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General and clinical immunology. Lecture notes: briefly, the most important

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Table of contents

1. Introduction to immunology. The body's defenses and disease
2. Organs of the immune system (Thymus. Lymph nodes. Spleen. Lymphoid tissue associated with mucous membranes. Excretory system. Cells of the immune system. Substances with protective complexes
3. Immunity is the shield of health. Mechanisms of immunity
4. immune status. Immunodeficiency states (Immune status. Congenital immunodeficiencies. Diseases of cellular immunity. Partial combined immunodeficiency states. Acquired immunodeficiencies
5. Pathological immune reactions of the body. Allergic diseases (General etiology of allergic diseases. Pathogenesis of allergic processes. Drug allergy
6. Ways to strengthen the immune system. Preventive immunization

During his life, every person in everyday life, at work, on vacation constantly interacts with numerous and very diverse natural objects and phenomena that determine the conditions of life in which a person exists. These are the sun, air, water, vegetable and animal foodstuffs, chemicals, plants and animals that provide the vital needs of man. The human body, due to biological evolution, is adapted to certain environmental conditions. At the same time, the normal vital activity of the organism and its interaction with the environment are quantitatively and qualitatively limited. Some interactions are healthy, others are harmful. The attitude of the organism to various factors is determined by the level of its adaptation. If the forces of influence of external factors exceed the norm or do not reach it, the body can be damaged, which will lead to illness. Causes of damage to the body, leading to disease, can be any natural phenomena: physical, chemical, biological. Physical factors include mechanical loads: impacts, stretching, squeezing, tissue bending. As a result, cuts, crushing, stretching and tearing of tissues, and bone fractures occur. The damaging factors also include changes in the temperature of the environment, which result in overheating of the body and burns of tissues or hypothermia of the body and frostbite of tissues. Biological influences include all types of human interaction with living beings. Roughly they can be divided into three groups: macropredators, micropredators and plants. Macropredators include animals that, when attacking a person with their bites or claws, can introduce poison into the human body that damages its tissues. But the most diverse ways of damaging the body are micropredators - the smallest parasites that live and multiply in the human body, ranging from viruses to various worms. Of the huge number of microorganisms, more than 2000 species have pathogenicity, including bacteria and rickettsia cause 1000 types of diseases, viruses - 500, fungi - 500, helminths - 200. The same parasite, depending on its localization, can contribute to the development of various diseases.

Thus, the body is constantly exposed to various pathogenic environmental factors. At the same time, many people remain healthy. Why can a person resist the harmful effects of the environment? What helps the body to fight them? In the process of human biological evolution, systems and mechanisms have been formed that protect it as an integrity in cases where physical, chemical or biological environmental factors can, when the organism interacts with them, lead to damage to any of its structures, which in turn causes their pathologies. As you know, with many diseases, a person recovers without the intervention of medicine, and damaged tissues are restored on their own. Consequently, the human body is able to protect itself from damage, fight pathology on its own.

Modern medical science bases the doctrine of the causes of pathology on the concept of "reactivity", i.e., the ability of the body, when interacting with various damaging effects, to give a protective "response" corresponding to the nature of this pathogenic effect. In the course of evolution, a person has developed biological mechanisms for protecting the body from the harmful effects of natural forces, certain protective reactions have been formed to any environmental influences. Changes in the environment lead to a change in its physiological processes in the body, corresponding to the new impact. In this way, balance is maintained with the environment that determines the possibilities of its vital activity. The protective reaction of the body is manifested in a certain change in its characteristics, which allows you to save the vital activity of the body as a whole. The way the body reacts to harmful effects in each particular case will be reflected in the type and number of effects experienced by a person. A person, for example, without harm to himself, endures physical activity within certain limits. However, the absence of loads (hypodynamia) or, conversely, overloads (hyperdynamia) can lead to pathology. A person does not react to some microorganisms as harmful, although they are pathogenic for animals. Others have a damaging effect on the body and activate protective mechanisms, that is, they cause a protective reaction that can lead to pathology. This shows the specific selectivity of the protective mechanisms of the human body. There are microorganisms that cause disease in humans and are not pathogenic for animals, and vice versa. The peculiarities of a particular human body are that some people do not get sick in the midst of an epidemic, while others just need to stand at an open window or drink a glass of cold water. The state of the body depends on the damaging factor: physical exhaustion, hypothermia, stress can cause a disease in a person whose body under normal conditions does not respond to one or another damaging factor. At the same time, elation and excitement can lead to an increase in the body's resistance to the disease. Protective reactions differ in the degree of manifestation and the nature of the systems involved in them. Up to a certain quantitative threshold (individual for each organism) of the impact of a pathogenic factor, the systems that carry out protective reactions do not allow it to cause damage to the body. If this threshold is exceeded, the reaction includes adaptive, adaptive-compensatory mechanisms that restructure the body and its elements to combat the pathogenic factor. The adaptive reactions of a particular organism depend on how well the defense mechanisms are adapted to interact with the pathogen. In the most general form, the following types of protective and adaptive mechanisms can be distinguished:

1) morphological: barrier membranes enclosing protected cells, tissues or organs; proliferation (recovery) of cells of the affected tissue; hyperplasia, i.e., a quantitative increase in a cell or tissue against the norm;

2) physiological: activation of metabolic processes, formation of new mediators, enzymes or metabolic cycles and deactivation of existing ones;

3) immunological cellular-humoral systems aimed at protecting the body from the effects of other biosystems.

Of all these types of protective-adaptive mechanisms, the most important is the immune system. It depends on how powerful it is, whether a person will get sick or not. A well-functioning immune system is the best guarantee of good health. Good immunity is the main indicator of health, vitality of any living organism. This is a powerful inner force with which nature has awarded all living beings. The immune system is a delicate organization: it reacts to the smallest changes in the internal and external environment of the body. It has long been noticed that a person who has had a dangerous infectious disease usually does not get sick a second time. In China, a method was invented to deal with severe cases of smallpox. The essence of this method was that smallpox crusts were ground into powder and brought into the nose of a healthy person. This was done in order to induce a mild form of smallpox. Immunity to re-infection with the same infection is due to immunity.

Immunity (from Latin immunitas - "getting rid of", "liberation from something") is the body's immunity to various infectious agents, as well as their metabolic products, substances and tissues that have alien antigenic properties (for example, animal and vegetable poisons origin). Once having been ill, our body remembers the causative agent of the disease, so the next time the disease proceeds faster and without complications. But often after long-term illnesses, surgical interventions, under adverse environmental conditions and in a state of stress, the immune system can malfunction. Reduced immunity is manifested by frequent and prolonged colds, chronic infectious diseases (tonsillitis, furunculosis, sinusitis, intestinal infections), constant fever, etc.

If we summarize all of the above, then we can say that immunity is a way to protect the body from living bodies and substances that carry signs of genetically alien information. The most ancient and stable mechanism of tissue interaction with any external damaging environmental factors (antigens) is phagocytosis. Phagocytosis in the body is carried out by special cells - macrophages, microphages and monocytes (cells - precursors of macrophages). This is a complex multi-stage process of capturing and destroying all micro-objects that are foreign to them in the tissues, without touching their own tissues and cells. Phagocytes, moving in the intercellular fluid of the tissue, upon meeting with the antigen, capture it and digest it before it comes into contact with the cell. This defense mechanism was discovered by I. M. Mechnikov in 1883 and was the basis of his theory of phagocytic defense of the body against pathogenic microbes. Wide participation of macrophages in various immunological processes has been established. In addition to protective reactions against various infections, macrophages are involved in antitumor immunity, antigen recognition, regulation of immune processes and immune surveillance, in the recognition and destruction of single altered cells of their own body, including tumor cells, in the regeneration of various tissues and in inflammatory reactions. Macrophages also produce various substances that have anti-antigenic effects.

Phagocytosis includes several stages:

1) directed movement of the phagocyte towards an object foreign to the tissue;

2) attachment of the phagocyte to it;

3) recognition of a microbe or antigen;

4) its absorption by a phagocyte cell (actual phagocytosis);

5) killing the microbe with the help of enzymes secreted by the cell;

6) digestion of the microbe.

But in some cases, the phagocyte cannot kill certain types of microorganisms, which are even able to multiply in it. That is why phagocytosis cannot always protect the body from damage. Promotes phagocytosis in the presence of intercellular fluid circulation systems in the body. The vascular transport of the intercellular fluid made it possible to concentrate phagocytes more quickly at the sites of penetration of the damaging factor into the tissue and, at the same time, contributed to the acceleration and direction of the action of chemicals (mediators) that attract phagocytes to the desired point. Thus, the inflammatory process is a local compensatory mechanism that ensures the restoration of a damaged tissue area that has been changed as a result of interaction with a damaging factor of any nature. In the process of evolution, a specific defense system appeared, which, unlike local defense during phagocytosis, operates at the level of the whole organism. This is the immune system, aimed at protecting the body from damaging factors of biological origin. The immune system protects the life support of the whole organism, is a highly specialized system that turns on when local non-specific defense mechanisms have exhausted their capabilities.

Initially, the immune system was designed to control the reproduction of a large number of differentiated cells with different structures and functions, as well as to protect against cell mutations. A mechanism arose designed to recognize and destroy cells that are genetically different from the cells of the body, but so similar to them that the phagocytosis mechanism could not recognize and destroy them, and prevent them from multiplying. The mechanism of immunity, originally formed for internal control over the cellular composition of the body, due to its effectiveness, was subsequently used against external damaging factors of a protein nature: viruses, bacteria and their metabolic products.

With the help of the immune system, the reactivity of the organism to certain types of microorganisms is formed and fixed genetically, for interaction with which it is not adapted, and the absence of a reaction of tissues and organs to other species. There are specific and individual forms of immunity. Both forms can be absolute, when the organism and the microbe do not interact directly under any conditions (for example, a person does not get sick with canine distemper), or relative, when the interaction between them can occur under certain conditions that weaken the body's immunity: hypothermia, hunger, overload, and etc. The function of the immune system is to compensate for the insufficiency of nonspecific forms of body defense against antigens in cases where phagocytes cannot destroy the antigen if it has specific defense mechanisms. So, for example, some bacteria and viruses can multiply inside the macrophage that has absorbed them. Moreover, drugs, such as antibiotics, do not work on them in this condition. Therefore, the immune system is characterized by great complexity, duplication of the functions of individual elements, includes cellular and humoral elements designed to accurately identify and then destroy microbes and their metabolic products. The system is self-regulating, reacting not only to the number of microbes, including successively its elements, increasing the sensitivity of non-specific levels of the defense reaction and stopping the immune reaction at the right time. Thus, the formation in the course of evolution and the comprehensive improvement of special anti-protein defenses play a huge role in protecting the health of the body.

Protein is the carrier of life, maintaining the purity of its protein structure is the duty of a living system. This defense, raised to the highest level in the living organism, includes two types of protective forces. On the one hand, there is the so-called innate immunity, which is of a non-specific nature, that is, directed generally against any foreign protein. It is known that from the huge army of microbes that constantly enter our body, only an insignificant part manages to cause a particular disease. On the other hand, there is acquired immunity - a striking protective mechanism that occurs during the life of a given organism and is of a specific nature, that is, directed at one specific foreign protein. Immunity, which arose after the transfer of a certain disease, is called acquired. Specific immunity is provided by immune mechanisms and has a humoral and cellular basis. Foreign particles-antigens can settle in the human body, penetrating into it through the skin, nose, mouth, eyes, ears. Fortunately, most of these "enemies" die when they try to get inside the body. The human body contains a large number of glands and tissues, which, at the command of the central nervous system, produce so-called immunocompetent cells. They, being in a state of constant "combat readiness", perform certain functions.

LECTURE No. 2. Organs of the immune system

The organs of the immune system are the bone marrow, thymus, spleen, appendix, lymph nodes, lymphoid tissue diffusely scattered in the mucous base of the internal organs, and numerous lymphocytes that are found in the blood, lymph, organs and tissues. In the bone marrow and thymus, lymphocytes differentiate from stem cells. They belong to the central organs of the immune system. The remaining organs are peripheral organs of the immune system, where lymphocytes are evicted from the central organs. The total weight of all organs representing the immune system of an adult is not more than 1 kg. Central to the immune system are lymphocytes, white blood cells whose function was a mystery until the 1960s. Lymphocytes normally make up about a quarter of all leukocytes. The body of an adult contains 1 trillion lymphocytes with a total mass of about 1,5 kg. Lymphocytes are produced in the bone marrow. They are round small cells, only 7-9 microns in size. The main part of the cell is occupied by the nucleus, covered with a thin membrane of the cytoplasm. As mentioned above, lymphocytes are found in the blood, lymph, lymph nodes, and spleen. It is lymphocytes that are the organizers of the immune reaction, or "immune response". One of the important organs of the immune system is the thymus gland, or thymus. It is a small organ located behind the breastbone. The thymus is small. It reaches its greatest value - approximately 25 g - during puberty, and by the age of 60 it significantly decreases and weighs only 6 g. The thymus is literally filled with lymphocytes that come here from the bone marrow. Such lymphocytes are called thymus-dependent, or T-lymphocytes. The task of T-lymphocytes is to recognize the "foreign" in the body, to detect a gene reaction.

Another type of lymphocytes is also formed in the bone marrow, but then it does not get into the thymus, but into another organ. So far, this organ has not been found in humans and mammals. It is found in birds - it is an accumulation of lymphoid tissue located near the large intestine. By the name of the researcher who discovered this formation, it is called the bursa of Fabricius (from Latin bursa - "bag"). If the bursa of Fabricius is removed from the chickens, then they stop producing antibodies. This experience shows that another type of lymphocytes, which produces antibodies, is "learning immunological literacy" here. Such lymphocytes were called B lymphocytes (from the word "bursa"). Although a similar organ has not yet been found in humans, the name of the corresponding type of lymphocytes has taken root - these are B-lymphocytes. T-lymphocytes and B-lymphocytes, as well as macrophages and granulocytes (neutrophils, eosinophils and basophils) are all the main cells of the immune system. In turn, several classes of T-lymphocytes are distinguished: T-killers, T-helpers, T-suppressors. T-killers (from the English kill - "kill") destroy cancer cells, T-helpers (from the English help - "help") help produce antibodies - immunoglobulins, and T-suppressors (from the English suppress - "suppress "), on the contrary, suppress the production of antibodies when it is necessary to stop the immune response. In addition to lymphocytes, the body has large cells - macrophages located in some tissues. They capture and digest foreign microorganisms. Leukocytes, in addition to invading foreign agents, also destroy malfunctioning, damaged cells that can degenerate into cancerous ones. They produce antibodies that fight specific bacteria and viruses. The circulating lymph picks up toxins and waste products from the tissues and blood and transports them to the kidneys, skin, and lungs for removal from the body. The liver and kidneys have the ability to filter toxins and waste products from the blood. In order for the functioning of the immune system to be normal, a certain ratio between all types of cells must be observed. Any violation of this ratio leads to pathology. This is the most general information about the organs of the immune system. They should be considered in more detail.

The state of immunity is associated mainly with the coordinated activity of three types of leukocytes: B-lymphocytes, T-lymphocytes and macrophages. Initially, the formation of them or their precursors (stem cells) occurs in the red bone marrow, then they migrate to the lymphoid organs. There is a peculiar hierarchy of organs of the immune system. They are divided into primary (where lymphocytes are formed) and secondary (where they function). All these organs are connected to each other and to other tissues of the body with the help of blood lymphatic vessels, through which leukocytes move. The primary organs are the thymus (thymus gland) and bursa (in birds), as well as the red bone marrow (possibly the appendix) in humans: hence the T- and B-lymphocytes, respectively. "Training" is aimed at acquiring the ability to differentiate one's own from another's (recognize antigens). To be recognized, body cells synthesize special proteins. Secondary lymphoid organs include the spleen, lymph nodes, adenoids, tonsils, appendix, peripheral lymph follicles. These organs, like the immune cells themselves, are scattered throughout the human body to protect the body from antigens. In the secondary lymphoid organs, the development of an immune response to the antigen occurs. An example is a sharp increase in lymph nodes near the affected organ in inflammatory diseases. The lymphoid organs at first glance appear to be a small body system, but it has been estimated that their total mass is more than 2,5 kg (which, for example, is more than the mass of the liver). In the bone marrow, cells of the immune system are formed from the progenitor stem cell (the ancestor of all blood cells). B-lymphocytes also undergo differentiation there. The transformation of a stem cell into a B-lymphocyte occurs in the bone marrow. The bone marrow is one of the main sites for antibody synthesis. For example, in an adult mouse, up to 80% of the cells that synthesize immunoglobulins are located in the bone marrow. It is possible to restore the immune system in lethally irradiated animals with the help of intravenous injection of bone marrow cells.

1. Thymus

The thymus is located directly behind the sternum. It is formed earlier than other organs of the immune system (already at the 6th week of pregnancy), but by the age of 15 it undergoes a reverse development, in adults it is almost completely replaced by fatty tissue. Penetrating from the bone marrow into the thymus, under the influence of hormones, the stem cell first turns into the so-called thymocyte (the cell - the precursor of the T-lymphocyte), and then, penetrating into the spleen or lymph nodes, it turns into a mature, immunologically active T-lymphocyte. Most of the T-lymphocytes become the so-called T-killers (killers). A smaller part performs a regulatory function: T-helpers (helpers) enhance immunological reactivity, T-suppressors (suppressors), on the contrary, reduce it. Unlike B-lymphocytes, T-lymphocytes (mainly T-helpers), with the help of their receptors, are able to recognize not just someone else's, but also their own, that is, a foreign antigen should be presented most often by macrophages in combination with the body's own proteins. In the thymus, along with the formation of T-lymphocytes, thymosin and thymopoietin are produced - hormones that ensure the differentiation of T-lymphocytes and play a certain role in cellular immune responses.

2. Lymph nodes

Lymph nodes are peripheral organs of the immune system that are located along the course of the lymphatic vessels. The main functions are the retention and prevention of the spread of antigens, which is carried out by T-lymphocytes and B-lymphocytes. They are a kind of filter for microorganisms carried by the lymph. Microorganisms pass through the skin or mucous membranes, enter the lymphatic vessels. Through them, they penetrate into the lymph nodes, where they linger and are destroyed. Functions of the lymph nodes:

1) barrier - they are the first to react to contact with a damaging agent;

2) filtration - they delay microbes, foreign particles, tumor cells penetrating with lymph current;

3) immune - associated with the production of immunoglobulins and lymphocytes in the lymph nodes;

4) synthetic - the synthesis of a special leukocyte factor, which stimulates the reproduction of blood cells;

5) exchange - lymph nodes are involved in the metabolism of fats, proteins, carbohydrates and vitamins.

3. Spleen

The spleen has a structure similar to that of the thymus gland. In the spleen, hormone-like substances are formed that are involved in the regulation of the activity of macrophages. In addition, phagocytosis of damaged and old red blood cells occurs here. Functions of the spleen:

1) synthetic - it is in the spleen that the synthesis of immunoglobulins of classes M and J is carried out in response to the entry of an antigen into the blood or lymph. The spleen tissue contains T and B lymphocytes;

2) filtration - in the spleen, the destruction and processing of substances alien to the body, damaged blood cells, coloring compounds and foreign proteins occur.

4. Lymphoid tissue associated with mucous membranes

This type of lymphoid tissue is located under the mucous membrane. These include the appendix, lymphoid ring, intestinal lymph follicles, and adenoids. Accumulations of lymphoid tissue in the intestine - Peyer's patches. This lymphoid tissue is a barrier to the penetration of microbes through the mucous membranes. Functions of lymphoid accumulations in the intestines and tonsils:

1) recognition - the total surface area of ​​​​the tonsils in children is very large (almost 200 cm²). On this area there is a constant interaction of antigens and cells of the immune system. It is from here that information about a foreign agent follows to the central organs of immunity: thymus and bone marrow;

2) protective - on the mucous membrane of the tonsils and Peyer's patches in the intestine, in the appendix there are T-lymphocytes and B-lymphocytes, lysozyme and other substances that provide protection.

5. Excretory system

Thanks to the excretory system, the body is cleansed of microbes, their waste products and toxins.

The set of microorganisms that inhabit the skin and mucous membranes of a healthy person is a normal microflora. These microbes have the ability to resist the defense mechanisms of the body itself, but they are not able to penetrate tissues. The normal intestinal microflora has a great influence on the intensity of the immune response in the digestive organs. Normal microflora inhibits the development of pathogenic microflora. For example, in a woman, the normal microflora of the vagina is represented by lactic acid bacteria, which in the process of life create an acidic environment that prevents the development of pathogenic microflora.

The internal environment of our body is delimited from the outside world by the skin and mucous membranes. They are the mechanical barrier. In the epithelial tissue (it is located in the skin and mucous membranes), the cells are very strongly interconnected by intercellular contacts. This obstacle is not easy to overcome. The ciliated epithelium of the respiratory tract removes bacteria and dust particles thanks to the oscillation of the cilia. The skin contains sebaceous and sweat glands. Sweat contains lactic and fatty acids. They lower the pH of the skin, harden it. The reproduction of bacteria is inhibited by hydrogen peroxide, ammonia, urea, bile pigments contained in sweat. The lacrimal, salivary, gastric, intestinal and other glands, whose secrets are secreted on the surface of the mucous membranes, intensively fight microbes. First, they simply wash them off. Secondly, some fluids secreted by the internal glands have a pH that damages or destroys bacteria (for example, gastric juice). Thirdly, the salivary and lacrimal fluids contain the enzyme lysozyme, which directly destroys bacteria.

6. Cells of the immune system

And now let us dwell in more detail on the consideration of cells that ensure the coordinated work of immunity. The direct executors of immune reactions are leukocytes. Their purpose is to recognize foreign substances and microorganisms, to fight them, and to record information about them.

There are the following types of leukocytes:

1) lymphocytes (T-killers, T-helpers, T-suppressors, B-lymphocytes);

2) neutrophils (stab and segmented);

3) eosinophils;

4) basophils.

Lymphocytes are the main figures in immunological surveillance. In the bone marrow, the precursors of lymphocytes are divided into two major branches. One of them (in mammals) ends its development in the bone marrow, and in birds - in a specialized lymphoid organ - the bursa (bag). These are B-lymphocytes. After B-lymphocytes leave the bone marrow, they circulate in the bloodstream for a short time, and then they are introduced into peripheral organs. They seem to be in a hurry to fulfill their mission, since the life span of these lymphocytes is short - only 7-10 days. A variety of B-lymphocytes is formed already during fetal development, and each of them is directed against a specific antigen. Another part of the lymphocytes from the bone marrow migrates to the thymus, the central organ of the immune system. This branch is T-lymphocytes. After completion of development in the thymus, some of the mature T-lymphocytes continue to be in the medulla, and some leave it. A significant part of T-lymphocytes become T-killers, a smaller part performs a regulatory function: T-helpers increase immunological reactivity, and T-suppressors, on the contrary, weaken it. Helpers are able to recognize the antigen and activate the corresponding B-lymphocyte (directly upon contact or at a distance with the help of special substances - lymphokines). The most well-known lymphokine is interferon, which is used in medicine in the treatment of viral diseases (for example, influenza), but it is effective only at the initial stage of the onset of the disease.

Suppressors have the ability to turn off the immune response, which is very important: if the immune system is not suppressed after neutralizing the antigen, the components of the immune system will destroy the body's own healthy cells, which will lead to the development of autoimmune diseases. Killers are the main link of cellular immunity, as they recognize antigens and effectively affect them. Killers act against cells that are affected by viral infections, as well as tumor, mutated, aging cells of the body.

Neutrophils, basophils and eosinophils are types of white blood cells. They got their names for the ability to perceive coloring matter in different ways. Eosinophils react mainly to acidic dyes (Congo red, eosin) and are pink-orange in blood smears; basophils are alkaline (hematoxylin, methyl blue), so they look blue-violet in smears; neutrophils perceive both of them, therefore they stain with a gray-violet color. The nuclei of mature neutrophils are segmented, that is, they have constrictions (therefore they are called segmented), the nuclei of immature cells are called stab. One of the names of neutrophils (microphagocytes) indicates their ability to phagocytize microorganisms, but in smaller quantities than macrophages do. Neutrophils protect against the penetration of bacteria, fungi and protozoa into the body. These cells eliminate dead tissue cells, remove old red blood cells and clean the wound surface. When evaluating a detailed blood test, a sign of an inflammatory process is a shift in the leukocyte formula to the left with an increase in the number of neutrophils.

Eosinophils take part in the destruction of parasites (they secrete special enzymes that have a damaging effect on them), in allergic reactions.

Macrophages (aka phagocytes) are "eaters" of foreign bodies and the most ancient cells of the immune system. Macrophages are derived from monocytes (a type of white blood cell). They pass the first stages of development in the bone marrow, and then leave it in the form of monocytes (rounded cells) and circulate in the blood for a certain time. From the bloodstream, they enter all tissues and organs, where they change their rounded shape to another, with processes. It is in this form that they acquire mobility and are able to stick to any potentially foreign bodies. They recognize some foreign substances and signal them to T-lymphocytes, and those, in turn, to B-lymphocytes. Then B-lymphocytes begin to produce antibodies - immunoglobulins against the agent, which was "reported" by the phagocyte cell and T-lymphocyte. Sedentary macrophages can be found in almost all human tissues and organs, which provides an equivalent response of the immune system to any antigen that enters the body anywhere. Macrophages eliminate not only microorganisms and foreign chemical poisons that enter the body from outside, but also dead cells or toxins produced by their own body (endotoxins). Millions of macrophages surround them, absorb and dissolve them in order to remove them from the body. A decrease in the phagocytic activity of blood cells contributes to the development of a chronic inflammatory process and the emergence of aggression against the body's own tissues (the appearance of autoimmune processes). With the inhibition of phagocytosis, dysfunction of the destruction and excretion of immune complexes from the body is also observed.

7. Substances with protective complexes

Immunoglobulins (antibodies) are a protein molecule. They combine with a foreign substance and form an immune complex, circulate in the blood and are located on the surface of the mucous membranes. The main feature of antibodies is the ability to bind a strictly defined antigen. For example, with measles, the body begins to produce "anti-measles" immunoglobulin, against influenza - "anti-influenza", etc. The following classes of immunoglobulins are distinguished: JgM, JgJ, JgA, JgD, JgE. JgM - this type of antibody appears very first upon contact with an antigen (microbe), an increase in their titer in the blood indicates an acute inflammatory process, JgM play an important protective role when bacteria enter the bloodstream in the early stages of infection. JgJ - antibodies of this class appear some time after contact with the antigen. They participate in the fight against microbes - they form complexes with antigens on the surface of a bacterial cell. Subsequently, other plasma proteins (the so-called complement) join them, and the bacterial cell is lysed (its membrane is torn). In addition, JgJ are involved in some allergic reactions. They make up 80% of all human immunoglobulins, they are the main protective factor in a child in the first weeks of life, as they have the ability to pass through the placental barrier into the fetal blood serum. With natural feeding, antibodies from mother's milk through the intestinal mucosa of the newborn penetrate into his blood.

JgA - are produced by lymphocytes of the mucous membranes in response to local exposure to a foreign agent, thus they protect the mucous membranes from microorganisms and allergens. JgA inhibit the adhesion of microorganisms to the surface of cells and thereby prevent the penetration of microbes into the internal environment of the body. This is what prevents the development of chronic local inflammation.

JgD is the least studied. Researchers suggest that it is involved in the body's autoimmune processes.

JgE - antibodies of this class interact with receptors that are located on mast cells and basophils. As a result, histamine and other mediators of allergy are released, resulting in an allergic reaction. Upon repeated contact with the allergen, JgE interaction occurs on the surface of blood cells, which leads to the development of an anaphylactic allergic reaction. In addition to allergic reactions, JgE is involved in antihelminthic immunity.

Lysozyme. Lysozyme is present in all body fluids: in tears, saliva, blood serum. This substance is produced by blood cells. Lysozyme is an antibacterial enzyme that can dissolve the shell of the microbe and cause its death. When exposed to bacteria, lysozyme needs the support of another factor of natural immunity - the complement system.

Complement. This is a group of protein compounds involved in the chain of immune reactions. Complement can participate in the destruction of bacteria, preparing them for absorption by macrophages. The complement system consists of nine complex biochemical compounds. By changing the concentrations of any of them, one can judge the place of a possible pathology in the link of immunity.

Interferons. These substances provide antiviral immunity, increase the resistance of cells to the effects of viruses, thereby preventing their reproduction in cells. These substances are produced mainly by leukocytes and lymphocytes. The result of the action of interferons is the formation of a barrier around the focus of inflammation from cells that are not infected with the virus. Of all the above organs of immunity, only the thymus undergoes reverse development. This process usually occurs after 15 years, but sometimes the thymus gland does not undergo age-related involution. As a rule, this happens with a decrease in the activity of the adrenal cortex and a lack of hormones that are produced in it. Then pathological conditions develop: susceptibility to infections and intoxications, the development of tumor processes. Children may have thymomegaly - an increase in the thymus. Often this leads to protracted courses of colds and is accompanied by allergic reactions.

LECTURE No. 3. Immunity is a shield of health. Mechanisms of immunity

A well-coordinated, well-regulated activity of the biological protective devices of the body allows it to interact without harm to health with various environmental factors in which it exists and acts. The immune response begins immediately after the penetration of a foreign agent into the body, but only when passing through the first line of defense of the immune system. Intact mucosal membranes and skin by themselves present significant barriers to pathogens and produce many antimicrobial agents themselves. More specialized defenses include high acidity (pH around 2,0) in the stomach, mucus, and mobile cilia in the bronchial tree.

The range of safe environmental influences is limited by the specifics of the species and the characteristics of the individual person, the rate of adaptation of the individual, his specific phenotype, that is, the totality of the properties of the organism that are congenital and acquired during his life. Each person inherits genetic traits in different amounts while maintaining the genotype in its defining features. Each person is biologically unique because, within certain genotypes, deviations of some specific traits are possible, creating the uniqueness of each organism, and, consequently, the individual rate of its adaptation when interacting with various environmental factors, including the difference in the level of protection of the organism from damaging factors.

If the quality of the environment corresponds to the rate of adaptation of the organism, its protective systems ensure the normal reaction of the organism to the interaction. But the conditions in which a person carries out his life activity are changing, in some cases going beyond the limits of the body's adaptation norm. And then, in extreme conditions for the body, adaptive-compensatory mechanisms are activated that ensure the adaptation of the body to increased loads. Protective systems begin to carry out adaptive reactions, the ultimate goals of which are to preserve the body in its integrity, to restore the disturbed balance (homeostasis). A damaging factor, by its action, causes a breakdown of a certain structure of the body: cells, tissues, sometimes an organ. The presence of such a breakdown turns on the mechanism of pathology, causes an adaptive reaction of protective mechanisms. The breakdown of the structure leads to the fact that the damaged element changes its structural connections, adapts, trying to maintain its "duties" in relation to the organ or organism as a whole. If he succeeds, then due to such an adaptive restructuring, a local pathology arises, which is compensated by the protective mechanisms of the element itself and may not affect the activity of the organism, although it will reduce its rate of adaptation. But with a large overload (within the limits of the organism's adaptation rate), if it exceeds the element's adaptation rate, the element can be destroyed in such a way that it changes its functions, i.e., it malfunctions. Then a compensatory reaction is carried out on the part of a higher level of the organism, the function of which can be impaired as a result of the dysfunction of its element. The pathology is on the rise. Thus, cell breakdown, if it cannot be compensated by its hyperplasia, will cause a compensatory reaction from the tissue. If tissue cells are destroyed in such a way that the tissue itself is forced to adapt (inflammation), then compensation will come from the healthy tissue, i.e., the organ will turn on. Thus, in turn, higher and higher levels of the body can be included in the compensatory reaction, which ultimately will lead to the pathology of the whole organism - a disease when a person cannot normally carry out his biological and social functions.

A disease is not only a biological phenomenon, but also a social one, in contrast to the biological concept of "pathology". According to WHO definition, health is "a state of complete physical, mental and social well-being". In the mechanism of the development of the disease, two levels of the immunological system are distinguished: nonspecific and specific. The founders of immunology (L. Pasteur and I. I. Mechnikov) originally defined immunity as immunity to infectious diseases. Currently, immunology defines immunity as a method of protecting the body from living bodies and substances that bear signs of foreignness. The development of the theory of immunity enabled medicine to solve such problems as the safety of blood transfusions, the creation of vaccines against smallpox, rabies, anthrax, diphtheria, polio, whooping cough, measles, tetanus, gas gangrene, infectious hepatitis, influenza and other infections. Thanks to this theory, the danger of Rh-hemolytic disease of newborns was eliminated, organ transplantation was introduced into the practice of medicine, and the diagnosis of many infectious diseases became possible. Already from the examples cited it is clear what tremendous importance for the preservation of human health was the knowledge of the laws of immunology. But even more important for medical science is the further disclosure of the secrets of immunity in the prevention and treatment of many diseases dangerous to human health and life. The non-specific defense system is designed to withstand the action of various damaging factors external to the body of any nature.

When a disease occurs, the nonspecific system carries out the first, early defense of the body, giving it time to turn on a full-fledged immune response from the specific system. Nonspecific protection includes the activity of all body systems. It forms an inflammatory process, fever, mechanical release of damaging factors with vomiting, coughing, etc., changes in metabolism, activation of enzyme systems, excitation or inhibition of various parts of the nervous system. Mechanisms of nonspecific protection include cellular and humoral elements that have a bactericidal effect on their own or in combination.

The specific (immune) system reacts to the penetration of a foreign agent in the following way: upon initial entry, a primary immune response develops, and upon repeated penetration into the body, a secondary one. They have certain differences. In a secondary response to an antigen, immunoglobulin J is immediately produced. The first interaction of an antigen (virus or bacterium) with a lymphocyte causes a reaction called the primary immune response. During it, lymphocytes begin to develop gradually, undergoing differentiation: some of them become memory cells, others are transformed into mature cells that produce antibodies. At the first encounter with an antigen, antibodies of the immunoglobulin class M first appear, then J, and later A. A secondary immune response develops upon repeated contact with the same antigen. In this case, there is already a faster production of lymphocytes with their transformation into mature cells and the rapid production of a significant amount of antibodies that are released into the blood and tissue fluid, where they can meet with the antigen and effectively overcome the disease. Let's consider both (non-specific and specific) body defense systems in more detail.

The nonspecific defense system, as mentioned above, includes cellular and humoral elements. Cellular elements of nonspecific protection are the phagocytes described above: macrophages and neutrophilic granulocytes (neutrophils, or macrophages). These are highly specialized cells that differentiate from stem cells produced by the bone marrow. Macrophages constitute a separate mononuclear (single-nuclear) system of phagocytes in the body, which includes bone marrow promonocytes, blood monocytes that differentiate from them, and tissue macrophages. Their feature is active mobility, the ability to adhere and intensively carry out phagocytosis. Monocytes, having matured in the bone marrow, circulate for 1-2 days in the blood, and then penetrate into tissues, where they mature into macrophages and live for 60 or more days.

Macrophages contain enzymes for the digestion of phagocytosed substances. These enzymes are contained in vacuoles (vesicles) called lysosomes and are able to break down proteins, fats, carbohydrates, and nucleic acids. Macrophages cleanse the human body of particles of inorganic origin, as well as bacteria, viral particles, dying cells, toxins - toxic substances formed during the decay of cells or produced by bacteria. In addition, macrophages secrete some humoral and secretory substances into the blood: complement elements C₂, FROM₃, FROM₄, lysozyme, interferon, interleukin-1, prostaglandins, α₂-macroglobulin, monokines that regulate the immune response, cytotoxins - substances that are toxic to cells. We will consider the issue of these substances and their role in the defense system in more detail later. Macrophages have a subtle mechanism for recognizing foreign particles of an antigenic nature. They distinguish and quickly absorb old and newborn erythrocytes, without touching the normal ones. For a long time, the role of "cleaners" was assigned to macrophages, but they are also the first link in a specialized defense system. Macrophages, including the antigen in the cytoplasm, recognize it with the help of enzymes. Substances are released from lysosomes that dissolve the antigen within approximately 30 minutes, after which it is excreted from the body. But some antigens cannot be completely digested; they are degraded and excreted from macrophages during the day. The antigen processed in this way carries a “mark” that cells or humoral elements of specific protection are able to perceive. The antigen is expressed and recognized by macrophages, after which it passes to lymphocytes. Neutrophil granulocytes (neutrophils, or microphages) are also formed in the bone marrow, from where they enter the bloodstream, where they circulate for 6-24 hours. Unlike macrophages, mature microphages receive energy not from respiration, but from glycolysis, like prokaryotes, i.e. become anaerobes, and can carry out their activities in anoxic zones, for example, in exudates during inflammation, complementing the activity of macrophages. Macrophages and microphages on their surface carry receptors for immunoglobulin JgJ and complement element C3, which help the phagocyte in recognizing and attaching the antigen to the surface of its cell. Violation of the activity of phagocytes quite often manifests itself in the form of recurrent purulent-septic diseases, such as chronic pneumonia, pyoderma, osteomyelitis, etc. So, mucocutaneous candidiasis is the result of a defect in neutrophils, which makes them unable to kill the Candida fungus. This disease proceeds as a massive destruction of tissues and is not amenable to conventional methods of treatment, including intensive combined antibiotic therapy. In a number of infections, various acquisitions of phagocytosis occur. Thus, tuberculosis mycobacteria are not destroyed by phagocytosis. Staphylococcus inhibits its absorption by the phagocyte. Violation of the activity of phagocytes also leads to the development of chronic inflammation and diseases associated with the fact that the material accumulated by macrophages from the decomposition of phagocytized substances cannot be removed from the body due to the deficiency of some phagocyte enzymes. The pathology of phagocytosis may be associated with impaired interaction of phagocytes with other systems of cellular and humoral immunity. So, in infections, the pathogens of which parasitize inside the cell (tuberculosis, leprosy, listeriosis), activation of macrophages by T-lymphocytes is of great importance. Thus, the process of phagocytosis is influenced by factors of both nonspecific and specific defense systems. Phagocytosis is facilitated by normal antibodies and immunoglobulins, complement, lysozyme, leukins, interferon, and a number of other enzymes and blood secretions that pre-process the antigen, making it more accessible for capture and digestion by the phagocyte.

Complement is an enzyme system that consists of 11 blood serum proteins that make up 9 components (from C₁ to C₉) complement. The complement system stimulates phagocytosis, chemotaxis (attraction or repulsion of cells), the release of pharmacologically active substances (anaphylotoxin, histamine, etc.), enhances the bactericidal properties of blood serum, activates cytolysis (cell breakdown) and, together with phagocytes, takes part in the destruction of microorganisms and antigens . Each component of complement plays a role in the immune response. Yes, complement deficiency₁ causes a decrease in bactericidal blood plasma and contributes to the frequent development of infectious diseases of the upper respiratory tract, chronic glomerulonephritis, arthritis, otitis media, etc.

Complement C₃ prepares the antigen for phagocytosis. With its deficiency, the enzymatic and regulatory activity of the complement system is significantly reduced, which leads to more severe consequences than complement deficiency C₁ and C₂up to and including death. Its modification C_3a is deposited on the surface of the bacterial cell, which leads to the formation of holes in the shell of the microbe and its lysis, i.e., dissolution by lysozyme. With hereditary deficiency of component C₅ there are violations of the development of the child, dermatitis and diarrhea. Specific arthritis and bleeding disorders are observed in C deficiency.₆. Diffuse lesions of the connective tissue occur with a decrease in the concentration of components C₂ and C₇. Congenital or acquired insufficiency of complement components contributes to the development of various diseases, both as a result of a decrease in the bactericidal properties of the blood, and due to the accumulation of antigens in the blood. In addition to deficiency, activation of complement components also occurs. So, activation₁ leads to Quincke's edema, etc. Complement is actively consumed in thermal burns, when complement deficiency is created, which can determine an unfavorable outcome of thermal injury. Normal antibodies are found in the serum of healthy people who have not previously been ill. Apparently, these antibodies arise during inheritance, or antigens come with food without causing the corresponding disease. The detection of such antibodies indicates the maturity and normal functioning of the immune system. Normal antibodies include, in particular, properdin. It is a high molecular weight protein found in blood serum. Properdin provides bactericidal and virus-neutralizing properties of blood (together with other humoral factors) and activates specialized defense reactions.

Lysozyme is an enzyme called acetylmuramidase that breaks down the membranes of bacteria and lyses them. It is found in almost all tissues and body fluids. The ability to destroy the cell membranes of bacteria, from which destruction begins, is explained by the fact that lysozyme is found in high concentration in phagocytes and its activity increases during microbial infection. Lysozyme enhances the antibacterial action of antibodies and complement. It is part of saliva, tears, skin secretions as a means of enhancing the body's barrier defenses. Inhibitors (retarders) of viral activity are the first humoral barrier that prevents the contact of the virus with the cell.

People with a high content of highly active inhibitors are highly resistant to viral infections, while viral vaccines are ineffective for them. Nonspecific defense mechanisms - cellular and humoral - protect the internal environment of the body from various damaging factors of organic and inorganic nature at the tissue level. They are sufficient to ensure the vital activity of low-organized (invertebrate) animals. The complication of the organism of animals, in particular, has led to the fact that the nonspecific protection of the organism was insufficient. The complication of organization has led to an increase in the number of specialized cells that differ from each other. Against this general background, as a result of a mutation, cells harmful to the body could appear, or similar, but foreign cells could be introduced into the body. Genetic control of cells becomes necessary, and a specialized system for protecting the body from cells that differ from its native, necessary ones appears. It is likely that lymphatic defense mechanisms initially developed not to protect against external antigens, but to neutralize and eliminate internal elements that are "subversive" and threaten the integrity of the individual and the survival of the species. Species differentiation of vertebrates in the presence of a base-cell common to any organism, differing in structure and functions, led to the need to create a mechanism for distinguishing and neutralizing body cells, in particular mutant cells that, multiplying in the body, could lead to its death.

The mechanism of immunity, which arose as a means of internal control over the cellular composition of organ tissues, due to its high efficiency, is used by nature against damaging antigen factors: cells and products of their activity. With the help of this mechanism, the reactivity of the organism to certain types of microorganisms, to the interaction with which it is not adapted, and the immunity of cells, tissues and organs to others are formed and fixed genetically. Species and individual forms of immunity arise, which are formed, respectively, in adaptatiogenesis and adaptiomorphosis as manifestations of compensationogenesis and compensationomorphosis. Both forms of immunity can be absolute, when the organism and the microorganism practically do not interact under any conditions, or relative, when the interaction causes a pathological reaction in certain cases, weakening the body's immunity, making it susceptible to the effects of microorganisms that are safe under normal conditions. Let us turn to the consideration of a specific immunological defense system of the organism, the task of which is to compensate for the insufficiency of nonspecific factors of organic origin - antigens, in particular microorganisms and toxic products of their activity. It begins to act when nonspecific defense mechanisms cannot destroy an antigen that is similar in its characteristics to the cells and humoral elements of the organism itself or provided with its own protection. Therefore, a specific protection system is designed to recognize, neutralize and destroy genetically alien substances of organic origin: infectious bacteria and viruses, organs and tissues transplanted from another organism, which have changed as a result of mutation of the cells of one's own organism. The accuracy of discrimination is very high, up to the level of one gene that differs from the norm. The specific immune system is a collection of specialized lymphoid cells: T-lymphocytes and B-lymphocytes. There are central and peripheral organs of the immune system. The central ones include the bone marrow and thymus, the peripheral ones include the spleen, lymph nodes, lymphoid tissue of the intestines, tonsils and other organs, blood. All cells of the immune system (lymphocytes) are highly specialized, their supplier is the bone marrow, from the stem cells of which all forms of lymphocytes are differentiated, as well as macrophages, microphages, erythrocytes, and blood platelets.

The second most important organ of the immune system is the thymus gland. Under the influence of thymus hormones, thymus stem cells differentiate into thymus-dependent cells (or T-lymphocytes): they provide the cellular functions of the immune system. In addition to T-cells, the thymus secretes into the blood humoral substances that promote the maturation of T-lymphocytes in peripheral lymphatic organs (spleen, lymph nodes), and some other substances. The spleen has a structure similar to that of the thymus, but unlike the thymus, the lymphoid tissue of the spleen is involved in humoral immune responses. The spleen contains up to 65% of B-lymphocytes, which provide the accumulation of a large number of plasma cells that synthesize antibodies. Lymph nodes contain predominantly T-lymphocytes (up to 65%), and B-lymphocytes, plasma cells (derived from B-lymphocytes) synthesize antibodies when the immune system is just maturing, especially in children of the first years of life. Therefore, the removal of the tonsils (tonsillectomy), produced at an early age, reduces the body's ability to synthesize certain antibodies. Blood belongs to the peripheral tissues of the immune system and contains, in addition to phagocytes, up to 30% of lymphocytes. T-lymphocytes predominate among lymphocytes (50-60%). B-lymphocytes make up 20-30%, about 10% are killers, or "null-lymphocytes" that do not have the properties of T- and B-lymphocytes (D-cells).

As noted above, T-lymphocytes form three main subpopulations:

1) T-killers carry out immunological genetic surveillance, destroying mutated cells of their own body, including tumor cells and genetically alien transplant cells. T-killers make up to 10% of T-lymphocytes in peripheral blood. It is T-killers that, by their action, cause rejection of transplanted tissues, but this is also the first line of defense of the body against tumor cells;

2) T-helpers organize an immune response by acting on B-lymphocytes and giving a signal for the synthesis of antibodies against the antigen that has appeared in the body. T-helpers secrete interleukin-2, which acts on B-lymphocytes, and γ-interferon. They are in peripheral blood up to 60-70% of the total number of T-lymphocytes;

3) T-suppressors limit the strength of the immune response, control the activity of T-killers, block the activity of T-helpers and B-lymphocytes, suppressing the excessive synthesis of antibodies that can cause an autoimmune reaction, that is, turn against the body's own cells.

T-suppressors make up 18-20% of T-lymphocytes in peripheral blood. Excessive activity of T-suppressors can lead to suppression of the immune response up to its complete suppression. This happens with chronic infections and tumor processes. At the same time, insufficient activity of T-suppressors leads to the development of autoimmune diseases due to the increased activity of T-killers and T-helpers that are not restrained by T-suppressors. To regulate the immune process, T-suppressors secrete up to 20 different mediators that accelerate or slow down the activity of T- and B-lymphocytes. In addition to the three main types, there are other types of T-lymphocytes, including immunological memory T-lymphocytes, which store and transmit information about the antigen. When they encounter this antigen again, they provide its recognition and the type of immunological response. T-lymphocytes, performing the function of cellular immunity, in addition, synthesize and secrete mediators (lymphokines), which activate or slow down the activity of phagocytes, as well as mediators with cytotoxic and interferon-like actions, facilitating and directing the action of a nonspecific system. Another type of lymphocytes (B-lymphocytes) differentiates in the bone marrow and group lymphatic follicles and performs the function of humoral immunity. When interacting with antigens, B-lymphocytes change into plasma cells that synthesize antibodies (immunoglobulins). The surface of a B-lymphocyte can contain from 50 to 150 immunoglobulin molecules. As B-lymphocytes mature, they change the class of immunoglobulins they synthesize.

Initially synthesizing JgM class immunoglobulins, upon maturation, 10% of B-lymphocytes continue to synthesize JgM, 70% switch to JgJ synthesis, and 20% switch to JgA synthesis. Like T-lymphocytes, B-lymphocytes consist of several subpopulations:

1) B₁-lymphocytes - precursors of plasmocytes, synthesizing JgM antibodies without interacting with T-lymphocytes;

2) B₂-lymphocytes - precursors of plasma cells, synthesizing immunoglobulins of all classes in response to interaction with T-helpers. These cells provide humoral immunity to antigens recognized by T-helper cells;

3) B₃-lymphocytes (K-cells), or B-killers, kill antigen cells coated with antibodies;

4) B-suppressors inhibit the function of T-helpers, and memory B-lymphocytes, preserving and transmitting memory of antigens, stimulate the synthesis of certain immunoglobulins upon re-encounter with an antigen.

A feature of B-lymphocytes is that they specialize in specific antigens. When B-lymphocytes react with an antigen encountered for the first time, plasma cells are formed that secrete antibodies specifically against this antigen. A clone of B-lymphocytes is formed, responsible for the reaction with this particular antigen. With a repeated reaction, only B-lymphocytes multiply and synthesize antibodies, or rather, plasma cells directed against this antigen. Other clones of B-lymphocytes do not participate in the reaction. B-lymphocytes are not directly involved in the fight against antigens. Under the influence of stimuli from phagocytes and T-helpers, they are transformed into plasma cells, which synthesize antibodies immunoglobulins that neutralize antigens. Immunoglobulins are proteins in the blood serum and other body fluids that act as antibodies that bind to antigens and neutralize them. Currently, there are five classes of human immunoglobulins (JgJ, JgM, JgA, JgD, JgE), which differ significantly in their physicochemical properties and biological functions. Class J immunoglobulins make up about 70% of the total number of immunoglobulins. These include antibodies against antigens of various nature, produced by four subclasses. They mainly perform anti-bacterial functions and form antibodies against polysaccharides of bacterial membranes, as well as anti-rhesus antibodies, provide a skin sensitivity reaction and complement fixation.

Class M immunoglobulins (about 10%) are the most ancient, synthesized in the early stages of the immune response to most antigens. This class includes antibodies against polysaccharides of microorganisms and viruses, rheumatoid factor, etc. Class D immunoglobulins make up less than 1%. Their role in the body is almost not studied. There is evidence of their increase in certain infectious diseases, osteomyelitis, bronchial asthma, etc. Class E immunoglobulins, or reagins, have an even lower concentration. JgE play the role of a trigger in the deployment of immediate-type allergic reactions. By binding to the complex with the allergen, JgE causes the release of mediators of allergic reactions (histamine, serotonin, etc.) into the body. Class A immunoglobulins make up about 20% of the total number of immunoglobulins. This class includes antibodies against viruses, insulin (in diabetes mellitus), thyroglobulin (in chronic thyroiditis). A feature of this class of immunoglobulins is that they exist in two forms: serum (JgA) and secretory (SJgA). Class A antibodies neutralize viruses, neutralize bacteria, prevent the fixation of microorganisms on the cells of the epithelial surface of the mucous membranes. Summing up, we will draw the following conclusion: a specific system of immunological protection is a multi-level mechanism of the elements of the body that ensures their interaction and complementarity, including, as necessary, components of protection against any interaction of the body with damaging factors, duplicating, in necessary cases, the mechanisms of cellular protection by humoral means, and vice versa .

The immune system that has developed in the process of adaptatiogenesis, which has fixed the genetically specific reactions of the organism to damaging factors, is a flexible system. In the process of adaptiomorphosis, it is corrected, it includes new types of reactions to damaging factors, newly appeared, with which the body has not met before. In this sense, it plays an adaptive role, combining adaptive reactions, as a result of which the body's structures change under the influence of new environmental factors, and compensatory reactions that preserve the integrity of the body, seeking to reduce the price of adaptation. This price is irreversible adaptive changes, as a result of which the organism, adapting to new conditions of existence, loses the ability to exist under the original conditions. So, a eukaryotic cell, adapted to exist in an oxygen atmosphere, can no longer do without it, although anaerobes can do this. The price of adaptation in this case is the loss of the ability to exist in anaerobic conditions.

Thus, the immune system includes a number of components that independently engage in the fight against any foreign factors of organic or inorganic origin: phagocytes, T-killers, B-killers, and a whole system of specialized antibodies aimed at a specific enemy. The manifestation of the immune response of a specific immune system is diverse. If a mutated body cell acquires properties that are different from the properties of its genetically inherent cells (for example, tumor cells), T-killers infect the cells on their own, without the intervention of other elements of the immune system. B-killers also destroy recognized antigens coated with normal antibodies on their own. A complete immune response occurs against some antigens that first enter the body. Macrophages, phagocytizing such antigens of viral or bacterial origin, cannot completely digest them and throw them away after a while. The antigen that has passed through the phagocyte bears a label indicating its "indigestibility". The phagocyte thus prepares the antigen for "feeding" into the specific immune defense system. It recognizes the antigen and labels it accordingly. In addition, the macrophage simultaneously secretes interleukin-1, which activates T-helpers. T-helper, faced with such a "labeled" antigen, signals B-lymphocytes about the need for their intervention, secreting interleukin-2, which activates lymphocytes. The T-helper signal includes two components. First, it is a command to start an action; secondly, it is information about the type of antigen obtained from the macrophage. Having received such a signal, the B-lymphocyte turns into a plasma cell, which synthesizes the corresponding specific immunoglobulin, i.e., a specific antibody designed to counteract this antigen, which binds to it and renders it harmless.

Therefore, in the case of a complete immune response, the B-lymphocyte receives a command from the T-helper and information about the antigen from the macrophage. Other variants of the immune response are also possible. The T-helper, having encountered an antigen before being processed by a macrophage, gives a signal to the B-lymphocyte to produce antibodies. In this case, the B-lymphocyte turns into a plasma cell that produces nonspecific immunoglobulins of the JgM class. If a B-lymphocyte interacts with a macrophage without the participation of a T-lymphocyte, then, having not received a signal about the production of antibodies, the B-lymphocyte is not included in the immune response. At the same time, the immune reaction of antibody synthesis will begin if the B-lymphocyte interacts with an antigen corresponding to its clone processed by a macrophage, even in the absence of a signal from the T-helper, since it is specialized for this antigen.

Thus, the specific immune response provides for various cases of interaction between the antigen and the immune system. It involves a complement that prepares the antigen for phagocytosis, phagocytes that process the antigen and supply it to lymphocytes, T- and B-lymphocytes, immunoglobulins and other components. In the process of evolution, various scenarios for dealing with foreign cells have been developed. Once again, it should be emphasized that immunity is a complex multi-element system. But, like any complex system, immunity has a drawback. A defect in one of the elements leads to the fact that the entire system may fail. There are diseases associated with immunosuppression, when the body cannot independently counteract the infection.

LECTURE № 4. Immune status. Immunodeficiency states

Violation of the mechanisms of implementation of the immune response leads to various pathologies of immunity that are dangerous to health and life. The most common form of such a pathology is immunological deficiency, or, according to generally accepted international terminology, immunodeficiency states. Let us briefly consider the general patterns of the functioning of the immune system.

First, the effectiveness of the immune system is based on the balance of its components. Each component of the immune system largely mimics the functions of the other components. Thus, a defect in a part of the components (or links) of the immune system can often be compensated by other components of the immune system. Therefore, if a person has a defect in any immune component, it is necessary to use drugs that improve cell metabolism as an adjuvant.

Secondly, the cells of the immune system carry out their basic functions in an active state. The main stimulus for the activation of all cells of the immune system is the antigen. But there are situations when the antigen acts as a suppressive factor. For example, the phenomenon of the so-called lazy leukocytes, which do not react actively enough to a foreign substrate, is known.

Thirdly, the degree of activation of the immune system is related to the level of the totality of its components. In healthy people, the number and intensity of interactions between the components of the immune system are usually minimal. When an inflammatory process occurs during the active work of the immune system, their number increases dramatically. With a favorable outcome (after recovery), the relationship between the components decreases again. The chronic process is characterized by maintaining a high level of the totality of immune components (mostly several times more than in healthy people), which is regarded as a syndrome of immune system tension. This is explained by the fact that under these circumstances, the immune system continues to actively fight the foreign agent, maintaining it at some compensated level, but is not able to completely eliminate it. The exacerbation of the chronic process can be explained by the disruption of the effective functioning of the immune system after prolonged stress. As a result, one of the tasks of immunocorrective therapy of chronic diseases is to prevent the disruption of the effective functioning of the immune system by reducing the infectious and parasitic effects on the body with the help of drugs with anti-infective activity. Since the ratio of the components of the immune system, the degree of activation of lymphocytes and the syndrome of tension of the immune system as a whole can be determined by analyzing peripheral blood immunograms, this is used in practice. The characteristic of the state of the body's immune system, expressed by the qualitative and quantitative indicators of its components, is called the immune status (immunogram). Determination of the immune status is carried out in order to establish the correct diagnosis and choose a method of treatment. The revealed changes in immunity are not evaluated in isolation, but in combination with the individual characteristics of the human condition and data from other studies.

Thus, the immune status determines in total the individual reactivity of the organism and reflects the boundaries of interaction with the environment, beyond which a normal reaction turns into a pathological one. Any acute disease is not a consequence of the fact that in the human environment there are all kinds of pathogenic bacteria. If that were the case, then people would get sick all the time. But only those who react to a certain type of bacteria that are pathological for him get sick. Based on this, we can say about three levels of the reactivity of the body, such as: tolerance, resistance and immunity. A tolerant organism has no protection against pathological factors. Lack of protection leads to the destruction of the body and death. This happens with immunodeficiencies. When a resistant organism encounters a pathological agent, it reacts by turning on the immune system to fight it. The result of this struggle will depend on the power of the defense mechanisms of the quantity and quality of the pathogen. This struggle manifests itself as a pathological process. The immune organism interacts with the pathogen, and the result of its reaction is the destruction of the pathogen at the level of the body's normal defenses. But such a division is very conditional and relative. For example, an organism that is tolerant to one antigen may be resistant to another and immune to a third. In addition, there are intermediate types of reactions. This applies to chronic diseases, when the immune defenses cannot completely destroy the antigen, but at the same time do not give it the opportunity to destroy the diseased organ or tissue. This struggle goes on with varying success, that is, periods of remission (recovery) are replaced by periods of exacerbation of a chronic disease. With insufficient protection of the body, caused by a defect in any of the elements of protection or weakness of the body itself, generalization of compensatory reactions occurs.

Thus, ever higher levels of the body, including vital systems, are involved in the fight against the pathogen. The body in this case works to the limit. Compensatory reactions can reach such strength that life support systems begin to be affected. For example, during a fever, the body temperature as a result of thermal reactions can exceed the permissible value and cause death. In this case, death is the price of adaptation. This is just a single example, but it also shows how important it is for the body to have a good immunological status.

The study of the immune status includes:

1) determination of blood group and Rh factor;

2) a general blood test with an expanded leukogram or formula;

3) determination of the amount of immunoglobulins;

4) study of lymphocytes;

5) study of the phagocytic activity of neutrophils.

In addition, there are two stages of immunological diagnostics. The first stage reveals "gross" defects in the immune system. Research is carried out using simple, so-called indicative methods. These are first level tests. Therefore, the method determines twenty indicators: the number of leukocytes, lymphocytes, various subgroups of T-lymphocytes, the levels of immunoglobulins (Jg) A, M, J, E, the concentration of circulating immune complexes, etc. At this stage, the number of cells, their percentage and functional activity are taken into account . At the second stage, a more thorough analysis of the state of immunity is carried out if deviations were found in the orientation tests. Second-level tests allow you to track changes in the content of complex substances involved in the regulation of the immune response (for example, interleukin), as well as the number of cells that carry a certain type of immunoglobulin. Analysis of the immune status indicators is carried out in the dynamics of the disease, so these studies should be repeated. This allows you to identify the nature and level of violations and trace their change in the course of treatment. It is necessary to dwell in more detail on the decoding of the immunogram indicators.

1. Immune status

leukocytes

Norm - 3,5-8,8 4 × 10⁹/ l. An increase in the number of leukocytes is leukocytosis, a decrease is leukopenia. Leukocytosis is divided into physiological and pathological. Causes of physiological leukocytosis may be food intake (in this case, the number of leukocytes does not exceed 10-12 × 10⁹/ l), physical work, hot and cold baths, pregnancy, childbirth, premenstrual period. For this reason, blood should be taken on an empty stomach and before that, do not engage in heavy physical work. For pregnant women, women in childbirth, children have their own rules. Pathological leukocytosis occurs in infectious diseases (pneumonia, meningitis, general sepsis, etc.), infectious diseases with damage to the cells of the immune system (infectious mononucleosis and infectious lymphocytosis), various inflammatory diseases caused by microorganisms (furunculosis, erysipelas, peritonitis, etc.) .). But there are also exceptions. For example, some infectious diseases occur with leukopenia (typhoid fever, brucellosis, malaria, rubella, measles, influenza, viral hepatitis in the acute phase). The absence of leukocytosis in the acute phase of an infectious disease is an unfavorable sign, which indicates a weak resistance of the organism. At the heart of inflammatory diseases of non-microbial etiology, the so-called autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, etc.), infarcts of various organs, is non-microbial inflammation (necrosis); extensive burns, large blood loss.

Causes of leukopenia:

1) exposure to certain chemicals (for example, benzene);

2) taking certain drugs (butadione, reopirin, sulfonamides, cytostatics, etc.);

3) radiation, x-rays;

4) violation of hematopoiesis;

5) blood diseases (leukemia) - leukopenic and aleukopenic forms;

6) overdose of cytostatics during chemotherapy;

7) metastases of tumors in the bone marrow;

8) diseases of the spleen, lymphogranulomatosis;

9) some endocrine diseases (acromegaly, Cushing's disease and syndrome, some of the infectious diseases mentioned above).

Norm: absolute content - 1,2-3,0 × 10⁹/l, but more often in a clinical blood test, the percentage of lymphocytes is indicated. This figure is 19-37%. There are also lymphocytosis and lymphopenia. Lymphocytosis is found in chronic lymphocytic leukemia, chronic radiation sickness, bronchial asthma, thyrotoxicosis, some infectious diseases (whooping cough, tuberculosis), and removal of the spleen. Anomalies in the development of the lymphoid system, ionizing radiation, autoimmune diseases (systemic lupus erythematosus), endocrine diseases (Cushing's disease, taking hormonal drugs), AIDS lead to lymphopenia.

T-lymphocytes

Norm: relative content 50-90%, absolute - 0,8-2,5 × 10⁹/ l. The number of T-lymphocytes increases with allergic diseases, during the recovery period, with tuberculosis. A decrease in the content of T-lymphocytes occurs with chronic infections, immunodeficiencies, tumors, stress, trauma, burns, some forms of allergies, heart attack.

T-helpers

Norm: relative content - 30-50%, absolute - 0,6-1,6 × 10⁹/ l. The content of T-helpers increases with infections, allergic diseases, autoimmune diseases (rheumatoid arthritis, etc.). A decrease in the content of T-helpers occurs in immunodeficiency states, AIDS, and cytomegalovirus infection.

B-lymphocytes

Norm: relative content - 10-30%, absolute - 0,1-0,9 × 10⁹/ l. An increased content occurs with infections, autoimmune diseases, allergies, lymphocytic leukemia.

A decrease in the number of B-lymphocytes is found in immunodeficiencies, tumors.

Their activity is assessed using methods that determine the proportion of cells capable of forming a phagosome (digestive vesicle) inside themselves. To assess the digestive capacity of neutrophils, the NBT test is used (NBT is a nitrosine tetrazolium dye). The norm of the NST-test is 10-30%. The phagocytic activity of leukocytes increases in acute bacterial infections, decreases in congenital immunodeficiencies, chronic infections, autoimmune diseases, allergies, viral infections, AIDS. The activity of phagocytes, i.e., “devourer” cells, is estimated by the so-called phagocytic number (normally, a cell absorbs 5-10 microbial particles), phagocytic blood capacity, the number of active phagocytes, and the phagocytosis completion index (should be more than 1,0) .

Immunoglobulin A. Norm: 0,6-4,5 g / l. JgA rises in acute infections, autoimmune diseases (often in the lungs or intestines), nephropathies. A decrease in JgA occurs in chronic diseases (especially the respiratory system and gastrointestinal tract), purulent processes, tuberculosis, tumors, and immunodeficiencies.

Immunoglobulin M. Norm: 0,4-2,4 g / l. The content of JgM increases with bronchial asthma, infections (acute and chronic), with exacerbations, autoimmune diseases (especially with rheumatoid arthritis). Decreased JgM in primary and secondary immunodeficiencies.

Immunoglobulin J. Norm: 6,0-20,0 g / l. The amount of JgJ increases in the blood with allergies, autoimmune diseases, past infections. A decrease in the content of JgJ occurs in primary and secondary immunodeficiencies.

Immunoglobulin E. Norm: 20-100 g / l. The amount of JgE increases with hereditary allergic reactions, allergic lesions of the respiratory organs with the fungus Aspergillus, helminthic invasion and parasitic infection (giardiasis). A decrease in JgE occurs with chronic infections, taking drugs that inhibit cell division, and congenital immunodeficiency diseases.

When examining the immune status, the number of immune complexes (IC) is also determined. The immune complex consists of an antigen, an antibody, and their associated components. The content of IC in the blood serum normally ranges from 30 to 90 IU / ml. The content of immune complexes increases in acute and chronic infections and makes it possible to distinguish these stages from each other, in allergic reactions (and determines the type of these reactions), intoxication of the body (kidney disease, immunoconflict), pregnancy, etc.

All of the above norms of immune status indicators may differ slightly in different immunological laboratories. It depends on the diagnostic technique and the reagents used. Normal indicators of the immune status indicate a reliable "shield" of the body and, therefore, that a person has good health. But the immune system, like any other system of the body, can have disorders in any part. In other words, the immune system itself can be "sick". There are so-called immunodeficiencies. The basis of immunodeficiency states are violations of the genetic code that do not allow the immune system to carry out one or another link of the immune response. Immunodeficiency states can be primary and secondary. In turn, the primary ones are congenital, and the secondary ones are acquired.

2. Congenital immune deficiencies

This pathology is genetically determined. Most often, congenital immunodeficiencies appear in the first months of life. Children very often suffer from infectious diseases, which often occur with complications. There is a working classification of congenital conditions of immune deficiency, proposed by WHO experts in 1971. According to this classification, primary immunodeficiencies are divided into five large groups.

The first group includes diseases that are associated only with a defect in B-cells: Bruton's sex-linked agammaglobulinemia, transient (transient) hypogammaglobulinemia, X-linked immune deficiency and M hyperimmunoglobulinemia, etc.

The second group includes diseases of immune deficiency with a defect only in T-cells: thymus hypoplasia (DiGeorge syndrome), episodic lymphocytopenia, etc.

The third group is diseases with simultaneous damage to B- and T-cells: immune deficiency with or without hypergammaglobulinemia, immune deficiency with ataxia, telangiectasia (Louis-Barr syndrome), thrombocytopenia and eczema (Wiskott-Aldridge syndrome), thymoma (tumor of the thymus ) and etc.

The fourth group includes immunodeficiency states in which B- and T-stem cells are simultaneously affected: immune deficiency with generalized hypoplasia of the hematopoietic system, severe, combined immunodeficiency linked to the X chromosome, etc.

The final fifth group includes the states of immune deficiency that are not qualified above.

In practice, congenital conditions of immune deficiency are limited to three main groups:

1) defects in phagocytosis;

2) insufficiency of cellular and humoral immunity (T-, B- and stem cells);

3) dysfunction of the complementary system.

Defects in phagocytosis constitute a large group of diseases. Here, there are mainly dysfunctions of granulocytes and related cells: chronic idiopathic neutrocytopenia with lymphocytosis (essential benign granulocytopenia, often affecting premature babies), inherited autosomal recessively agranulocytosis, which begins in early infancy and ends with the death of a child from bacterial infections in the first years his life, dysfunction of granulocytes, degranulation syndrome (congenital dysphagocytosis), congenital hypoplasia of the spleen, etc.

Defects in humoral and cellular immunity cause the following conditions:

1) severe combined immune defect syndrome with impaired cellular immunity and antibody formation;

2) thymus hypoplasia (DiGeorge syndrome);

3) absence of purine nucleoside phosphorylase;

4) ataxia-telangiectasia syndrome;

5) thymoma with immunodeficiency syndrome, etc.

Clinical manifestations of congenital immunodeficiency states are very diverse. They range from severe symptoms caused by previous infections or vaccinations to moderate to mild recurrent and difficult to diagnose disease events. Congenital or primary immunodeficiencies are among the most common causes of early childhood death. In patients with immune deficiency in a family history, there is evidence of severe recurrent inflammation of the skin, mucous membranes, respiratory and digestive tract (otitis media, bronchopneumonia, enteritis, pyoderma, candidiasis, sepsis, etc.). With a deficiency of B-lymphocytes, bacterial infections develop caused by pneumococci, streptococci, meningococci. T-lymphocyte deficiency is characterized by viral, fungal and mycobacterial infections. In children with T-system deficiency, viral infections are severe. With immune deficiency, children find it difficult to tolerate antiviral and antibacterial vaccinations, and even death.

Deficiency of humoral immunity is manifested in the second half of the year by bacterial infections. With a deficiency of cellular immunity, fungal and viral infections develop immediately after birth. Now about congenital immunodeficiency states in more detail.

This disease is based on an isolated defect of B-lymphocytes that cannot mature into plasma cells, is inherited recessively, is X-linked, and is the first described state of immune deficiency. This disease affects only boys. The body cannot produce all classes of immunoglobulins, and without treatment, children die at an early age from recurrent infections. In many cases, patients develop well until 6-8 months of age. This appears to be due to the transplacental transfer of immunoglobulins from the mother. Pathology manifests itself with the final exhaustion of the received reserves. This is a relatively rare disease - approximately 13 patients per 1 boys.

Clinically, the disease is manifested by the fact that boys often suffer from recurrent infections caused by pneumococci, streptococci, and the influenza virus. Less often there are infections caused by meningococci, staphylococci. The infectious process is localized in the paranasal sinuses, middle ear, bronchi, lungs, and in the membranes of the brain. In such patients, the course of viral infections is the same as in healthy children, with the exception of viral hepatitis and enterovirus infections. Affected boys do not have tonsils (tonsillar tissue) and lymph nodes. In a laboratory study, the number of lymphocytes is usually normal. When determining B- and T-lymphocytes, a very pronounced decrease in the number of B-lymphocytes and a normal number of T-lymphocytes are found.

It is an isolated JgA deficiency with normal or elevated levels of other immunoglobulins. It is the most common immunodeficiency condition, found in healthy individuals from 1:300 to 1:3000 cases in various studies. The absence of JgA is quite often combined with chromosomal abnormalities (especially the 18th pair of chromosomes), with developmental defects after intrauterine infections. It is likely that in the 18th pair of chromosomes there is a gene that regulates the synthesis of JgA ... The clinical manifestations of this pathology are very diverse: from the complete absence of symptoms to severe illness. The most frequently observed pulmonary infections, diarrhea and autoimmune diseases. The defeat of the digestive and respiratory systems is explained by the absence of the secretory component of JgA ... Patients with selective deficiency of JgA have an increased tendency to form immune complexes. This explains the often observed selective deficiency of JgA in systemic lupus erythematosus, rheumatoid arthritis, pernicious anemia, thyroiditis, diabetes mellitus, Addison's disease, chronic active hepatitis, etc.

The disease is genetically determined, inherited recessively, transmitted with the X chromosome and is characterized by an increase in JgM with normal or reduced levels of JgJ and JgA in blood plasma. There is another name for this immunodeficiency - dysgammaglobulinemia I and II.

Clinical signs appear in the first or second year of life in the form of severe, frequently recurring bacterial infections. Purulent infections are the most frequent: skin abscesses, ulcerations of the oral cavity, otitis media, tonsillitis, lymphadenitis, sinusitis, and respiratory tract lesions. Sometimes the disease generalizes and leads to sepsis. Patients with hyperimmunoglobulinemia M often develop autoimmune diseases. The disease is complicated by neutropenia.

It is known that only antibodies of the JgJ class pass into the placenta. After incomplete breakdown of immunoglobulins, antibodies accumulate in the placenta. Having penetrated into the fetus in this form, they are again resynthesized into whole JgJ molecules. As a result, some newborns may have JgJ blood levels higher than their maternal blood levels. Maternal antibodies and infant immunoglobulins are usually metabolized after birth, and JgJ levels begin to decline, reaching their minimum between the 3rd and 6th months of life.

Clinically, these changes are manifested by low resistance to infections in the second half of the child's life. Healthy infants can overcome this physiological hypogammaglobulinemia because, immediately after birth, the infant is exposed to antigens that induce their own production of immunoglobulins. The JgM system is activated first, as a result of which, a few days after birth, antibodies of this system are detected in the blood. JgJ react more slowly - within a few weeks, and the concentration of JgA reaches their values ​​in adults only after a few months or even years. Secretory JgA is formed in large quantities in a much shorter time. Activation of the own synthesis of immunoglobulins in the fetus is possible with intensive antigenic stimulation. In this case, the JgM system reacts especially rapidly and intensively. Therefore, the detection of an increased level of JgM in the blood serum of newborns indicates the presence of intrauterine infection.

In infants, there are several types of transient (transient) hypogammaglobulinemia. The most common physiological hypogammaglobulinemia, which usually disappears by the end of the first six months of a child's life. Pathological hypogammaglobulinemia occurs in preterm infants, as transfer of immunoglobulins across the placenta begins by the end of the 20th week and continues until birth. There is a clear relationship between gestational age and immunoglobulin levels. Their low value is affected by the limited possibility of immunoglobulin synthesis in premature infants. Also, pathological hypogammaglobulinemia in infants can be observed with maternal hypogammaglobulinemia, which is compensated under the influence of their own products. And finally, pathological transient hypogammaglobulinemia occurs in cases of delayed maturation of the immunoglobulin production system. This may be due to lack of contact with antigens, as well as unknown reasons. The diagnosis of transient hypogammaglobulinemia in infants is based on low immunoglobulin values ​​and the ability to form antibodies after vaccination, which is not seen in persistent (aggressive) hypogammaglobulinemia.

This disease is manifested by immune deficiency and an increased tendency to develop lymphoma. The syndrome is named after the first described family - Duncan's disease. In this family, three brothers died from infectious mononucleosis, and four male relatives of the mother had lymphoma and unusual complications of infectious mononucleosis in the form of immunoblastic sarcoma, hypogammaglobulinemia and immune deficiency with hypergammaglobulinemia M. Subsequently, this disease was described in other families.

Most of the patients had clinical and laboratory signs of long-term infectious mononucleosis. At the same time, patients had rapidly progressive and fatal diseases with pathological proliferation of lymphoid tissue, such as plasmacytoma, Burkitt's African lymphoma, B-cell immunoblastic sarcoma, histiocytic lymphoma.

3. Diseases of cellular immunity

These diseases are rare due to their severe course and deaths already in early childhood.

Children with partial or complete T-lymphocyte deficiency are most likely to develop severe infections that do not respond to treatment. In these conditions, serum immunoglobulin levels are either normal or elevated. Of this group, two syndromes are the main ones: DiGeorge's syndrome (thymus hypoplasia) and cellular immunodeficiency syndrome with immunoglobulins.

With this syndrome, embryonic cells are affected in utero, from which the parathyroid glands and thymus develop. As a result, the parathyroid glands and thymus are either underdeveloped or completely absent in the child. The tissues from which the face is formed are also affected. This is expressed by underdevelopment of the lower jaw, a short upper lip, characteristic palpebral fissures, low position and deformation of the auricles. In addition, children have congenital disorders of the heart and large vessels. The disease appears sporadically, but there are suggestions that it is genetically determined and inherited in an autosomal recessive manner.

Clinically, DiGeorge syndrome manifests itself already at birth. Disproportions of the face, heart defects are characteristic. The most characteristic symptom in the neonatal period is hypocalcemic convulsions (due to underdevelopment of the parathyroid glands). Immunodeficiency syndrome develops more often in the second half of the life of an infant and is clinically manifested by frequently recurring infections caused by viruses, fungi and opportunistic bacteria, up to severe septic processes. Depending on the degree of underdevelopment of the thymus, the symptoms of immune deficiency can be very different (from severe to mild), and therefore, in mild cases, they speak of partial DiGeorge syndrome. In the blood, a reduced level of calcium and an increased level of phosphorus and a decrease or complete absence of parathyroid hormone are found, which confirms the underdevelopment or absence of the parathyroid glands.

A group of diseases of the immune system, called severe combined immunodeficiency states, has been identified. Enzyme (enzyme) defects were revealed in the pathogenesis. Such immunodeficiencies are relatively rare diseases. They occur in cases from 1:20 to 000:1 in newborns. Despite a similar clinical picture, severe combined immunodeficiencies are divided into several subgroups based on pathogenetic and pathophysiological principles.

In most cases, it is hereditary. Inheritance can be either X-linked recessive or autosomal recessive. In these diseases, the reproduction and differentiation of B-lymphocytes and T-lymphocytes are impaired. A decrease in the concentration of T-cells and immunoglobulins (antibodies) in the blood is characteristic. Often this pathology is accompanied by other malformations.

In severe combined immunodeficiencies, approximately 1/3 and 1/2 of patients have a deficiency of the enzyme adenosine deaminase. The lack of this enzyme leads to the accumulation of adenosine monophosphate, which in high concentrations is toxic to lymphocytes. The manifestations of the disease are typical for patients with severe combined immunodeficiency, but in about 50% of cases, cartilage tissue abnormalities are also observed. Previously, these patients were classified as immunodeficient with short stature and short limbs. In the blood, a pronounced leukopenia is found, as well as the absence of granulocytes and their precursors in the bone marrow. There are no JgA and JgM in the blood, and the amount of JgJ corresponds to the values ​​of JgJ that entered the child's body through the placenta from the mother.

The main clinical symptom of this group of diseases is a pronounced tendency to infectious diseases that appear from the first month of a child's life and are most often extensive: all contact surfaces of the body (skin, digestive system, respiratory tract) are affected. Pyoderma, abscesses and various types of rash are observed. Lesions of the gastrointestinal tract manifest as recurrent, refractory diarrhea that causes severe malnutrition. Respiratory tract infections are complicated by deep dry, whooping cough, pneumonia. Children often have prolonged hyperthermia, which is an expression of hematogenous sepsis or meningitis. Under such conditions, infectious processes are caused by a wide variety of microorganisms: saprophytic bacteria and bacteria that cause purulent inflammation, viruses, protozoal pathogens and fungi. In laboratory studies, severe lymphopenia is established. In the blood, the number of B and T cells is significantly reduced, and the thymus gland is not detected on x-ray. Usually, the clinic manifests itself after the third month of the child's life, that is, when the JgJ transferred from the mother's body through the placenta before delivery is exhausted. Hemagglutinins and specific antibodies are not found in the blood after immunizations. Cellular immunity is significantly impaired. In such patients, the nodes are very small with structural changes, in the intestinal mucosa there is severe atrophy of the lymphatic system. If the thymus gland is found, then very characteristic changes in morphology, structural disturbances, severe lymphopenia, and the absence of Hassal's bodies are noted in it.

4. Partial combined immunodeficiency states

This syndrome is characterized by a triad: thrombocytopenia, eczema, and an increased susceptibility to infectious diseases.

It is inherited recessively, transmitted with the X chromosome, and is relatively rare.

Clinically, this disease manifests itself very early, already in the neonatal period. Children have skin hemorrhages, mostly petechial, and bloody diarrhea. In a later period, nosebleeds appear. Hemorrhages are fatal. In the first three months of life, eczema appears, often complicated by hemorrhages. There may be other manifestations of allergy with high eosinophilia. In the first half of a child's life, severe respiratory tract infections, complicated eczema, meningitis, and sepsis appear during the course of the disease. With age, the immune deficiency deepens and aggravates. The most common infectious agents are pneumococci, which cause recurrent pneumonia, otitis media, meningitis, and sepsis. These diseases occur in early infancy. When cellular immunity is already affected, diseases can be caused by fungi and viruses. Of interest is the fact that in the Wiskott-Aldrich syndrome, a rather high risk of diseases with malignant tumors, amounting to 10-15%, was revealed.

Louis-Barr syndrome is a complex disease of the immune, nervous and endocrine systems, with frequent damage to the skin and liver. The disease is inherited through an abnormal autosomal recessive gene.

A characteristic symptom of the disease is progressive cerebral ataxia, which usually appears at school age in children who were healthy before this age. At the age of three to six years, telangiectasias (changes in the vessels) are established. Most often, the conjunctiva is affected (small veins are greatly dilated and tortuous). Such expansions are observed on the auricles and on the cheeks. In this case, the skin looks prematurely aged, and graying of the hair during puberty is common. In patients, in 80% of cases, a tendency to infections that affect mainly the respiratory tract is found. Generalization of the infectious process and damage to the digestive system is not observed.

In addition to the main symptoms, there are also endocrinological abnormalities (genital disorders, short stature, glucose intolerance, insulin resistant diabetes mellitus) and hepatic dysfunction. Patients have a tendency to malignant diseases of the lymphoreticular type. In this disease, selective JgA deficiency is a frequent immunological abnormality, while JgJ values ​​are normal or slightly reduced, and JgM concentration is normal or elevated. The level of JgE is usually low. Most patients have signs of impaired cellular immunity. The total number of lymphocytes is reduced slightly, and the number of circulating T-lymphocytes is significantly reduced.

This pathology is referred to as congenital immune diseases associated with impaired phagocytic function of neutrophilic leukocytes. In this disease, granulocytes are unable to destroy microorganisms. It occurs relatively rarely. It can be inherited through a recessive, X-linked, abnormal gene, or through an autosomal recessive gene.

It is clinically manifested by numerous recurrent infections that appear in the earliest period of life. The skin is most often affected, on which small abscesses first appear, which quickly penetrate into the underlying tissues and are very difficult to heal. Most have lesions of the lymph nodes (especially the cervical) with the formation of abscesses. Often there are also cervical fistulas. The lungs may be affected, which is manifested by recurrent pneumonia, the digestive system in the form of inflammatory processes in the esophagus, liver, and also in the mediastinum.

In the blood, a pronounced leukocytosis with a shift to the left, an increase in ESR, hypergammaglobulinemia, and anemia are detected. The prognosis of chronic granulomatous disease is poor. Most of the patients die in preschool age.

Complement refers to humoral immunity (from Latin gumor - "liquid"). This is a group of proteins circulating in the blood serum that prepare bacteria and their toxins for phagocytosis, and are also capable of directly destroying microorganisms. An insufficient amount of complement leads to the fact that the body struggles with microbes with great difficulty, and this leads to the development of severe infectious diseases (up to sepsis).

In some diseases, such as systemic lupus erythematosus, secondary complement deficiency may develop.

5. Acquired immune deficiencies

They are also called secondary immunodeficiencies, as they appear during a person's life for a variety of reasons. In other words, they arise as a result of the impact of many damaging factors on the body, which at birth had a healthy immune system. These damaging factors can be:

1) unfavorable ecology (pollution of water, air, etc.);

2) eating disorders (irrational diets that cause metabolic disorders, starvation);

3) chronic diseases;

4) prolonged stress;

5) not completely cured acute bacterial and viral infections;

6) diseases of the liver and kidneys (organs that provide detoxification of the body);

7) radiation;

8) incorrectly selected medicines.

Scientific and technological progress has led our civilization to the use of a huge number of artificial (synthetic) additives in food, medicines, hygiene products, etc. If these factors affect the body for a long time, then toxic products and metabolic products accumulate in the blood and lymph in such concentration that chronic diseases develop. As a result, some types of bacteria that have been absorbed by macrophages (phagocytes) do not die, but begin to actively multiply, which leads to the death of the phagocyte. Under normal conditions, microorganisms should die. The problem of secondary immunodeficiencies is very relevant for today. They can seriously change and aggravate diseases, affect their outcome and the effectiveness of treatment.

There are temporary violations of the immune system, the so-called functional disorders. They respond well to correction (most often in children). A temporary decrease in the activity of immune indicators can also occur in healthy people. This is usually associated with seasonal phenomena (decreased solar activity, wet weather), which leads to epidemic outbreaks of colds and flu. With timely detection, functional changes in immunity are easily restored to normal. If secondary immunodeficiencies disrupt the self-cleansing processes of the body, then over time this imbalance can lead to autoimmune diseases, oncology, and AIDS. All these types of secondary immunodeficiency states are quite serious diseases, have severe clinical manifestations and often unfavorable prognosis and outcome.

These diseases can occur when exposed to adverse environmental factors. The basis of the pathogenesis of autoimmune pathologies is a violation of the work of T-lymphocytes (suppressors). As a result, the immune system begins to show aggression against its own (healthy) cells of its own body. There is a "self-harm" of tissues or organs.

Autoimmune diseases have a hereditary predisposition. These diseases include rheumatoid arthritis, systemic lupus erythematosus, periarthritis nodosa, scleroderma, systemic vasculitis, dermatomyositis, rheumatism, ankylosing spondylitis (Bekhterev's disease), some diseases of the nervous system (for example, multiple sclerosis), etc. All autoimmune diseases have development in a vicious circle. Schematically, this circle can be described as follows. When foreign agents (bacteria, viruses, fungus) invade the cell, an inflammatory reaction develops, which aims to isolate and reject the harmful agent. At the same time, the own tissue changes, dies off and becomes foreign to the body itself, and the production of antibodies already begins on it, as a result of which inflammation develops again. When it reaches the stage of necrosis, the necrotic tissue also becomes an antigen, a harmful agent, against which antibodies are again produced, resulting in inflammation again. Antibodies and inflammation destroy this tissue. And so it goes on endlessly, forming a painful and destructive circle. The primary agent (bacteria, virus, fungus) is gone, and the disease continues to destroy the body. The group of autoimmune diseases is quite large, and the study of the mechanisms of development of these diseases is of great importance for the development of tactics for their treatment and prevention, since most of these diseases lead patients to disability.

A particularly significant proportion of autoimmune diseases is occupied by collagenoses, vasculitis, rheumatic lesions of the joints, heart, and nervous system.

This is a systemic disease of the connective tissue, which is manifested mainly by progressive inflammation of the joints. The causes of occurrence are not well known. The most probable is the immunogenetic theory. It suggests the presence of a genetically determined defect in the immune system. The mechanism of the development of the disease is associated with autoimmune disorders. The main disorders concern the so-called rheumatoid factors, which are antibodies to immunoglobulins. Immunocomplex processes lead to the development of synovitis, and in some cases to generalized vasculitis. In the synovial membrane, granulation tissue is formed and grows, which eventually destroys cartilage and other parts of the bones with the occurrence of erosions (usur). Sclerotic changes develop, fibrous and then bone ankylosis occurs (the joint is deformed and becomes stiff). Pathological changes occur in the tendons, serous bags and joint capsule.

Clinically, the disease is manifested by persistent inflammation of the joint (arthritis). But the most common is polyarthritis, which affects mainly small joints (metacarpophalangeal, interphalangeal and metatarsophalangeal). There are all signs of inflammation (pain, swelling of the joints, local fever). The disease is characterized by a gradual, slow, but steady progression of arthritis and the involvement of new joints in the pathological process. The advanced stage of the disease is characterized by deforming arthritis. Deformities of the metacarpophalangeal (flexion contractures, subluxations) and proximal (distant) interphalangeal joints are especially typical. These changes form the so-called rheumatoid hand and rheumatoid foot.

In rheumatoid arthritis, it is rare, but extra-articular manifestations are also observed. These include subcutaneous nodules, often located in the elbow joints, serositis (inflammation in the pleura and pericardium), lymphadenopathy, and peripheral neuropathy. The severity of extra-articular manifestations, as a rule, is small. Usually they do not come to the fore in the overall picture of the disease. Approximately 10-15% of patients develop kidney damage in the form of amyloidosis with gradually increasing proteinuria, nephrotic syndrome, which ends with renal failure. Laboratory indicators are nonspecific. In 70-80% of patients, rheumatoid factor (Waaler-Rose reaction) is detected in the blood serum. This form of rheumatoid arthritis is called seropositive. From the very beginning of the disease, an increase in ESR, fibrinogen, α₂-globulins, the appearance of C-reactive protein in the blood serum, a decrease in hemoglobin levels. All of these indicators usually correspond to the activity of the disease.

This is a group of diseases in which there is a systemic vascular lesion with an inflammatory reaction of the vascular wall. There are primary and secondary systemic vasculitis. In primary, systemic vascular lesions are an independent disease, while secondary ones develop against the background of some infectious-allergic or other disease. Secondary systemic vasculitis in diseases such as rheumatoid arthritis, systemic lupus erythematosus, scleroderma, is of paramount importance in the clinical picture of these diseases.

Primary systemic vasculitis includes hemorrhagic vasculitis, giant cell temporal arteritis, Wegener's granulomatosis, thromboangiitis obliterans, Goodpasture's, Moshkovich's, and Takayasu's syndromes.

This is a systemic lesion of capillaries, arterioles, venules. The process takes place mainly in the skin, joints, abdominal cavity, kidneys. The disease usually occurs in children and adolescents, less often in adults of both sexes. The development of the disease occurs after an infection (streptococcal tonsillitis or exacerbations of chronic tonsillitis or pharyngitis), as well as after vaccination, due to drug intolerance, hypothermia, etc.

Damage to blood vessels in the form of microthrombosis, hemorrhages (hemorrhages), changes in the inner lining of the artery (endothelium) has an immune genesis. Damaging factors are immune complexes circulating in the blood.

Clinically, the disease is manifested by a triad:

1) small-celled, sometimes merging hemorrhagic rashes on the skin (purpura);

2) pain in the joints or inflammation of the joints, mostly large ones;

3) abdominal syndrome (pain in the abdominal cavity).

The rash is more common on the legs. Initially, skin rashes are located on the extensor surfaces of the limbs, sometimes on the trunk, often ending with residual pigmentation. More than 2/3 of patients have migrating symmetrical polyarthritis, usually of large joints. Inflammation of the joints is often accompanied by hemorrhages inside the cavity of the joints, which leads to pain of a different nature: from slight aches to severe pain, up to immobility. Abdominal syndrome is manifested by sudden intestinal colic, which simulates appendicitis, cholecystitis, pancreatitis. Often, the kidneys are involved in the pathological process in the form of glomerulonephritis due to damage to the glomerular capillaries. There is an acute course of the disease with a sudden, violent onset, a multi-symptom clinic, and a frequent complication of the kidneys. In chronic course, recurrent skin-articular syndrome is more often observed.

Granulomatous-necrotic vasculitis with a primary lesion of the respiratory tract, lungs and kidneys. The reason is not yet known. The disease is provoked by colds (ARVI), cooling, overheating in the sun, trauma, drug intolerance, etc. The leading mechanisms for the development of the disease are autoimmune.

The disease develops more often in men. First, the respiratory tract is affected, which manifests itself in two ways. In the first variant, there is a persistent runny nose with serous-sanitary, purulent discharge, nosebleeds, in the second - a persistent cough with bloody-purulent sputum, pain in the chest. Further the clinical picture with many syndromes develops. This is the stage of generalization, which is accompanied by fever, transient polyarthritis or only pain in the joints and muscles, skin lesions (up to severe necrotic lesions of the skin of the face), etc. The most typical occurrence is purulent-necrotic and ulcerative-necrotic rhinitis, sinusitis, nasopharyngitis and laryngitis. Clinical and radiological symptoms in the lungs are manifested in the form of focal and confluent pneumonia with the formation of abscesses and cavities. At this stage, the kidneys, heart, nervous system, etc. are involved in the pathological process.

In blood tests, changes are not specific (bright signs of inflammation - leukocytosis, accelerated ESR). The prognosis of the disease is often unfavorable. Patients die of pulmonary heart or kidney failure, pulmonary hemorrhage. The diagnosis is made on the basis of a biopsy of the mucous membranes of the respiratory tract, lungs, where the granulomatous nature of the disease is revealed.

This is a systemic disease with a predominant lesion of the temporal and cranial arteries. A viral etiology is assumed, and the mechanism of development (pathogenesis) is an immunocomplex lesion of the arteries, which is confirmed by the detection of fixed immune complexes in the wall of the arteries. The granulomatous type of cellular infiltrates is also characteristic. Elderly people of both sexes get sick. With the most common variant, the disease begins acutely, with high fever, headaches in the temporal region. There is a visible thickening of the affected temporal artery, its tortuosity and pain on palpation, sometimes reddening of the skin. When the diagnosis is made late, damage to the vessels of the eye and the development of partial or complete blindness are observed. From the first days of the disease, the general condition also suffers (lack of appetite, lethargy, weight loss, insomnia).

In blood tests, high leukocytosis, neutrophilia, accelerated ESR, hyper-α₂ and gammaglobulinemia. The course of the disease is progressive, but early treatment can lead to permanent improvement.

This is a systemic capillaritis with a primary lesion of the lungs and kidneys in the form of hemorrhagic pneumonia (with hemorrhages in the lung tissue) and glomerulonephritis (damage to the renal glomeruli). Men of young age (20-30 years) get sick more often. The reason is not clear, but a connection with a viral or bacterial infection, hypothermia is considered more likely. It is characteristic that for the first time this disease was described during the influenza pandemic in 1919. The pathogenesis is autoimmune, since antibodies to the basement membranes of the kidneys and lungs are found circulating and fixed in the tissues. Electron microscopic examination shows changes in the basement membranes of the alveoli of the lungs and renal capillaries in the form of fixation of antibodies to these basement membranes.

Clinically, the disease begins acutely, with high fever, hemoptysis or pulmonary hemorrhage, shortness of breath. In the lungs, an abundance of moist rales is heard in the middle and lower sections, and on x-rays there are many focal or confluent opacities on both sides. Almost simultaneously, severe, with rapid progression of glomerulonephritis with nephrotic syndrome (edema, protein and blood in the urine) and the rapid development of renal failure. The prognosis is often unfavorable, patients die in the next six months or a year from the onset of the disease from pulmonary and cardiac and renal failure. Anemia, leukocytosis and accelerated ESR are found in the blood. The immunological sign of the disease is antibodies to the basement membranes of the kidney.

This is a systemic thrombotic microangiopathy, which is accompanied by thrombocytopenic purpura, intravascular coagulation (hemolysis), cerebral and renal symptoms. The cause and mechanism of the development of the disease is not yet known. Assume the immune nature of a disease. Mostly young women get sick. The disease begins suddenly, with fever, signs of intravascular coagulation, thrombocytopenic purpura, and a variety of neuropsychiatric disorders due to brain damage. Other organs are also affected, primarily the kidneys with the rapid development of renal failure.

Clinically, the disease is manifested by hemorrhagic syndrome, petechial (small cell) hemorrhages on the skin, nasal, gastric, gynecological, renal bleeding, hemorrhages in the fundus. Blood tests reveal anemia, reticulocytosis (immature blood cells), thrombocytopenia (lack of platelets), elevated bilirubin, and hypergammaglobulinemia. The course is steadily progressive with a rapid lethal outcome.

This syndrome is an inflammatory process in the aortic arch (aortitis) and in the branches extending from it. At the same time, their partial or complete obliteration develops. Other parts of the aorta may also be affected.

The causes (etiology) and mechanisms (pathogenesis) of this disease are not yet clear. The importance of immune disorders, which are based on genetic defects in the formation of the aortic wall, is assumed. More often young women are ill.

The syndrome is manifested by a gradual increase in signs of circulatory disorders in the areas of the affected vessels. The main symptom is the absence of a pulse in one or both hands, less often in the carotid, subclavian, temporal arteries. Patients feel pain and numbness in the limbs, which are aggravated by physical exertion, weakness in the arms, dizziness, often with loss of consciousness. When examining the eyes, cataracts, changes in the vessels of the fundus (narrowing, the formation of arteriovenous anastomoses) are detected. Significantly less often, coronary arteries with corresponding symptoms are involved in the process. When the abdominal aorta with renal vessels is affected, vasorenal (renal) hypertension develops. Of the common signs of the disease, subfebrile condition and asthenia are characteristic. Laboratory indicators are moderate. The disease progresses slowly, with exacerbations in the form of ischemia of a particular zone. Diagnosis can be made at an early stage by arteriography.

This is a systemic inflammatory vascular disease with a predominant lesion of the arteries of the muscular type, as well as veins. The etiology and pathogenesis are not yet known. An allergic reaction to various influences of the external and internal environment of the body is assumed. Mostly men aged 30-45 years are ill. The disease begins gradually, with migrating thrombophlebitis, fatigue and heaviness in the legs (primarily when walking in the calf muscles), paresthesia (sensitivity disorders). Later, intermittent claudication develops, pain in the legs persists even at rest, especially at night. There is a decrease in pulsation in the arteries of the lower extremities, which later disappears. Already in the early stages, trophic disorders appear on the affected limbs, which can turn into necrosis as a result of increasing ischemia. The disease can acquire the character of a systemic process with damage to the coronary, cerebral, mesenteric arteries with the development of ischemia phenomena, respectively, to the feeding zone of a particular artery. There is a deterioration in the general condition, subfebrile reactions, in particular accelerated ESR. The course is chronic, steadily progressing, with an increase in ischemic phenomena. With a systemic process, myocardial infarctions, ischemic strokes, intestinal necrosis and other serious conditions that worsen the prognosis are possible.

It is a chronic systemic autoimmune disease of the connective tissue and blood vessels. This serious autoimmune disease is caused by a chronic viral infection. These are RNA viruses that are close to measles or measles-like. The mechanism of the development of the disease is quite complex. Circulating auto-antibodies are formed in the body, of which antinuclear antibodies to the whole nucleus and its individual components are of the most important diagnostic value, circulating immune complexes, primarily DNA antibodies to complement DNA, which are deposited on the basement membranes of various organs, causing their damage. with an inflammatory response.

Such is the pathogenesis of nephritis, dermatitis, vasculitis, etc. Such a high reactivity of humoral immunity is explained by a decrease in control from T-lymphocytes, i.e., cellular immunity. There may be a family genetic predisposition. Mostly teenage girls and young women are ill. The disease can be provoked by pregnancy, abortion, childbirth, the onset of menstruation, infections (especially in adolescents), prolonged exposure to the sun, vaccination, and the use of drugs.

The disease has a gradual onset. Appear asthenia (weakness), recurrent polyarthritis. Much less often there is an acute onset, characterized by fever, dermatitis, acute polyarthritis, and then there is a course with relapses and multisyndromic symptoms. Multiple joint lesions (polyarthritis) and pain in them are the most frequent and early symptoms. The lesions mainly affect the small joints of the hands, wrists, ankles, but the knee joints can also be affected. The severity and persistence of the lesion are different. A characteristic symptom of the disease is skin lesions in the form of erythematous rashes on the face (redness) in the form of a butterfly, i.e. on the bridge of the nose, cheeks and in the upper half of the chest in the form of a decollete, as well as on the extremities. Almost all patients have polyserositis in the form of pleurisy, pericarditis, perihepatitis, perisplenitis. Dermatitis, polyarthritis, and polyserositis are the diagnostic triad of systemic lupus erythematosus. Characterized by damage to the cardiovascular system. Pericarditis usually develops with further addition of myocarditis. Libman-Sachs verrucous endocarditis is often observed with damage to the mitral, aortic and tricuspid valves. Vascular damage occurs in individual organs, but Raynaud's syndrome is possible, which appears long before the development of a typical picture of the disease.

Lung damage is associated with a vascular connective tissue syndrome that develops with the underlying disease and with a secondary infection. The so-called lupus pneumonia is manifested by cough, shortness of breath, unvoiced moist rales in the lower parts of the lungs. X-ray reveals an increase and deformation of the pulmonary pattern due to the vascular component in the lower parts of the lungs, sometimes focal-like shadows are found. Pneumonia develops against the background of polyserositis, therefore, on x-rays, in addition to the main changes, a high standing of the diaphragm with signs of adhesions and the so-called linear shadows parallel to the diaphragm (disc-shaped lung tissue seals) are found. The pathological process also affects the gastrointestinal tract. Anorexia, aphthous (ulcerative) stomatitis, dyspepsia (indigestion) are noted. There may be an abdominal pain syndrome, which is caused by the involvement of the peritoneum in the process or by vasculitis itself (damage to the mesenteric, splenic and other arteries). In the early stages of the disease, there is an increase in the liver, although lupus hepatitis itself is extremely rare. As a rule, liver enlargement is due to heart failure, pancarditis (damage to the pericardium, myocardium and endocardium), or severe effusion pericarditis. Could be fatty liver.

A frequent and early sign of systemic disease is an increase in all groups of lymph nodes and spleen, which indicates damage to the reticuloendothelial system. Lupus nephritis, the so-called lupus nephritis, develops in 50% of patients. Its development usually occurs during the period of generalization of the process. Kidney damage in systemic lupus erythematosus has several options: urinary, nephritic or nephrotic syndrome. In the diagnosis of lupus nephritis, intravital puncture biopsy with a deep study of the biopsy (immunomorphological and electron microscopic) is of great importance. The combination of fever, recurrent articular syndrome and persistently accelerated ESR requires the exclusion of lupus nephritis. Observations show that almost every fifth patient with nephrotic syndrome has systemic lupus erythematosus.

In many patients in all phases of the disease, damage to the neuropsychic sphere is noted. At the initial stage of the disease, asthenovegetative syndrome is observed, and then signs of damage to all parts of the central and peripheral nervous system develop in the form of encephalitis, myelitis, polyneuritis. Often there are combined lesions (systemic) of the nervous system in the form of meningoencephalo-, myelopolyradiculoneuritis. Laboratory data are of great diagnostic value, especially for the detection of a large number of LE cells (lupus cells, or lupus).

High titers of antibodies to DNA are specific for systemic lupus erythematosus. In the case of an acute (rapid) development of the disease, lupus nephritis is detected already after 3-6 months, which proceeds according to the type of nephrotic syndrome. In the subacute course, undulation is characteristic with the involvement of various organs and systems in the pathological process, which in the clinical picture is manifested by polysyndromicity. The chronic long-term course of the disease is characterized by relapses of polyarthritis and (or) polyserositis, Raynaud's syndrome and epileptiform convulsions. Only at the 5-10th year characteristic polysyndromicity gradually develops. In accordance with the clinical and laboratory characteristics, three degrees of activity of the process are distinguished: high (III degree), moderate (II degree) and minimal (I degree). Patients need long-term continuous treatment. The best results are observed with early treatment, then a stable clinical remission develops.

Refers to systemic diseases of the connective tissue with a primary lesion of the muscles and skin. It is assumed that the trigger of this disease is a viral infection, and the provoking factors are cooling, trauma, prolonged exposure to the sun, pregnancy, drug intolerance. 20-30% of patients may have tumor dermatomyositis. The pathogenesis is based on autoimmune disorders. Neuroendocrine reactivity is important, since women predominate among patients (2: 1), and the peak of the disease falls on two age periods. These periods are puberty (the period of sexual development) and menopause, i.e. peaks of hormonal changes in the body. A family genetic predisposition is also possible.

The clinical onset of the disease can be either acute or gradual. The muscle syndrome comes to the fore in the form of muscle weakness and muscle pain (myasthenia gravis and myalgia). No less significant manifestations of the disease are arthralgia, fever, skin lesions, dense widespread edema. In the future, the disease acquires a relapsing course. In all patients, skeletal muscles are affected. This is manifested by myalgia during movement and at rest, as well as with pressure, and increasing muscle weakness is characteristic.

There is a compaction and an increase in the volume of the muscles of the shoulder and pelvic girdle, active movements are significantly disturbed, and to such an extent that patients cannot sit down on their own, raise their limbs, head from the pillow, hold it while sitting or standing. If the process spreads significantly, then the patients become immobilized, and in severe cases are in a state of complete prostration. If the pathological process extends to the mimic muscles of the face, then this leads to a mask-like face, damage to the pharyngeal muscles leads to dysphagia, and the intercostal muscles and diaphragm lead to respiratory failure, a decrease in the ventilating function of the lungs and, as a result, to frequent pneumonia.

In the early stages of the disease, the muscles are painful and often swollen, later they undergo dystrophy and myolysis (resorption of muscle fibers). In even later stages of the disease, myofibrosis develops in place of muscle fibers (replacement of muscle tissue with connective tissue), which leads to muscle atrophy and contractures. There may be calcification (calcium deposition) in the muscles, subcutaneous tissue, especially often in young people. Calcification is easily detected on x-ray. With electromyography, changes are nonspecific. A variety of skin lesions are characteristic. These are all kinds of rashes in the form of reddened areas of the skin, the appearance of tubercles and blisters, expansion of skin vessels, keratinization of certain areas of the skin, depigmentation or hyperpigmentation, etc. Often these rashes are accompanied by itching. The presence of periorbital (around the eyes) edema with purple-purple erythema is very pathognomonic - the so-called dermatomyositis glasses.

The joints are affected in the form of polyarthralgia (pain in many joints at once), up to the development of joint stiffness. There is a lesion of the myocardium of an inflammatory or dystrophic plan. With diffuse myocarditis, a severe picture of heart failure develops. Raynaud's syndrome is observed in 1/3 of patients. Frequent lung damage due to hypoventilation. In almost half of the patients, the gastrointestinal tract is involved in the pathological process. This is manifested by anorexia, abdominal pain, gastroenterocolitis, decreased tone of the upper third of the esophagus. Sometimes there are symptoms that simulate intestinal obstruction. Data from laboratory studies are nonspecific. Usually it is moderate leukocytosis with severe eosinophilia (up to 25-70%), persistent moderate acceleration of ESR, hypergammaglobulinemia. Biochemical studies of blood and urine, muscle biopsy are important for diagnosis. Thickening of muscle fibers with loss of transverse striation, fragmentation and dystrophy, up to necrosis, accumulation of lymphocytes, plasma cells, etc. in the muscles, etc. are found. In an acute course, a catastrophically increasing generalized lesion of the striated muscles is observed, up to complete immobility. Patients cannot swallow or speak. There is a general serious condition with fever, toxicosis and various skin rashes. If left untreated, death usually occurs within 3-6 months. The main causes of poor outcome are aspiration pneumonia, pulmonary heart failure. The subacute course is marked by cyclicity, but there is also a steady increase in adynamia, damage to the skin and internal organs. The most favorable form is the chronic course of the disease, in which only individual muscles are affected, and patients remain able to work. The exception is young people who develop extensive calcifications in the skin, subcutaneous tissue, muscles with the formation of persistent contractures and almost complete immobility.

This is a systemic vascular disease with a predominant lesion of the arteries of the muscular type and vessels of a smaller caliber. A disease occurs for an unknown reason. In pathogenesis, the main thing is the highest (hyperergic) reaction of the body in response to the influence of various factors. An essential role is played by immune complexes circulating and fixed in the vessel wall. Mostly men aged 30-40 years get sick.

The onset of the disease is acute or gradual, with such general symptoms as fever, progressive weight loss, pain in the joints, muscles, abdomen, skin rashes, lesions of the gastrointestinal tract. Over time, the heart, kidneys, and peripheral nervous system are affected, i.e., polyvisceral symptoms develop (all organs are affected). Almost all patients have glomerulonephritis of varying severity: from mild nephropathy with transient (transient) hypertension and moderate urinary syndrome to diffuse glomerulonephritis with persistent hypertension and a rapidly progressive course. Unfavorable in terms of prognosis is the development of the syndrome of malignant hypertension and nephrotic syndrome, which quickly leads to renal failure. In addition, there are kidney infarcts, aneurysms due to arteritis. Almost 70% of patients have heart disease. Since the coronary arteries are affected, angina attacks are noted up to the development of myocardial infarction, but without clear clinical signs. Sometimes aneurysm and exudative (effusion) pericarditis are formed. Perhaps the development of Raynaud's syndrome, which is occasionally complicated by gangrene of the fingers. Sometimes there are migrating phlebitis (vein lesions).

Acute pain in the abdomen is very characteristic of periarteritis nodosa. They are associated with the pathological process in the vessels of the abdominal cavity. Damage to the vessels of the stomach leads to gastritis, damage to the vessels of the small intestine leads to enteritis, etc. Appendicitis, acute cholecystitis, pancreatitis, intestinal perforation due to necrosis, infarction, and hemorrhages may develop. In 50% of patients, damage to the nervous system is manifested by multiple neuritis associated with pathology in the vessels that feed one or another nerve. Possible meningoencephalitis with impaired speech and hearing, headache and dizziness, convulsions, as well as focal brain lesions due to thrombosis, aneurysm rupture. One of the early symptoms of the disease is eye damage. Examination of the fundus reveals arterial aneurysms, thrombosis of the central retinal artery, etc.

Pain in the joints (arthralgia) is noted, less often - arthritis of large joints, muscle pain, various skin lesions. In a small group of patients, subcutaneous nodules, which are very characteristic of periarteritis nodosa, are found, which are vascular aneurysms or a granuloma associated with the affected vessel.

A feature of periarteritis nodosa is the rapidly developing pronounced pallor of patients, which, in combination with exhaustion, creates a picture of chlorotic insanity. Lung damage is manifested by pneumonia and bronchial asthma. Pulmonary symptoms are associated with vascular damage. There are observations indicating that bronchial asthma may precede the full picture of periarteritis nodosa by many years.

Laboratory data are uncharacteristic. Possible leukocytosis with neutrophilic shift, eosinophilia, sometimes high. In severe cases, moderate anemia and thrombocytopenia occur. To clarify the diagnosis, a muscle biopsy is performed from the lower leg or abdominal wall. At the same time, vascular changes characteristic of this disease are revealed.

Systemic inflammatory disease of the connective tissue with predominant localization in the heart. Children and young people usually get sick. Women get sick about 3 times more often than men. The main cause of the disease is group A β-hemolytic streptococcus. However, in patients with prolonged and continuously recurrent forms of rheumatic heart disease (rheumatic heart disease), the relationship of the disease with streptococcus is often not established, although heart damage fully meets all the main criteria for rheumatism. This indicates other reasons for the development of rheumatism: allergic (out of connection with streptococcus or infectious antigens in general), infectious-toxic, viral.

Allergy plays an important role in the development of rheumatism. It is assumed that sensitizing agents (streptococcus, virus, nonspecific allergens, etc.) can lead to allergic inflammation in the heart at the first stages, and then to a change in the antigenic properties of its components with their transformation into autoantigens and the development of an autoimmune process. Genetic predisposition plays an important role. Morphologically, the systemic inflammatory process in rheumatism manifests itself in characteristic phase changes in the connective tissue. This is mucoid swelling - fibrinoid change - fibrinoid necrosis. Also in the morphology of rheumatism, cellular reactions play an important role (infiltration by lymphocytes and plasmocytes). These cellular reactions are the histological reflection of allergy in rheumatic fever. From the stage of fibrinoid changes, complete tissue restoration is no longer possible, the process ends with sclerosis (i.e., replacement with connective tissue).

Clinical manifestations of the disease in typical cases develop 1-2 weeks after suffering a sore throat or other infection. But with repeated attacks, this period may be shorter. In some patients, even primary rheumatism occurs 1-2 days after cooling without any connection with infection. Exacerbations develop after any concomitant diseases, operations, physical exertion. Characteristic is the fact that the patient can clearly and accurately indicate the day of onset of the disease. In the first period of the disease, fever is often noted (usually subfebrile), the general condition is unchanged. In some patients with polyarthritis or serositis, the condition may be severe: with a high persistent fever up to 38-40 ^oC with daily fluctuations of 1-2 ^oWith and profuse sweats (but no chills). However, in recent years, this condition has been observed extremely rarely.

The most common manifestation of rheumatism is an inflammatory lesion of the heart. Any membranes of the heart can be involved in the process, but primarily the myocardium. It should be noted that rheumatism often proceeds without any obvious changes in the heart. A regularity is noted: the older the patient who first fell ill with rheumatism, the less serious the rheumatic heart disease.

Rheumatic myocarditis. This disease in adults, as a rule, is not particularly severe. Patients complain of mild pain and vague discomfort in the region of the heart, slight shortness of breath during exertion, less often - of palpitations or interruptions in the heart. On x-ray, the heart is of normal size or moderately enlarged. Circulatory failure practically does not develop. In some patients in childhood, the so-called diffuse rheumatic myocarditis can occur, which is manifested by violent allergic inflammation of the myocardium with its pronounced edema and dysfunction.

The disease from the very beginning is manifested by severe shortness of breath up to the adoption of a forced position to facilitate breathing (orthopnea). Patients complain of constant pain in the region of the heart, palpitations. Characterized by the so-called pale cyanosis, swelling of the cervical veins. The heart is considerably and evenly dilated. Very characteristic of diffuse myocarditis is the development of circulatory failure, both in the left ventricular and right ventricular types. In adults, this variant of rheumatic myocarditis is currently practically not found.

Rheumatic endocarditis. It proceeds in isolation and is very poor in general symptoms. The main signs of rheumatic endocarditis are systolic and diastolic murmurs, which appear to be due to thrombotic overlays on inflammatory valves.

Occasionally, these overlays serve as sources of embolism in the vessels of the small or large circulation with the development of infarctions of the lungs, kidneys, spleen, gangrene of the extremities, central paralysis, etc. If endocarditis is the only localization of rheumatism, then patients constitute the so-called outpatient group. This means that with this course of rheumatism, good general health and ability to work are maintained for a long time. After a certain time, a heart disease is formed with concomitant hemodynamic disorders, and this makes patients see a doctor for the first time.

Pericarditis. For modern rheumatism is very rare. Dry pericarditis is manifested by constant pain in the region of the heart and pericardial friction rub. Exudative pericarditis is characterized by the accumulation of serous-fibrous exudate in the heart sac and is essentially the next stage of dry pericarditis. Characterized by shortness of breath, which increases in the supine position. With a significant accumulation of exudate, the region of the heart swells somewhat, the intercostal spaces are smoothed, the apex beat is not palpable. The enlargement of the heart is significant, it takes the characteristic shape of a trapezoid or a round decanter. Tones and noises are very muffled. Often the outcome of rheumatic pericarditis are small adhesions between the outer sheet and surrounding tissues. Much less common is the complete fusion of the sheets of the heart bag, i.e., an adhesive obliterating pericarditis develops, the so-called armored heart.

Rheumatic vascular disease. With rheumatism, the vessels in the internal organs (arteritis of the internal organs) are mainly affected, which is the basis for the manifestations of rare rheumatic visceritis: nephritis, meningitis, encephalitis, etc.

Joint damage. Currently, acute rheumatic fever is relatively rare. Characteristic manifestations of rheumatic polyarthritis are increasing acute pain in the joints, aggravated by movement and palpation. Within a few hours, the pain becomes extremely sharp. Very quickly, symptoms of joint damage join the pains: swelling, sometimes hyperemia. Symmetrical lesions of large joints and volatility of arthritis are characteristic. Rheumatoid arthritis is completely reversible: all articular manifestations (regardless of their severity at the onset of the disease) disappear without a trace.

At present, only pronounced arthralgias are much more common without swelling of the joints, swelling is mild or completely absent, inflammation of small joints is predominantly observed. Also often there is no symmetry of the lesion. Very rarely there is rheumatic myositis with characteristic severe pain in the muscles.

Skin lesions. With rheumatism, skin lesions occur in the form of rheumatic nodules, annular or nodular erythema, urticaria, etc. Rheumatic nodules are usually located in the area of ​​the affected joints, over bony prominences, in the occipital region, on the forearms and legs.

It is characteristic that under the influence of treatment (and sometimes without it) they disappear within a few days and are now practically not found. A very characteristic sign of rheumatic skin lesions is erythema annulare, which is pink ring-shaped elements that never itch, located mainly on the skin of the inner surface of the arms and legs, abdomen, neck and trunk. This symptom, like rheumatic nodules, is pathognomonic for rheumatism, but is found infrequently, only in 1-2% of patients.

Rheumatic lesions of the lungs. There are rheumatic pneumonias and pleurisy, but this is extremely rare. Usually they occur against the background of already developed rheumatism. The distinguishing features of rheumatic pneumonias are their resistance to antibiotics and the good effect of the use of antirheumatic drugs (without antibacterials). Pleurisy in rheumatism is often bilateral and well reversible. Rheumatic nephritis is rare, and antirheumatic drugs are especially effective in their treatment.

Rheumatic affections of the digestive organs. Such rheumatic lesions have no significant clinical significance. Gastritis or ulcers of the stomach and intestines are the consequences of long-term medication, especially steroid hormones. Only children suffering from rheumatism sometimes have severe abdominal pain associated with allergic peritonitis, which quickly passes, that is, is completely reversible. Distinctive features of rheumatic peritonitis are the diffuse nature of pain, their combination with other signs of rheumatism and the very rapid effect of the use of antirheumatic drugs. Often, pain can disappear without treatment.

In some patients with high activity of the rheumatic process, the liver may be enlarged and slightly painful due to interstitial hepatitis (damage to the connective tissue elements of the hepatic parenchyma).

Changes in the nervous system. Such changes are specific. The so-called chorea is a nervous form of rheumatism. It occurs mainly in children, more often in girls.

It is clinically manifested by emotional instability, muscle weakness and violent fanciful movements of the torso, limbs and mimic muscles of the face. When excited, these movements increase, and during sleep they disappear. Chorea minor can relapse, but by the age of 17-18 it almost always ends. With this form of rheumatic damage, the heart suffers slightly, laboratory indicators of rheumatism activity are also slightly expressed (ESR is often not accelerated).

The central nervous system rarely suffers from rheumatism. If this occurs, then usually the lesions proceed as a combination of encephalitis and meningitis. Central nervous system lesions respond well to antirheumatic therapy.

Laboratory data. Patients with the maximum degree of activity of the process have neutrophilic leukocytosis up to 12-15 × 10³. At the same time, there is a shift of the formula to the left due to an increase in stab leukocytes. In the leukogram, metamyelocytes and myelocytes may appear. In most patients, the number of leukocytes and the leukogram are not significant. In the acute period of the disease, the number of platelets is increased, but this increase does not last long. Most patients with rheumatism have an accelerated ESR, reaching maximum numbers (40-60 mm / h) with polyarthritis and polyserositis. Shifts in immunological indicators are very characteristic. These include an increase in titers of antistreptococcal antibodies (antistreptohyaluronidase, antistreptokinase, antistreptolysin). An increase in the level of these antibodies reflects the body's reaction to exposure to streptococci, and therefore often occurs after any streptococcal infections (as well as the detection of streptococcal antigens in the blood or urine). But the height of titers of antistreptococcal antibodies and their dynamics do not reflect the degree of activity of rheumatism. In very many patients with chronic forms of rheumatism, there are no signs of participation of streptococcal infection at all. Biochemical indicators of the activity of the rheumatic process are non-specific, that is, they occur in various types of inflammation and tissue decay. In cases where the diagnosis of rheumatism is justified by clinical and instrumental data, biochemical studies are important to determine the activity of the disease.

These biochemical studies include an increase in fibrinogen levels, an increase in α₂-globulins, γ-globulins, hexoses, ceruloplasmin, seromucoid, diphenylamine reactions, etc. But the most revealing and accessible of all biochemical studies is the detection of C-reactive protein in the blood. In most cases, biochemical indicators of activity are parallel to the values ​​of ESR, which is the best laboratory sign of the activity of rheumatism, as well as its dynamics.

There are two phases of rheumatism: inactive and active. The activity of the disease can be of three degrees: the first degree is minimal, the second degree is average, the third degree is maximum. The activity of rheumatism is judged by the severity of clinical manifestations and changes in laboratory parameters.

In modern conditions, the nature of the course of the disease has changed significantly. The number of patients with bright, violent manifestations and a protracted and continuously relapsing course has sharply decreased. Other visceral lesions became casuistry.

Suspicion of rheumatism should be caused by any disease that occurs 1-3 weeks after a sore throat or other nasopharyngeal infection and is characterized by signs of damage to the joints and heart. Significant diagnostic criteria are objective evidence of cardiac involvement, rapidly reversible arthritis of the large joints, chorea minor, erythema annulare, and subcutaneous nodules with rapid regression. The prognosis for rheumatic lesions is based mainly on the degree of reversibility of the symptoms of rheumatic heart disease. The most unfavorable are continuously recurrent rheumatic carditis, which lead to the formation of heart defects, myocardiosclerosis. Rheumatism is more severe in children. In them, it often leads to persistent changes in the valves of the heart. Also, the likelihood of developing heart defects increases with late treatment. If the primary disease occurs in a patient over the age of 25, then the process, as a rule, proceeds favorably, and heart disease is extremely rare.

It is a disease of unclear etiology with a characteristic combination of arthritis, urethritis, conjunctivitis, and in some cases, a kind of dermatitis. In the development of the disease, it is considered likely that the genetic characteristics of the immune system play a decisive role. The disease affects mainly young men. Often the disease is preceded by non-gonococcal urethritis or acute intestinal upset.

Clinically, arthritis ranges from moderate, transient to severe, prolonged, or recurrent. More often one large joint is affected. The duration of arthritis in Reiter's syndrome ranges from 2 to 6 months, less often - longer. Many patients have lesions of the spine. The severity of urethritis can be different, often it is found only during special examinations or urine tests, i.e., it is almost asymptomatic. Conjunctivitis is usually also not severe, quickly passing. In some cases, there may be dermatitis. Rarely, but lesions of internal organs can occur: arthritis with the development of aortic valve insufficiency, myocarditis, pericarditis, enteritis, polyneuritis, meningoencephalitis.

Laboratory data are nonspecific. Disease activity is determined by the value of ESR (acceleration) and an increase in the level of biochemical indicators of inflammation (fibrinogen, C-reactive protein, etc.). The course of the disease varies, spontaneous recovery is often noted. Diagnosis in the presence of the entire triad of symptoms does not cause difficulties.

Chronic systemic connective tissue-vascular disease characterized by progressive fibrosis. The etiology is probably viral, since when examining the affected tissues with an electron microscope, virus-like particles were detected and an increase in the titers of a number of antiviral antibodies was noted.

Pathogenetic mechanisms are quite complex and are associated with metabolic and structural disorders on the part of collagen formation and the main substance of the connective tissue. Also in pathogenesis an important role is played by disorders of microcirculation, as well as humoral and cellular immunity. The role of family genetic predisposition is significant. Women get sick three times more often than men.

The onset of the disease is usually gradual, rarely acute. Provoking factors are cooling, trauma, infections, vaccinations, etc. More often, the disease begins with Raynaud's syndrome (vasomotor disorders). There are also violations of tissue trophism, joint pain, weight loss, asthenia, fever. As a rule, systemic scleroderma, starting with a single symptom, gradually or rather quickly becomes a generalized multisyndromic disease.

The pathognomonic (specific) sign of the disease is a skin lesion. This is a widespread dense edema, and in the future - thickening and atrophy of the skin. The greatest changes occur with the skin of the face and limbs. But often the skin of the entire body becomes dense. At the same time, focal or widespread pigmentation develops with areas of depigmentation and expansion of small vessels. Ulcerations and pustules on the fingertips are characteristic, very painful and do not heal for a long time, deformation of the nails, hair loss (up to baldness) and other trophic disorders.

Fibrolyzing interstitial myositis is often noted. Muscle syndrome is manifested by muscle pain, progressive compaction, then muscle atrophy, and a decrease in muscle strength. In rare cases, many muscles are affected (acute polymyositis) with pain, muscle swelling, etc. The replacement of muscle fibers with connective tissue is also accompanied by tendon fibrosis, which leads to muscle-tendon contractures, which are one of the main causes of early disability in patients. In 80-90% of cases, pain in the joints is observed, often accompanied by joint deformity, often quite pronounced due to changes in the periarticular tissues.

X-rays did not reveal significant lesions. An important diagnostic sign is osteolysis (resorption) of the terminal, and in severe cases, the middle phalanges of the fingers, less often of the legs. With scleroderma, deposits of calcium salts are observed in the subcutaneous tissue. These deposits are localized mainly in the area of ​​​​the fingers and in the periarticular tissues and appear as uneven, painful formations that can spontaneously open with the rejection of crumbly calcareous masses.

In almost all patients, the cardiovascular system is affected by the type of myocarditis, endocarditis, and rarely - pericarditis. As a result of inflammatory lesions of the heart, scleroderma cardiosclerosis is formed, which is clinically manifested by pain in the region of the heart, shortness of breath, arrhythmia in the form of extrasystole, muffled tones, systolic murmur at the apex, and expansion of the heart to the left. Localization of the process in the endocardium leads to the formation of scleroderma heart disease. The mitral valve is usually affected. Scleroderma heart disease is characterized by a benign course. Heart failure rarely develops, only with widespread, pronounced myocarditis or with damage to all membranes of the heart at once.

Peripheral symptoms of scleroderma are caused by damage to small arteries, arterioles. The consequences of these lesions are Raynaud's syndrome, telangiectasia, gangrene of the fingers. Damage to the vessels of internal organs leads to severe visceral pathology. Hemorrhages, ischemic phenomena and even necrotic changes in organs are observed. There may be a breakdown of lung tissue, a true scleroderma kidney, etc. Vascular pathology determines the speed of the process, its severity, and even the outcome of the disease. It is also possible to damage large vessels with a picture of thromboangiitis obliterans, the development of ischemic phenomena, migrating thrombophlebitis with trophic ulcers in the feet and legs, etc. Lung damage is usually accompanied by emphysema and bronchiectasis due to focal or diffuse pneumofibrosis. Focal nephritis often develops in the kidneys, but in some cases diffuse glomerulonephritis with hypertension and renal failure is possible.

Damage to the nervous system is manifested by polyneuritis, vegetative instability, characterized by impaired sweating, thermoregulation, and vasomotor reactions of the skin. There may also be emotional lability, irritability, tearfulness, suspiciousness, insomnia. In very rare cases, a picture of encephalitis or psychosis occurs. In connection with scleroderma lesions of the cerebral vessels, symptoms of sclerosis are possible even in young people. Lesions of the reticuloendothelial system are possible, which are manifested by an increase in the number of lymph nodes and the spleen, as well as damage to the endocrine system in the form of a pathology of any endocrine gland. In the subacute course, the disease begins with pain in the joints, fever, weight loss, the pathology of the internal organs is rapidly growing. In this case, the disease acquires a steadily progressive course with the spread of the pathological process to many organs and systems. Usually patients die in 1-2 years from the onset of the disease. Much more often there is a chronic course. The disease lasts for decades with minimal activity of the process and the gradual spread of lesions to internal organs, the functions of which are not disturbed for a long time.

Patients suffer mainly from damage to the skin, joints and trophic disorders. In chronic systemic scleroderma, calcification, Raynaud's syndrome, telangiectasia, and finger damage are isolated. All these pathologies are characterized by a long benign course with an extremely slow development of damage to internal organs. Laboratory data are not representative. Usually there is a moderate leukocytosis and eosinophilia, transient thrombocytopenia. ESR is normal or moderately accelerated in chronic course and very high (up to 50-60 mm / h) - in subacute.

Chronic inflammatory disease of the joints of the spine with a tendency to develop a gradual limitation of movements in them. The etiology and pathogenesis are not yet clear. Great importance is attached to the genetic characteristics of the immune system. The disease affects mainly men.

An obligatory symptom of Bechterew's disease is a lesion of the spine. But this defeat is often limited for a long time only to the sacroiliac joints (sacropleitis). Manifestations of sacropleitis can be vague (in the form of discomfort, mild pain) and inconsistent. Sometimes subjective sensations may be completely absent, and only an X-ray examination reveals a lesion of the sacroiliac joint. As the small joints of the spine are involved in the process, pains appear in one or another of its departments (sometimes in the entire spine). Very often the pain intensifies at night, and in the morning there is stiffness. Later, restrictions on the movements of the spine join: the patient cannot reach the floor with his fingers without bending his knees, his chin - the sternum, there is a decrease in the respiratory excursion of the chest. Gradually, the physiological curves of the spine are smoothed out, hyperkyphosis of the thoracic region is formed, i.e., a very characteristic supplicant posture appears. The course of this form of Bechterew's disease (central) is usually slow, long-term, with periods of exacerbations and remissions. Damage to non-vertebral joints, which has some features, is also characteristic. The large joints of the lower extremities (hip, knee, ankle) are more often affected, often also the shoulder and sternoclavicular joints. Oligoarthritis and asymmetric joint damage (peripheral form) are typical. Most often, the disease is short-lived (1-2 months), but it can also be protracted.

Pain in the muscles, especially in the back, the development of inflammation in the region of the Achilles tendon are also characteristic. In some cases, the internal organs are affected: the eyes (lesion of the iris), the aorta (aortitis), the myocardium (sometimes with impaired atrioventricular conduction), the endocardium with the formation of valve insufficiency, the kidneys (glomerulonephritis, urethritis). With a long course, amyloidosis often develops with a primary lesion of the kidneys.

The diagnosis is made on the basis of an x-ray examination (radiography), where characteristic changes are found. Sacropleitis is the earliest X-ray symptom of a spinal lesion; in some cases, it develops as early as 4-6 months from the onset of the disease.

It is a chronic inflammation of the endocrine glands, mainly salivary and lacrimal, leading to their secretory insufficiency. It may be an isolated syndrome (this is the so-called dry syndrome). The name speaks for itself, since the most striking clinical signs are dry mouth and eyes. The cause of the disease has not been fully elucidated, but the most likely opinion is about autoimmune genesis, which is confirmed by the frequent combination with other diseases of an autoimmune nature: rheumatoid arthritis, systemic lupus erythematosus, systemic scleroderma, etc. Mostly middle-aged women get sick. Sjögren's syndrome is characterized by a combination of dry keratoconjunctivitis (xerophthalmia) and dry stomatitis (xerostomia), which are associated with damage to the lacrimal and salivary glands and secretory insufficiency. There are also recurring parotitis (lesions of the parotid glands), usually symmetrical, pain and swelling in the region of the submandibular glands. Dry eyes (xerophthalmia) is manifested by a constant burning sensation, sensation of a foreign body in the eyes, photophobia, a sharp decrease or complete disappearance of tears. Consequences of constant dryness in the mouth are difficult chewing and swallowing. Glossitis (inflammation of the tongue), cheilitis (inflammation of the red border of the lips), progressive dental caries develop.

Patients are concerned about constant pain in the joints, periodically swelling, but there are no severe deformities and destructions with dry syndrome. Raynaud's syndrome is also observed, and drug intolerance is often present. Laboratory data are quite characteristic: positive rheumatoid factor, accelerated ESR. Diagnosis is based on two of three features: xerophthalmia, xerostomia, and autoimmune disease. Sjögren's syndrome proceeds as a chronic relapsing disease with involvement of the lymph nodes and internal organs in the process.

In addition to such a large group of acquired immunodeficiencies as collagenoses, which occur as autoimmune lesions, there are also autoimmune diseases of other body systems. For example, these include diseases of the blood system (agranulocytosis, autoimmune hemolytic anemia), the nervous system (multiple sclerosis).

Agranulocytosis is a decrease in the number of leukocytes (less than 1000 in 1 μl of blood) or the number of granulocytes (less than 750 in 1 μl of blood). As a rule, agranulocytosis is a symptom of some general disease. The most common are myelotoxic agranulocytosis (cytostatic disease) and immune. Immune agranulocytosis is caused by the appearance of autoantibodies (for example, in systemic lupus erythematosus) and antibodies to granulocytes after taking medications (the so-called haptens). Haptens are drugs that, when ingested, combine with a protein and acquire the properties of an antigen. Hapten agranulocytosis is caused by diamox, amidopyrine, antipyrine, acetylsalicylic acid, barbiturates, isoniazid (tubazid), meprobamate, phenacetin, butadione, plasmoquine, indomethacin, levamisole, sulfonamides, biseptol, chloroquine, antidiabetic sulfanilamide drugs, insecticides (insecticides).

The mechanism of development of agranulocytosis is not well understood. In autoimmune forms of damage, premature death of granulocytes and their bone marrow precursors is caused by autoantibodies. The very mechanism of the body's individual reaction to the ingestion of a drug in hapten agranulocytosis is not yet clear. It is characteristic that, once having arisen, haptenic agranulocytosis will invariably repeat when the same drug, hapten, is introduced into the body. Clinical manifestations are due to agranulocytosis itself (i.e., a sharp decrease in the number of leukocytes, defender cells). Therefore, septic complications are typical: tonsillitis, pneumonia, etc. In a laboratory study, granulocytes in the blood are not detected, but the number of lymphocytes, platelets, and reticulocytes is normal. There is no bleeding or hemorrhage. Occasionally, the appearance of antibodies to platelets is also possible, then thrombocytopenic hemorrhagic purpura occurs. The prognosis of autoimmune agranulocytosis is determined by the underlying diseases (systemic lupus erythematosus, rheumatoid arthritis, etc.). Hapten agranulocytosis gives a high percentage of deaths (up to 80%). The prognosis is sharply aggravated with repeated ingestion of haptens into the body. Since it is often very difficult to determine which drug was a hapten, all suspected drugs have to be excluded from use for life. It is this rule that is the main preventive measure for repeated hapten-type agranulocytosis.

These are anemias that are caused by the action of antibodies on red blood cells. There are several forms of immune hemolytic anemia. These are autoimmune anemias caused by the formation in the body of antibodies against its own red blood cells; haptenic, caused by the fixation on erythrocytes of hapten antigens alien to the body (drugs, viruses, etc.) with antibodies formed in response to the combination of the hapten with the protein of the body; isoimmune, associated with the ingestion of maternal antibodies directed against the child's erythrocytes into the body of the newborn (with incompatibility between the child and the mother by the Rh factor and much less often by the blood group).

The basis of the pathological process is the breakdown of immunological insensitivity to its own antigen. The leading symptom of the clinical picture is anemic syndrome. The severity of the condition is determined by the severity and severity of anemia. When the process develops slowly, the first sign of the disease may be a slight jaundice (due to indirect bilirubin), and anemia is also detected at the same time. In other cases, the onset of the disease is rapid, with hemolysis (destruction of red blood cells), rapidly increasing anemia, and jaundice. Often the body temperature rises. Sometimes the spleen and liver are enlarged. A systolic murmur is heard at the apex and base of the heart, which has a functional nature. In the blood test, normochromic anemia is determined, and in the acute course of the disease, the hemoglobin level can drop to catastrophic numbers. Then the patient may fall into an anemic coma. In acute hemolysis, single erythrokaryocytes can be determined in the blood. The level of reticulocytes is also high. The leukogram does not change significantly, but a hemolytic crisis may be accompanied by a short neutrophilic leukocytosis. The platelet count is usually normal. However, autoimmune cytolysis (cell breakdown) occurs, affecting two germs: platelet and erythrocyte (Ivens-Fischer syndrome). In this case, there are signs of hemolytic anemia and thrombocytopenic purpura. With autoimmune hemolytic anemia, irritation of the red germ occurs in the bone marrow, i.e., when hemolysis is combined with thrombocytopenia, high megakaryocytosis is noted in the bone marrow. In a biochemical study, in addition to hyperbilirubinemia, there is an increase in α-globulins.

The prognosis of the disease cannot be given. It may be the only episode of the breakdown of red blood cells, or it may turn into a chronic hemolytic process. In addition to this most common form of autoimmune hemolytic anemia, in which hemolysis occurs intracellularly, there is a form of the disease with intravascular hemolysis. The difference between these forms is that with intravascular hemolysis, dark urine is released due to hemoglobinuria and hemosiderinuria. In severe hemolysis, thrombosis is possible in the system of mesenteric vessels with the appearance of severe paroxysmal pain in the abdomen. In rare cases, there may be intravascular hemolysis on cooling (cold hemoglobinuria). Another form of autoimmune hemolysis is also associated with exposure to cold, in which intracellular hemolysis occurs, provoked by the cooling of the body. In this case, autoagglutination (gluing) of erythrocytes is noted immediately after taking blood from a finger when it is cooled to room temperature.

The diagnosis of autoimmune hemolytic anemia is made on the basis of the general signs of hemolysis: an increase in the level of bilirubin in the blood or the appearance of bilirubin in the urine, an increase in the percentage of reticulocytes in the blood, and the detection of autoantibodies on the surface of red blood cells using the Coombs test (a special laboratory test), which is positive in almost 60% cases of autoimmune hemolysis.

A disease of the nervous system, which is based on the occurrence of demyelination foci scattered throughout the brain and spinal cord, which either disappear with time or are replaced by plaques (glial scars). The cause of this disease is not clear enough. Most likely, autoimmune reactions are involved in the mechanism. The demyelinating process mainly affects the white matter of the central nervous system. The affected area undergoes remyelination, after the breakdown of myelin, the axial cylinders are also damaged, followed by the formation of a characteristic dense glial plaque ranging in size from several millimeters to several centimeters. Remyelination (restoration of myelin) underlies clinical remissions. With the development of scars, the functions of the affected areas of the central nervous system are irreversibly lost.

The disease usually occurs at a young age. In childhood and after 50 years, the disease develops extremely rarely. The first symptoms of the disease are transient motor, sensory (often numbness) or visual disturbances. Over time, newly emerging lesions are no longer subject to reverse development. There is a steady increase in the severity of the clinical picture. More often than others, the pyramidal and cerebellar systems and the optic nerves are affected. Almost always (in 90% of cases) in the advanced stage of the disease there is lower spastic paraparesis or tetraparesis (weakness in the lower extremities or in the upper and lower extremities). At the same time, cerebellar disorders are expressed: gait disturbances, speech disorders, involuntary movements of the eyeballs (nystagmus). There is a pronounced tremor of the limbs and head, and the trembling is detected during active movements and tension, but it can also be at rest. The combination of nystagmus, speech disorders (chanted speech), and trembling together form the Charcot triad, which is a characteristic feature of multiple sclerosis.

Damage to the optic nerves leads to a decrease in visual acuity. On the fundus there is blanching of the temporal discs. Urinary disorders are common. Many patients have a kind of euphoria, and in advanced cases, dementia (dementia) is not uncommon. In about 85% of cases, multiple sclerosis is characterized by a remitting course, that is, periods of exacerbation are replaced by a significant improvement, and often the complete disappearance of all or individual signs of the disease. The duration of improvements can range from a few hours to several years. Especially good remissions are observed in the first years of the disease. However, after a few years, most patients become disabled to some extent. In advanced and irreversible stages of the disease, a combination of paresis with ataxia (staggering gait) is especially characteristic. The onset of the disease in many patients may be preceded by febrile illness, vaccination, trauma, surgery, pregnancy.

Studies of the cerebrospinal fluid help to confirm the diagnosis, in which in almost 90% of cases there are certain anomalies, for example, such as a moderate increase in protein, a paralytic type of colloidal Lange reaction, and an increase in the level of α-globulins.

AIDS is an acquired immunodeficiency syndrome that is caused by the human immunodeficiency virus (HIV), so the disease has a double name: AIDS or HIV infection. The human immunodeficiency virus was isolated in 1983 by French and then American researchers. The detection of the virus in certain substrates associated with the diseased (blood, saliva, semen) made it possible to clarify the ways of transmission of the disease. In turn, the establishment of the etiology made it possible to develop work on the serological diagnosis of the infection. Thus, AIDS was clearly differentiated from other acquired immunodeficiencies.

AIDS is a severe disease, with a far advanced disease, the death of the patient is almost inevitable. In terms of mortality, AIDS came in third after atherosclerosis and cancer. True, this applies to forms of the disease with a pronounced clinical picture. Despite the fact that AIDS is not a widespread disease, the increase in the number of cases, according to scientists, is growing exponentially. It is believed that the number of cases is doubling every six months. It is also alarming that, according to the latest data, the contingent with antibodies to the virus - the causative agent of AIDS, is in the millions. All this raises fears that acquired immunodeficiency may become a mass disease in the future. There is also a wide geographical distribution of AIDS. There is currently no inhabited continent free of this disease.

The human immunodeficiency virus belongs to the so-called retroviruses. Retroviruses are the only living creatures in the world that can synthesize DNA from RNA, while the rest can only synthesize RNA from DNA. For this purpose, the viruses of this group have the enzyme reverse transcriptase. Hence the name of the retrovirus (from Latin "retro" - "reverse"). Among the animal viruses that cause immunodeficiency states, simian retroviruses are of the greatest interest. Once in the human body, the human immunodeficiency virus attaches to special formations located on the lymphocyte cell, then penetrates inside it, integrates into the genetic apparatus of the cell and causes it to produce virus particles until the cell dies. New viruses infect new cells, and so on. Before the number of lymphocytes drops to such an extent that immunodeficiency develops, it can take a dozen years. But all this time, an infected person, feeling healthy, can be a source of infection for others.

This infection has a number of clinical and epidemiological features. These include:

1) an unusually (for the vast majority of infections) long incubation period (sometimes exceeding 5 years), so AIDS can be attributed to the so-called slow viral infections;

2) an exceptionally "narrow" application of the virus - it affects only some categories of immunocompetent cells, but this does not prevent the occurrence of a total defeat of the entire defense system of the body;

3) the infection does not have a definite clinical picture - its manifestations are determined by opportunistic conditions (i.e., adapting to certain conditions), the clinic of which is extremely diverse, which makes a purely clinical diagnosis of the disease impossible.

Many features of the disease are currently not amenable to rational explanation. The origin of AIDS remains unclear. However, the mechanism of the impact of the AIDS virus on the body has already been sufficiently studied and the clinical manifestations of the disease in the advanced stage have been described. The main thing in the pathogenesis of HIV infection is the revealed ability of the virus to selectively turn off T-helpers, as a result of which the immune response does not develop, and the person becomes completely defenseless against any infection or pathology (it can even die from opportunistic bacteria). The virus, getting into T-helpers, can be in an inactive state for many years, but a person is already infected. When HIV for some reason becomes active, AIDS develops, most patients die within 1-2 years.

Pathoanatomical changes in those who died from AIDS are diverse and largely depend on the nature of the opportunistic diseases that led to death. In those who died from AIDS, widespread inflammatory and suppurative processes are found: lung abscesses, damage to the liver, kidneys, heart, and lymph nodes. Ulceration of the esophagus and intestines were noted. If there were infections (toxoplasmosis and cryptococcosis), then corresponding changes are found in the substance of the brain.

Histological examination of the material shows the absence of granulomas as a characteristic sign of AIDS. Electron microscopy in biopsies of various tissues revealed multiple tubular-reticular inclusions in the cytoplasmic reticulum of endothelial cells, histocytes and lymphocytes. In preparations made from bronchial swabs, saliva, urine, gastric juice, pronounced cellular atypia, an increase in mature and immature lymphoreticular elements are found. In the bone marrow, a normal and somewhat increased number of nucleated cells is noted with a normal ratio of myeloid and erythrocyte cells, moderate plasmacytosis, and a slight increase in reticulin. The number of lymphocytes is reduced. Bone marrow puncture shows histiocytes, many of which are engulfed by nucleated erythroid cells or granulocytes, which is similar to the virus-associated phagocytic syndrome described in patients with immune system dysfunction. In the lymph nodes - intense follicular hyperplasia, the size and shape of the follicles, cellular composition disorders similar to those in the blood, in particular, the predominance of T-suppressors. Thymus pathology in children with AIDS was studied. A sharp decrease in the number of lymphocytes and Hassal's bodies was noted. In those who died from the malignant course of AIDS, there was no division into the cortical and medulla in the thymus gland, Hassall's bodies and accumulations of epithelial cells were not detected. Thymus tissue was infiltrated with plasma and mast cells.

Changes in the thymus in AIDS and congenital immunodeficiency are associated with damage to the T-system, but a thorough pathological and anatomical study makes it possible to clearly differentiate AIDS from congenital immunodeficiency.

AIDS is characterized by a normal anatomical position and configuration of the thymus with normal blood vessels. The described changes in immunodeficiencies and one of the central organs of the immune system (thymus gland) lead to serious violations of its function. Delayed-type hypersensitivity reactions (to tuberculin, streptokinase, trichophytin) are sharply suppressed. The proliferative activity of lymphocytes when stimulated by their soluble antigens is reduced. At the same time, the level of immunoglobulins (JgM, JgJ, JgA) is increased.

The presence of lymphocytotoxic antibodies in the blood serum of AIDS patients, which are combined with a deficiency of cellular immunity, has been established. AIDS patients lack the synthesis of interleukin-2. The production of interleukin-2 is inhibited by hypersecretion of prostaglandins. After the isolation of the causative agent of AIDS, the development of methods for determining antibodies to the virus, it was found that the number of people with antibodies to the pathogen significantly (about 50-100 times) exceeds the number of patients with clinically expressed AIDS. With regard to the ways of transmission of infection, there is no doubt that AIDS is transmitted by direct contact during sexual intercourse. Another way of transmitting the infection is considered to be the contact-household route - through objects contaminated with the blood of sources of infection, when the virus enters the body through small defects on the skin and mucous membranes. The possibility of "vertical" transmission of infection from virus-carrying mothers or patients is undoubted. Already the first work of US scientists made it possible to identify a contingent that has an increased risk of AIDS, that is, the so-called risk groups. It includes homosexuals, intravenous drug addicts, patients with hemophilia, persons receiving numerous blood transfusions (blood transfusions).

Characterizing the clinic of this serious and dangerous disease, there is reason to distinguish three main forms of infection: asymptomatic; an infection that proceeds according to the type of generalized lymphadenopathy and AIDS itself, when, in addition to the general symptoms characteristic of immunodeficiency, various opportunistic diseases occur with a predominant lesion of certain systems. The main feature of this infection is the duration of the incubation period. Without a doubt, AIDS is an infection with a very long incubation (from several months to several years). Moreover, the duration of incubation for different age groups is not the same. For example, in patients who had homosexual contact with other AIDS patients, the incubation period ranged from 9 to 22 months. With blood transfusion, incubation can be extended up to 58 months. The average duration of the incubation period in children is 12 months, in adults - 29 months, with infection during blood transfusion, incubation increases by 4 years.

At the end of the incubation period, the disease phase begins, which in various sources is indicated by different terms: generalized lymphadenopathy, persistent generalized lymphadenopathy, AJDS side complex, lymphadenopathy syndrome, chronic lymphadenopathy, prolonged unmotivated lymphadenopathy syndrome, prodrome phase, preAIDS. It is believed that generalized lymphadenopathy in some cases is a transitional phase of the development of infection (prodroma, preAIDS), in other (favorably current) cases, the clinic of the disease does not receive further development, i.e. generalized lymphadenopathy ends with recovery and acts as an independent form of the disease.

All of the above names for this condition emphasize the characteristic feature - lymphadenopathy. In patients, lymph nodes increase in several parts of the body at once. Diagnostic value is an increase in at least two groups of lymph nodes outside the inguinal region. Lymph nodes are moderately painful (but may be painless), not associated with fiber, mobile, 1-3 cm in diameter. The duration of lymphadenopathy is very characteristic - at least 3 months, often for a number of years. In addition to lymphadenopathy, in this condition, a temperature reaction of a recurrent type, night sweats, and increased fatigue are noted. Characteristic signs are weight loss (a decrease in body weight by at least 10%), as well as chronic diarrhea. Skin manifestations are less common: rashes, in some cases fungal diseases, seborrheic dermatitis of the face, frontal alopecia.

Laboratory studies reveal lymphopenia, a change in the ratio of T-helpers to T-suppressors in favor of T-suppressors, a decrease in the response of T-cells to mitogens, and a violation of delayed-type hypersensitivity reactions. The presence of antibodies to the human immunodeficiency virus (HIV) is detected in approximately 80% of patients. The levels of JgM, JgJ and JgA are increased. Increased amount of LJ-thymosin. Thus, laboratory data correspond to classical AIDS, but are less pronounced. In a minority of patients with generalized lymphadenopathy (about 1 in 10), the disease turns into "real" AIDS.

Characterizing the course of AIDS, the researchers point out that the AIDS clinic does not have clear nosological contours. There is a peculiar combination of causal and co-causal factors that create a severe pathology, the nature of which is determined by opportunistic infections.

Early signs of AIDS are worsening symptoms of the previous period - the pre-AIDS period:

1) fever of unknown etiology with a course that is not amenable to conventional treatment;

2) lymphadenopathy;

3) increasing general weakness;

4) loss of appetite;

5) diarrhea;

6) weight loss;

7) enlargement of the liver and spleen;

8) cough;

9) leukopenia with possible addition of erythroblastopenia.

Later, visual disturbances associated with retinitis (inflammation of the retina) may occur. There are several types of the course of the disease. Respiratory system lesions are the most common manifestation of AIDS. They were noted in 60% of patients. The so-called pulmonary type includes hypoxemia, chest pain, diffuse pulmonary infiltrates on x-ray. The most common opportunistic infection associated with lung involvement is pneumocystis pneumonia, with legionella lung disease and cytomegaly being much less common.

Damage to the central nervous system occurs in about 1/3 of AIDS patients, and there are several main forms:

1) abscesses caused by toxoplasma;

2) progressive multifocal leukoencephalopathy;

3) cryptococcal meningitis, subacute encephalitis (usually cytomegalovirus etiology);

4) tumors, such as primary and secondary brain lymphomas;

5) vascular lesions (non-bacterial thrombotic endocarditis and cerebral hemorrhage associated with thrombocytopenia);

6) lesions of the central nervous system with focal brain damage with non-diffuse (self-limiting) meningitis.

In addition to infection, AIDS patients have hypoxic phenomena and thromboembolism. According to clinical observations, in approximately 25% of patients, the immediate cause of death was damage to the central nervous system. As a result of clinical studies, data were obtained on the possibility of an indefinitely long-term preservation of the AIDS virus in brain cells, from where the pathogen can enter the bloodstream, causing disorders of the immune system. The AIDS virus located in the brain cells can cause dementia (dementia), which is not associated with damage to the immune system.

Another type of AIDS course is gastrointestinal, which is characterized by diarrhea and a significant decrease in body weight. The pathological process in the small and large intestines has a specific character. But these types of diseases are not limited to the pathologies of various systems observed in AIDS. The specificity of AIDS is such that specialists of various profiles have been studying this infection: virologists, immunologists, epidemiologists, parasitologists, dermatologists, and oncologists. There is an opinion among clinicians that in order to know AIDS, one must know all of medicine.

In patients with AIDS, the kidneys are affected, and glomerulonephritis with nephrotic syndrome is more common. Most patients with AIDS kidney disease quickly develop end-stage renal failure. Pathological anatomical examination revealed focal segmental glomerulonephritis with deposition of JgM in the glomeruli. Approximately 40% of AIDS patients have various ophthalmic lesions: conjunctivitis, keratitis, retinitis, retgonal periphlebitis, retinal hemorrhages, the appearance of a white spot, which causes a decrease in vision. Characteristically, the appearance of a white spot and cytomegalovirus retinitis is a negative prognostic sign. Skin lesions most often present with, but are not limited to, Kaposi's sarcoma. Seborrheic dermatitis, folliculitis, vasculitis, xerodermatitis, herpes zoster, and various manifestations of a fungal infection may also occur.

The most common opportunistic conditions in AIDS are grouped by etiology as follows:

1) malignant neoplasms: Kaposi's sarcoma, brain lymphoma;

2) invasions: pneumocystis pneumonia, toxoplasmosis causing pneumonia or damage to the central nervous system, cryptosporodiosis (intestinal form with prolonged diarrhea), stronglioidosis (pneumonia, damage to the central nervous system, disseminated process);

3) mycoses: candidiasis (most often the esophagus and oral cavity), cryptococcosis (damage to the lungs, central nervous system, disseminated process);

4) bacterial infections: legionella pneumonia, atypical mycobacteriosis (disseminated infection), salmonella infection (enteritis, sepsis);

5) viral infections: cytomegalovirus infection (damage to the lungs, gastrointestinal tract, central nervous system), progressive leukoencephalopathy (apparently caused by papavirus), infections caused by herpes viruses, infections caused by HTLV-I and HTLV-II viruses. But with all the variety of opportunistic states, a number of the most frequent ones can be distinguished. These are, firstly, pneumocystis pneumonia and Kaposi's sarcoma. According to numerous sources, approximately 50% of AIDS patients have pneumocystis pneumonia as an opportunistic disease, and 25% have Kaposi's sarcoma. About 6% of patients are affected by both conditions. Less than 20% of opportunistic diseases are accounted for by all other infectious agents, and in which infections caused by cytomegalovirus, herpes virus and Candida fungi are most common.

The causative agent of the disease is a protozoan pneumocystis, first described in 1909. This microorganism can cause interstitial pneumonia in premature and debilitated children. The disease has a wide geographical distribution, but is quite rare. Extremely rarely, diseases occur in adults suffering from blood diseases, tumors, in persons treated with corticosteroids and immunosuppressants, during organ transplantation. Cases of generalized infection have been reported. With pneumocystis pneumonia, inflammatory infiltration of the interalveolar septa leads to the filling of the alveoli with a foamy mass, which reduces the respiratory surface of the lungs, causing a violation of gas exchange, oxygen deficiency.

Clinically, the disease develops gradually; in some cases there may be an undulating course. In the beginning, shortness of breath, shortness of breath, and cyanosis appear. The temperature is often subfebrile. In the future, shortness of breath, rapid breathing, cyanosis progress, which are later joined by a dry, obsessive cough, respiratory acytosis, and pneumothorax may form. Cardiopulmonary insufficiency develops. The liver and spleen are enlarged. Pneumocystis pneumonia can be complicated by a bacterial infection.

A presumptive diagnosis can be made on the basis of clinical, epidemiological data and a characteristic x-ray picture, the final one - on the basis of the detection of the pathogen in the mucus of the upper respiratory tract, as well as using an immunofluorescence reaction. This infection affects only people, it spreads by airborne droplets, as well as through dust. Pneumocystis pneumonia in AIDS patients often recurs and has an exclusively malignant course with a mortality rate of 90 to 100%, while usually this disease is relatively mild.

It was first described in 1872. It is also known under many other names (about 70 terms). Kaposi's sarcoma is a malignant neoplastic disease of the reticulohistiocytic system with a predominant skin lesion. According to the classification of skin tumors, Kaposi's sarcoma refers to malignant diseases from blood vessels - hemorrhagic hemangioendotheliomas.

Clinically, in the normal course of the disease (not in AIDS patients), skin lesions occur in the form of spots, plaques, nodes with foci of hemorrhage. The lesions are symmetrical. The size of the elements is up to 5 cm in diameter, the color is reddish-bluish, reddish-brown, later the color becomes darker. The elements are sharply limited from the surrounding skin, their surface is smooth with slight peeling. Pain is not felt. There is a gradual increase in size and number of elements, their grouping in the form of arcs and rings, followed by compaction, retraction of the center, the formation of plaques and tumor nodes 1-5 cm in size, hemispherical in shape, protruding above the skin surface. Possible ulceration of tumors. Kaposi's sarcoma is most often localized on the anterior surface of the lower leg, much less often on the auricles, abdomen, and penis. Sometimes elephantiasis of the extremities develops (severe swelling due to stagnation of the lymph), there is a sharp pain in the tumor-like formations, and a generalization of the process is noted with the formation of tumor nodes in the gastrointestinal tract, liver, lungs, lymph nodes and bones. Kaposi's sarcoma, not associated with AIDS (as an independent disease), in 3/4 cases has a long (6-10 years, less often - 15-20 years) course. Less often there is a subacute course (2-3 years); in some cases - an acute form with a rapid death of patients. Without an association with AIDS, Kaposi's sarcoma is a rare disease (0,06 per 100 population), although it has recently become much more active. As a rule, men over 000 years of age get sick. The highest incidence was observed in the indigenous population of Central Africa. There are European, African and North American variants of the disease. Kaposi's sarcoma, which occurs in AIDS patients, does not differ histologically from the usual one, but has a number of features. It primarily affects not the lower limbs, but is associated with the lymph nodes, mucous membranes and membranes of the internal organs. The disease acquires a disseminated malignant character. There may also be a lightning current. There is an opinion that Kaposi's sarcoma is an opportunistic disease in AIDS due to the fact that the AIDS virus induces oncogenesis by stimulating B-cell proliferation with a predominance of one clone.

This disease is caused by yeast-like fungi of the genus Candida. A clinically pronounced disease develops, as a rule, in violation of the functions of the protective system, which is primarily characteristic of AIDS. The most common localization of candidiasis in AIDS is the oral cavity, and especially the esophagus. There may also be skin candidiasis and a common form (up to 80%).

Caused by the virus of the same name. The name of the disease is associated with the mechanism of infection. Giant cells with characteristic intranuclear inclusions are formed in the affected tissues (from the Greek citos - "cell" and megalos - "large"). There may be changes in the lungs, gastrointestinal tract, and central nervous system. In the pulmonary form, interstitial pneumonia occurs, sometimes multiple cysts form in the lungs. In the gastrointestinal form, persistent diarrhea occurs with abdominal pain. There is ulcerative enteritis, sometimes pancreatitis. With the defeat of the central nervous system, a clinic of meningoencephalitis develops. In the absence of AIDS, cytomegalovirus infection affects only children. In AIDS, cytomegalovirus infection is found in 70% of patients. The malignant nature of this infection is usually noted.

Diseases caused by herpes simplex viruses (herpes simplex) and herpes zoster virus (herpes zoster) are less common in patients than diseases associated with cytomegalovirus. Of the two herpes viruses, opportunistic infections caused by the herpes simplex virus are more frequent. As a rule, with AIDS, these diseases are malignant. Interstitial pneumonia, chorioretinitis (eye damage), hepatitis, damage to the kidneys, brain, and endocrine glands develop. Herpes zoster infection is twice as rare. Herpes zoster, which occurs without a connection with AIDS, affects more often people over 60 years of age. With AIDS, this infection occurs in people aged 20-30 years. Opportunistic conditions in AIDS have a number of features.

1. Opportunistic pathogens often appear as pathogens, which under normal conditions do not cause pathological processes or cause them only in a certain contingent (small children, elderly people treated with hormones or irradiated).

2. Microorganisms that stay in the body for a long time and in its normal state do not cause pathology act as pathogens.

3. Opportunistic infections that complicate AIDS are characterized by a malignant course, a tendency to spread, duration, and high mortality.

4. Opportunistic infections often recur, one infection can change to another, sometimes several opportunistic diseases occur simultaneously.

All these features are due to the very pathogenesis of the disease - a sharp suppression of immunity.

Features of the course of AIDS in children. Children make up a relatively small proportion of AIDS patients. They are mainly infected in utero, as well as during blood transfusions and the treatment of hemophilia. On average, the disease occurs 5 months after birth. In children with AIDS, prolonged fever, underdevelopment, hypergammaglobulinemia and impaired cellular immunity were noted. Opportunistic infections are dominated by pneumocystis and cytomegalovirus pneumonia, salmonella sepsis. In some sick children, several forms of infections and pathologies are observed simultaneously, caused by different etiological factors. Kaposi's sarcoma in children with AIDS is very rare. At the same time, infections caused by bacterial microflora are found in children more often than in adult patients. In children under one year of age, diarrhea is especially common.

AIDS diagnosis. Diagnosis of AIDS is a highly complex and responsible task. Overdiagnosis is completely unacceptable. The difficulty in diagnosing AIDS is primarily due to the polymorphism of the clinical picture of the disease due to the wide variety of opportunistic conditions. Many of them require rather complex laboratory diagnostics. If there is a combination of clinical findings with an immunodeficiency state confirmed by appropriate tests, then the diagnosis becomes justified. But even in these cases, caution is required, since immunodeficiency states can be etiologically and pathogenetically different. Putting an equal sign between AIDS and immunodeficiency, even T-cell, is impossible. Specific serological tests play an important role in making the diagnosis, but they must be performed repeatedly. Only a combination of epidemiological, clinical, immunological and specific serological diagnostic methods allows specialists to make a diagnosis of AIDS. Careful history taking, dynamic monitoring of the patient can reveal the symptom complex characteristic of pre-AIDS: lymphadenopathy, weight loss, persistent diarrhea, febrile reaction. Each of these symptoms in itself is not very proof, but in combination with the risk contingent (drug addicts, prostitutes, etc.), they make it possible to suspect preAIDS. Since the emergence of opportunistic conditions, the grounds for diagnosing AIDS have become much greater. This is especially true of such opportunistic conditions most characteristic of AIDS as pneumocystis pneumonia, Kaposi's sarcoma, candidiasis, and cytomegalovirus infection.

Prior to the development of specific serological and virological tests, the diagnosis of AIDS was made on the basis of clinical data and immunological tests, provided that all other factors that could cause immunodeficiency (primary immunodeficiencies, immunodeficiencies due to radiation, chemotherapy, fasting, administration of adrenal hormones - corticosteroids) were excluded.

Diagnosis of AIDS in children is especially difficult, since in early childhood the immune system is not yet fully formed, and in newborns and in the absence of AIDS, opportunistic infections are possible. In children, when diagnosing AIDS, the collection of anamnesis (history of the disease) is of great importance. The anamnesis concerns both the child himself (does he have hemophilia, did he have blood transfusions) and his parents (drug addiction, numerous sexual contacts, arrival from AIDS centers).

If AIDS is suspected on the basis of epidemiological and clinical data, it is advisable to study the state of the immune system and establish the nature of the violations. The complexity of the immunological examination is determined by the difficulties in correctly assessing the results obtained and the technical formulation of the reactions, which are not available to all laboratories. Patients with manifest (pronounced) forms of AIDS are characterized by changes in the form of a decrease in the total number of lymphocytes: from 1,0 to 1,5 × 10⁹/ l. With lymphadenopathy and asymptomatic infection, lymphopenia is noted in 40% of cases. Great importance in the immunological study is given to a change in the normal ratio of helpers to suppressors. In healthy people, helpers account for 60% of T-lymphocytes. With manifest (manifested) AIDS, the ratio of helpers to suppressors is always below 1. With lymphadenopathy, the ratio of less than 1 is noted in 55%. The degree of immunodeficiency is judged by the ratio of helpers and suppressors.

To determine cellular immunity, an intradermal test method is used. This is a multitest using 7 antigens and a control. Healthy people have at least two positive skin reactions (with a diameter of more than 10 mm in men, more than 5 mm in women). In patients with manifest forms of AIDS and in patients with lymphadenopathy, in almost all cases there is hyperergy or anergy. In asymptomatic carriers, hyperergy occurs in 20-40%. The change in humoral immunity is that in 50-60% of patients with manifest AIDS and in 30-40% of patients with lymphadenopathy, the content of JgA and JgJ is increased. In AIDS, the humoral response is qualitatively insufficient: B-lymphocytes react incompletely to microbial antigens, that is, they do not produce antibodies enough. This circumstance complicates the serological diagnosis of opportunistic infections. Additional tests are an increase in acute phase proteins, an increase in the content of low molecular weight protein β in serum₂- microglobulin. The results of immunological tests should be evaluated taking into account the characteristics of reactions in individual age groups. For example, in children, a change in the ratio of T-helpers and T-suppressors for the diagnosis of AIDS is less important than in adults. This is due to the fact that deviations from the norm in children are less pronounced. In children, AIDS can be differentiated from congenital immunodeficiencies by polyclonal hypergammaglobulinemia. In general, immunological tests are considered as one of the important components of a comprehensive diagnosis of AIDS. Isolation of the causative agent of AIDS (human immunodeficiency virus - HIV) made it possible to specifically diagnose the disease. Specific laboratory diagnostics goes along the following lines:

1) virus detection;

2) detection of virus components (antigens, nucleic acid, reverse transcriptase);

3) detection of antibodies.

It should be noted that although rare (in 0,2% of cases), false positive reactions are also possible. Therefore, serological tests, like other diagnostic methods, should only be evaluated in combination with other data. According to scientists, the most important for the serological diagnosis of AIDS is the enzyme-labeled antibody test (REMA). All positive and doubtful sera must be verified by other complex tests that are based on different principles. Improving the reactions of enzyme-labeled antibodies makes it possible to avoid false positive reactions, therefore, it helps to prevent errors in the final diagnosis of AIDS.

Having considered an extensive group of immunodeficiency states, it should be concluded that, with all the universality of the body's defense system that nature has created, it is not absolute, but only adapted to a certain set of natural conditions, the level and lifestyle of a particular person, which correspond to the individual norm of adaptation. Since the conditions of human life change, new environmental factors appear, the body is forced to adapt. Adaptation occurs even when changes in conditions correspond to the limits of adaptation laid down in the genotype. And such an adaptation necessarily includes mechanisms of adaptation and compensation, that is, in other words, it can cause a pathological reaction of the body.

LECTURE No. 5. Pathological immune reactions of the body. Allergic diseases

The possibility of a pathological reaction is especially high in cases where a change in the conditions of a person's life occurs in a short time. Such examples are climate change, a change in diet, a change in physical activity, etc. An even greater danger is the interaction with factors that, in quality or quantity, exceed the rate of adaptation of the species. In modern conditions, this is, in particular, due to environmental factors that are caused by human activity. The current scale of the impact of these factors is enormous, and mankind has not previously encountered such factors in such quantities.

An increase in the proportion of the urban population in relation to the rural - urbanization, depriving people of their natural habitat, chemicalization, which gave rise to a huge amount of artificial substances used in all spheres of human life, changes in diets, an increase in the proportion of canned and refined foods, the use of potent drugs and other, caused the impact on the human body of such factors with which the protective mechanisms had not previously interacted. The expression "diseases of civilization" was formed, which means a quantitative increase in such diseases as cardiovascular pathologies, cancer, various allergies, etc. Previously unknown diseases appeared: "legionnaires' disease" (acute pneumonia), AIDS, etc. All these facts indicate that the systems of protection of the human body against pathogens develop in response to changing conditions of existence by the formation of new elements of compensatory protection. These facts are confirmed by the wide development of allergic reactions, which have taken on a massive scale. Allergies have been known since ancient times. Hippocrates also described bronchial asthma. Currently, in medicine, allergology is separated into a separate science that tries to uncover the causes of allergies and develops new methods of treating and preventing them.

The term "allergy" refers to the increased sensitivity of the body to the action of certain substances of the external and internal environment. Substances that can cause this hypersensitivity are called allergens. Allergens, like antigens, cause the formation of antibodies in the body. But unlike antigens of a biological nature, allergens can be a variety of substances found in foods, chemicals, cosmetics, medicines, therapeutic serums, house dust, plant pollen, etc. For many people, these are absolutely harmless substances. , but for a person who is predisposed to allergies, they become the causes of bronchial asthma, hay fever, urticaria, allergic rhinitis, and sometimes severe anaphylactic shock. A feature of an allergic reaction is that the first interaction of the allergen with the body does not manifest itself externally. The immune system reacts to it by producing antibodies to a specific allergen, for example class E antibodies (or reagins). In addition, T-lymphocytes that are sensitive to this allergen are also formed. Thus, the first interaction with the allergen makes the body sensitive to it. Upon repeated interaction with the allergen, the clone of reagins corresponding to it includes an allergic reaction of the immediate (after 1-2 days) type. Allergic reactions are characterized by:

1) the allergen and the antibody combine on the cytoplasmic membrane of the target cell;

2) as a result of the action of the allergen-antibody complex on certain cells (mast cells), chemically active substances (histamine, serotonin, bradykinin, etc.) are released, which initiate an allergic reaction;

3) chemically active substances that were formed in the second stage affect the body, causing damage to tissue cells and inflammation.

Thus, unlike a purely immune reaction, in which the body's cells are destroyed by an antigen, and T- and B-lymphocytes destroy antigens, in an allergic reaction, the pathological destruction of cells occurs under the influence of substances produced by the body itself. Therefore, it is believed that the hypersensitivity reaction, allergy, is not part of the protective mechanism, but, on the contrary, tissue damage during allergies is an unfavorable factor and even a "miscalculation" of the immune process. But there is another opinion, according to which allergic reactions of various types include non-specific defense mechanisms, which are a typical pathological process and are aimed at localizing, destroying and removing any pathogens, including antigens. This indicates the protective role of allergy. But with an allergic reaction, the inflammatory process is highly active and significantly damages the tissues. In addition to inflammation, reactions such as bronchospasm, edema, shock, etc. occur with allergies. These damages are caused by an immune response, since other components of the immune system are also involved in the allergic process, which, of course, have a harmful effect. According to scientists, allergies are reactions that have both destructive and protective features. Normally, immunological damage and destruction of cells are carried out by the body constantly and are one of the elements of vital activity and an important component of maintaining the genetic individuality of the body. T-killers constantly destroy mutant cells that have a disturbed gene composition, including tumor and dying cells.

Substances of an antigenic nature constantly enter the body from the outside: through the skin, the respiratory system, and the gastrointestinal tract. In the body itself, in the process of metabolism, substances of an antigenic nature are formed, which are destroyed by the mechanisms of humoral and cellular non-specific and immune (specific) protection. Foreign cells and antigens, constantly formed or entering the body, by themselves do not cause damage or do not have time to cause them, because the defense mechanisms limit their number to a minimum level that does not exceed the threshold. Above this threshold, a pathological reaction begins.

Thus, for the development of pathological reactions, it is not the presence of destruction that matters, but their scale and strength. In some cases, the immune mechanism provides protection for the body, and in others - destruction. The same antigen can cause an immune or allergic reaction in different people. However, many antigens cause predominantly allergies, such as plant pollen, food products, dandruff, animal hair, room dust, etc. When they enter the body through the skin and mucous membranes, they cause the formation of immunoglobulin E and, as a result, allergies. But their introduction into the esophagus, even in large quantities, leads to the formation of immune antibodies, which, when combined with the allergen, do not cause tissue damage.

Thus, an antigen may or may not exhibit allergenic properties, depending on the amount and routes of entry. In the mechanism of the response, the reactivity of the organism, i.e., its ability to qualitatively and quantitatively respond to antigenic irritation, is also of great importance. The ability of the organism to form immunity largely depends on the reactivity of the organism or, in the event of immunity failure, to form an allergic reaction, i.e., a pathological process that has the features of protection and destruction. With allergic reactivity, it is more likely that the antigen will exhibit allergic properties, i.e., upon repeated administration, a reaction will occur that leads to tissue damage. The conditions that contribute to the translation of the immune reaction into an allergic one are an increase in the permeability of integumentary tissues, which contributes to the entry of antigens into the body, a change in the nature of the immune response, a violation of the ratio of different classes of immunoglobulins and their quantity, an increase in the formation of mediators of allergic reactions and a decrease in their inactivation.

Allergy is the subject of the study of immunology, which studies the inadequate response of the immune mechanism to the introduction of an antigen, leading to damage in the body. The increase in the number of allergic diseases is due to several reasons. First, the reduction or even complete elimination of epidemic diseases reduced human contact with strong allergens of their pathogens, which inhibited the reaction to predominantly weak environmental allergens. Secondly, the introduction of vaccines, sera and other substances of an antigenic nature causes increased sensitivity (sensitization) of organisms predisposed to this. Thirdly, the number of new chemicals that do not even occur in nature has increased dramatically. These substances include drugs, the uncontrolled intake of which causes a change in the reactivity of the body, affects the neuroendocrine system. Fourth, changing the conditions of lifestyle and nutrition. Violation of contact with nature, urban living conditions lead to the fact that the natural products of nature (plant pollen, dandruff, animal hair, etc.), which a person used to meet from the moment of birth, become alien, and uncontrolled chemicalization of agriculture leads to increase in the content of chemicals in food. Each class of immunoglobulins is designed to protect the body from certain groups of antigens, so it can be assumed that the immune system forms a new element of protection - reagins to fight unusual allergen antigens, since immunoglobulins of other classes do not cause a universal protective reaction with these antigens - inflammation, t i.e. the immune system undergoes evolution, adapting to new environmental conditions, strengthening the corresponding element of protection. The result of adaptation is the increased reactivity of individuals, caused by the individual characteristics of their immune system.

1. General etiology of allergic diseases

Thus, the causes of allergic diseases are allergens. The conditions for the occurrence of allergies are certain features of the external environment and the state of the reactivity of the body. Despite the many allergens surrounding a person, a certain percentage of people fall ill, and not all, since a significant role in the development of allergic diseases belongs to those specific adverse conditions that are developing at the moment and contribute to the implementation of the allergen's effect on the body. An allergen is a substance that causes an allergic reaction. How is an allergen different from an antigen? The main difference is the end result of the action. If a substance causes an allergic reaction, then it is called an allergen, if it leads to the development of an immune reaction, it is called an antigen. It turns out that allergens have all the properties of antigens (this is mainly a protein nature, macromolecularity, foreignness for a given organism, etc.).

But allergic reactions can cause not only substances of an antigenic nature, but also substances that have these properties. These include many micromolecular compounds, such as drugs, simple chemicals (bromine, iodine, chromium, nickel, etc.), as well as more complex non-protein products (some microbial products, polysaccharides, etc.). These substances are called haptens. When they enter the body, they do not turn on immune mechanisms, but become antigens (allergens) only after they combine with body tissue proteins. In this case, the so-called conjugated (or complex) antigens are formed, which sensitize the body. When re-entering the body, these haptens (allergens) can often combine with the formed antibodies and (or) sensitized lymphocytes on their own, without prior binding to proteins.

The specificity of the complex antigen is determined by the specificity of the hapten. In this case, changes in the properties of the protein (carrier) can be different. In some cases, its spatial configuration (i.e., conformation) does not change or changes slightly. It does not become alien to the body, so sensitization goes only to the hapten. In other cases, the attachment of the hapten causes significant changes in the carrier conformation. Protein molecules are denatured. This is observed during the addition of a halogen, nitration, acetylation, addition of chromium, etc. In these cases, sensitization develops not only to the hapten, but also to the altered regions of the protein molecule.

Thus, summarizing the above, it should be concluded that if the conformation of the carrier does not change, then allergic reactions develop that proceed according to the type of reactions to an exogenous (external) allergen, i.e. with the development of allergic diseases, when the conformation of the carrier changes, autoallergic reactions are added, which with its extreme severity, it can develop into autoallergic diseases. However, not every combination of a chemical with a protein results in the formation of an antigen. Many drugs in the body combine with serum proteins, but the resulting complexes do not always become antigens for the body. Whey proteins also combine with many endogenously formed micromolecular compounds (for example, steroid hormones, copper and iron ions, metabolic products), performing a transport function in relation to them. But this also does not lead to the appearance of antigenicity. The combination of transport proteins with the corresponding endogenous product or metabolite can change the conformation of the carrier, but does not lead to its denaturation, since these structural changes, developed in the course of evolution, are “own” for the organism, there is immunological tolerance to them, i.e. they are not perceived as foreign.

Another thing is if chemical compounds enter the body from outside, which are not products of natural metabolism and sometimes enter not through the gastrointestinal tract, but through the skin or respiratory tract. All these substances in the body are usually metabolized (most often in the liver) and excreted. But if among these substances or their metabolites there are those that have an active, reactive site in the molecular structure or a rigid structure, then such substances are connected to the carrier protein by chemical bonds. This leads to the formation of a complex allergen.

However, it should be borne in mind that the role of a hapten can sometimes be performed not by the entire chemical substance, but by a certain part of it, a grouping. Identical groupings can be in the composition of different chemicals. Therefore, with sensitization to one chemical, allergic reactions to other chemicals with similar groups are possible. This is of particular importance when dividing allergic reactions into medicinal and industrial allergens. Allergens are exogenous, entering the body from the outside, and endoallergens, formed in the body itself.

There is a classification based on the way the allergen enters the body:

1) air, inhalation allergens (household and industrial dust, plant pollen, epidermis and animal hair, etc.);

2) food allergens;

3) contact allergens that penetrate the skin and mucous membranes (chemicals, drugs);

4) injectable allergens (drugs, serums);

5) infectious allergens (bacteria, viruses);

6) medicinal allergens.

Each group of this classification includes allergens of different origin. There is also a more convenient classification, which is based on the origin of exogenous allergens. They are divided into the following groups:

1) allergens of non-infectious origin - household, epidermal, pollen, food, industrial;

2) allergens of infectious origin - bacterial, fungal, viral.

House dust plays the main role among them. This is a complex allergen in its composition, which includes dust particles (from clothes, bed linen, mattresses), fungi (in damp rooms), particles of domestic insects, bacteria (non-pathogenic staphylococci, etc.). The main allergens in house dust are mites and their waste products. They live in beds, pillows, where they feed on particles of human epidermis. When shaking the bed, ticks, their particles and excrement enter the respiratory tract. This type of tick is very widespread. Daphnia, which are included in the feed of aquarium fish, are highly allergenic. Household allergens most often cause allergic respiratory diseases.

These are allergens of venom of stingers, saliva of biting insects and particles of the body cover of insects. These allergens cause both local and general allergic reactions. People who are hypersensitive to one insect have the same hypersensitivity to other insects within the order and family, since they have common antigens.

This group includes dandruff, animal hair, bird feathers, fish scales. One particular allergen is horse dander. This type of allergen causes occupational allergies in vivarium workers, sheep breeders, poultry workers, horse breeders, and hairdressers. Manifested by rhinitis, bronchial asthma, urticaria.

Almost any drug can lead to the development of drug allergies. Drugs or their metabolites are, as a rule, haptens and become full-fledged allergens only after binding to tissue proteins. The drug molecule has a site in which antibodies are formed, i.e. this site (and not the entire molecule as a whole) plays the role of an antigenic determinant. Such sites may be the same for different drugs and are called common, cross-reactive determinants. Therefore, when sensitized to one drug, allergic reactions will occur to all other drugs that have the same determinant.

Thus, in case of allergy to one drug, it is necessary to exclude the use of all drugs that have a common determinant with it.

Allergic diseases are not caused by pollen of all types of plants, but only rather small (no more than 35 microns in diameter), and also have a good volatile effect. Most often it is the pollen of various types of wind-pollinated plants. An allergy caused by plant pollen is called hay fever. The antigenic composition of pollen is quite complex and consists of several components. For example, ragweed pollen contains 5-10 antigens, and timothy pollen contains up to 7-15 antigenic components. Different types of pollen can have common allergens, so people who are sensitive to one type of pollen may react to other types of pollen. Common allergens were found in the pollen of cereal grasses (timothy, rye, fescue, bluegrass). Each climatic and geographical zone has its own plant species, the pollen of which most often causes the development of hay fever. In the Krasnodar and Stavropol Territories, this is the pollen of the ragweed weed and wild hemp, in Moscow, the pollen of meadow grasses, etc.

Allergens can be many foods. But most often they are fish, meat (especially pork), eggs, milk, chocolate, wheat, beans, tomatoes. In addition, allergens can also be food additives that are included in products and are chemicals. These are antioxidants, dyes, aromatic and other substances.

The rapid development of the chemical industry has significantly increased the amount of various chemicals in production and at home, and therefore, people's contact with them. This caused the appearance of allergic reactions of various nature. Industrial allergens are overwhelmingly haptens, which bind to proteins through their reactive group. For example, through the halogen atom, aromatic nitro compounds are attached, the mercapto groups of a number of pesticides react with the HS groups of proteins, etc. It is believed that the higher the ability of the hapten to form a chemical bond with the protein, the higher its allergenic activity. The most common industrial allergens are turpentine, oils, nickel, chromium, arsenic, tar, resins, tannins, many dyes, etc. In hairdressing and beauty salons, allergens can be dyes for hair, eyebrows and eyelashes, perm fluid etc. In everyday life, allergens can be soap, detergents, synthetic fabrics, etc.

Allergic processes can cause a variety of pathogens of infectious diseases, as well as their metabolic products. These processes become an integral part of the pathogenesis of the disease. Those infectious diseases in the pathogenesis of which allergy plays a leading role are called infectious-allergic diseases. These include all chronic infections (tuberculosis, leprosy, brucellosis, syphilis, rheumatism, chronic candidiasis, etc.). With the elimination of epidemic diseases, allergic processes, which are caused by opportunistic and saprophytic flora, have become increasingly important. The source of sensitization is usually the flora of chronic foci of inflammation in the paranasal sinuses, middle ear, tonsils, carious teeth, gallbladder, etc. In this case, some forms of bronchial asthma, angioedema, urticaria, rheumatism, ulcerative colitis and other diseases can develop. Mushrooms are very common allergens. About 350 species of mushrooms show allergenic activity. Among them, there are species pathogenic for humans that cause diseases with allergies at the basis of pathogenesis. Such diseases are, for example, aspergillosis, actinomycosis, coccidioidomycosis, histoplasmosis, etc. However, many fungi that are not pathogenic for humans, when they enter the body, cause sensitization and the development of various allergic diseases (bronchial asthma, etc.). Such fungi are found in the atmospheric air, dwellings, house dust, moldy foods, etc. Their concentration depends on the season, humidity, temperature and other conditions.

2. Pathogenesis of allergic processes

There are various classifications of allergic reactions. The most common divides all allergic reactions into immediate-type allergic reactions and delayed-type allergic reactions. This classification is based on the time of occurrence of the reaction after contact with the allergen. The reaction of the immediate type develops within 15-20 minutes, the delayed type - after 1-2 days. But this classification does not cover the whole variety of manifestations of allergies. For example, some reactions develop after 4-6 or 12-18 hours, i.e., they cannot be attributed to either delayed reactions or immediate reactions. Therefore, the differences between allergic reactions began to be associated with different mechanisms of their development and a classification based on the pathogenetic principle was made. All allergic reactions are divided into true, or actually allergic, and false, or pseudo-allergic (non-immunological). In turn, true, or actually allergic, are divided into chimergic (B-dependent) and kitergic (T-dependent).

True, actually allergic, reactions have an immunological stage in their development, false ones do not have it. The division of true reactions into two types is based on the nature of the immunological mechanism. Chimergic ones are caused by the reaction of the allergen with antibodies (from the Greek himos - "juice"), and the kitergic ones are caused by the combination of the allergen with sensitized lymphocytes (from the Greek citos - "cell"). Later this classification was improved. It detailed the immunological mechanisms. Chimergic reactions began to be called B-dependent, since the formation of antibodies is associated with B-lymphocytes. Depending on the class of immunoglobulins to which the formed antibodies belong, A, J, E and M-globulin reactions have been identified in B-dependent allergic reactions. Kytergic reactions are called T-dependent, among them reactions of the tuberculin type, such as contact dermatitis and transplant rejection. There is another widespread classification, also based on the pathogenetic principle. It is based on the features of immune mechanisms. In accordance with this classification, 4 types of allergic reactions are distinguished:

1) anaphylactic (JgE- and less often JgJ-antibodies);

2) cytotoxic (JgJ- and JgM-antibodies);

3) Arthus type - damage by the immune complex (JgJ- and JgM-antibodies);

4) delayed hypersensitivity (sensitized lymphocytes).

Despite the fact that several immunological mechanisms are involved in the development of an allergic disease, it is possible to single out the main, leading mechanism, which is essential for pathogenetically substantiated treatment.

The antigen, when it enters the body, causes its sensitization. Sensitization is an immunologically mediated increase in the body's sensitivity to antigens (allergens) of exogenous or endogenous origin. The concepts of sensitization and allergy are different. Allergy includes not only an increase in sensitivity to any antigen, but also the realization of this increased sensitivity in the form of an allergic reaction. Initially, sensitivity to the antigen increases, and only then, if the allergen (antigen) remains in the body or enters it again, does an allergic reaction develop, that is, the allergic reaction itself has two components. These parts are separated in time. In this case, sensitization is the first (or preparatory) part, and the second part is actually an allergic reaction.

Thus, an allergic reaction is the realization of a state of sensitization into some clinical form of an allergic disease. Very often, a person whose body is sensitized to an allergen is practically healthy until this allergen enters his body, for example, pollen from pollinosis, a drug, etc. It follows that an increase in sensitivity is specific, i.e. only to the antigen that causes it. According to the method of obtaining, active and passive sensitization are distinguished. Active sensitization develops with artificial introduction or natural ingestion of the allergen into the body. Passive sensitization is reproduced in the experiment when blood serum or lymphoid cells are administered to a passive recipient from an actively sensitized donor. If there is a sensitization of the fetus during its intrauterine development, then such sensitization is called intrauterine. Sensitization can be monovalent when there is hypersensitivity to one allergen, and polyvalent when sensitized to many allergens. There is also the so-called cross-sensitization, when there is an increase in the sensitivity of the sensitized organism to other antigens that have common determinants with the allergen that caused the sensitization.

By the nature of the mechanisms that are involved in the development of allergies, stage III is distinguished.

I - immunological stage. It covers all changes in the immune system that occur from the moment the allergen enters the body, the formation of antibodies and sensitized lymphocytes and their connection with the allergen that has repeatedly entered or exists in the body.

II - pathochemical stage. At this stage, biologically active mediators are formed. Mediators are formed when the allergen is combined with antibodies or sensitized lymphocytes at the end of the immunological stage.

III - pathophysiological stage, or stage of clinical manifestations. It is characterized by the fact that the resulting mediators have a pathogenic effect on the cells, organs and tissues of the body.

There are several types of tissue damage in allergic reactions:

1) reaginic type of tissue damage. The name of this type comes from the name of the reagin antibodies involved in its development. Reagins belong mainly to the JgE class, but there are also JgJ class reagins among them. This type has synonyms: atonic (from the Greek atonos - "unusual", "alien"), anaphylactic, immediate type allergic reaction. In response to the ingestion of an allergen, reagins are formed. They are fixed mainly on mast cells and their analogues in the blood - basophils. The result is a state of sensitization. Repeated entry into the body of the same allergen leads to its combination with the formed reagins, which causes the release of a number of mediators from mast cells and basophils, as well as their formation by other cells. The formed and released mediators have both protective and pathogenic effects. Pathogenic action is manifested by symptoms of various diseases. Mediators of reaginic type reactions are histamine, serotonin, slowly acting substance (MDV), prostaglandins;

2) cytotoxic type of tissue damage. It is called cytotoxic because antibodies formed against cell antigens combine with cells and cause damage and even lysis (cytological action). An antigen is a cell, or rather, those antigenic determinants that are present on cells. Antibodies are formed against these determinants, which then bind to them. Damage can occur in three ways:

a) due to complement activation, active complement fragments are formed that damage the cell membrane;

b) due to the activation of phagocytosis of cells coated with antibodies;

c) through activation of antibody-dependent cellular cytotoxicity.

The role of damage mediators in the second type is played by lysosomal enzymes, which are secreted by phagocytes. The action of cytotoxic antibodies does not always end in cell damage. At the same time, their number matters. With a small amount of antibodies, instead of damage, a stimulation phenomenon can be obtained;

3) damage by immune complexes. In this type of allergic reaction, damage is caused by immune complexes. Synonyms are the immunocomplex type and the Arthus type. Ideas about this type were formed on the basis of observations of the local toxic effect on tissues of the antigen-antibody complex formed in excess of the antigen. An antigen that enters the body, having a soluble form, is the formation of antibodies. The greatest role in this case is played by antibodies of the JgJ- and JgM-classes. Under certain conditions, the antigen-antibody complex can cause damage and the development of the disease. In these cases, the damaging effect of the complex is realized mainly through complement activation, release of lysosomal enzymes, and activation of the kinin system. This type of allergic reactions is leading in the development of serum sickness, exogenous allergic alveolitis, in some cases of drug and food allergies, in a number of autoallergic diseases (such as rheumatoid arthritis, systemic lupus erythematosus, etc.). With significant complement activation, systemic anaphylaxis can develop in the form of anaphylactic shock. Some of the resulting mediators (kinins, serotonin, histamine) can cause bronchospasm, which is the main symptom of bronchial asthma;

4) an allergic reaction of a delayed type. This term refers to a group of allergic reactions that develop in sensitized people 24-48 hours after exposure to an allergen. A typical example of such a reaction is a positive tuberculin skin reaction of tuberculosis mycobacteria sensitized to antigens. Initially, a characteristic feature was the time of development of the reaction. Then it was found that the main role in the mechanism of their occurrence belongs to the action of sensitized lymphocytes on the allergen. Synonyms for this type:

a) delayed type hypersensitivity;

b) cellular hypersensitivity (due to the fact that the role of antibodies is performed by the so-called sensitized lymphocytes);

c) cell-mediated allergy;

d) tuberculin type;

e) bacterial hypersensitivity.

In response to an allergen entering the body, so-called sensitized lymphocytes are formed. They belong to the T-population of lymphocytes, and structures that play the role of antibodies that can bind to the corresponding antigen are also built into their cell membrane. When the allergen re-enters, it combines with sensitized lymphocytes. This leads to a number of morphological, biochemical and functional changes in lymphocytes. They manifest themselves in the form of increased synthesis of DNA, RNA and proteins, secretions of various mediators, which are called lymphokines. With the help of lymphokines, various cells are mobilized. Under the influence of some lymphokines, non-sensitized lymphocytes acquire increased sensitivity to the allergen. A special type of lymphokines has a cytotoxic and inhibitory effect on cell activity. Sensitized lymphocytes also have a direct effect on target cells (cytotoxic effect). Accumulation of cells, cell infiltration of the area where the connection of the lymphocyte with the corresponding allergen occurs, develop over several hours and reach a maximum after 1-3 days. In this area, destruction of target cells, their phagocytosis, and increased vascular permeability are noted. All this manifests itself in the form of an inflammatory reaction of a productive type. If the allergen or immune complex is not inactivated, then granulomas begin to form around them, with the help of which the allergen is separated from the surrounding tissues. The granulomas may include various mesenchymal macrophage cells, epithelioid cells, fibroblasts, and lymphocytes. The fate of the granuloma is different. Usually, necrosis develops in its center, followed by the formation of connective tissue and sclerosis.

The main mediators of the fourth type of allergic reactions are lymphokines, which are macromolecular substances of a polypeptide, protein or glycoprotein nature, formed during the interaction of T- and B-lymphocytes with allergens. Lymphokines act on various cells (macrophages, lymphocytes, fibroblasts, epithelial cells, etc.) through the corresponding receptors on these cells. The most studied lymphokines are the following:

1) a factor that inhibits the migration of macrophages. Promotes the accumulation of macrophages in the area of ​​an allergic reaction and may enhance their activity and phagocytosis. It also participates in the formation of granulomas in infectious and allergic diseases and enhances the ability of macrophages to destroy certain types of bacteria;

2) a factor that stimulates the formation of endogenous pyrogens. Stimulates the formation of endogenous pyrogens by macrophages;

3) mitogenic factors. They are a combination of several factors. These are lymphocytic mitogenic factor, interleukin-1 of macrophage origin and T-growth factor, or interleukin-2, secreted by T-helpers;

4) chemotactic factors. There are several types of these factors, each of which causes chemotaxis of the corresponding macrophage leukocytes, neutrophilic, eosinophilic and basophilic granulocytes;

5) lymphotoxins. Cause damage or destruction of various target cells. In the body, cells that are located at the site of the formation of lymphotoxins can be damaged. At high concentrations, they cause damage to a wide variety of target cells, and at low concentrations, their activity depends on the type of cells;

6) interferon is secreted by lymphocytes under the influence of a specific allergen (the so-called immune interferon) and nonspecific mitogens. It is species-specific;

7) skin-reactive factor. In the experiment, after intradermal administration to an animal, an inflammatory reaction develops after 4–6 hours, which reaches a maximum after 16–24 hours. The severity of inflammation depends on the source of the skin-reactive factor. The factor is species-specific. A decrease in the release of skin-reactive factor by blood lymphocytes indicates the suppression of cellular immunity;

8) transfer factor. Isolated from dialysate of lymphocytes of sensitized guinea pigs (in the experiment) and humans. This factor, when administered to intact gilts or humans, imparts "immunological memory" of the sensitizing antigen and sensitizes the organism to that antigen. In addition to lymphokines, lysosomal enzymes are involved in the damaging effect, which are released during phagocytosis and cell destruction.

Having considered the types of allergic reactions, the following conclusion should be made. The inclusion of one or another type of allergic reaction is determined by many factors, but they can be reduced to two main ones. These are the properties of the antigen and the reactivity of the organism. Among the properties of an antigen, its chemical nature, physical state and quantity play an important role. Weak antigens that are found in the environment in small quantities (plant pollen, house dust, dander and animal hair) often give an atonic type of allergic reactions. Insoluble allergens (bacteria, fungal spores, etc.) often lead to a delayed-type allergic reaction. Soluble allergens (antitoxic serums, γ-globulins, bacterial lysis products, etc.), especially in large quantities, usually cause an allergic reaction of the immunocomplex type.

An allergen as the cause of an allergic disease acts on the body under certain conditions, which can either promote its action, which will lead to the development of the disease, or hinder its action and thereby prevent the development of the disease. Therefore, despite the presence in the environment of a large number of potential allergens, allergic diseases develop only in a certain percentage of cases. Conditions can be external (the amount of the allergen, the duration and nature of its action) and internal. Internal conditions are the reactivity of the organism.

The reactivity of the organism is the property of the organism as a whole to respond with changes in vital activity to the influence of the environment. It depends on the hereditary features of the structure and functioning of body systems and those properties that the body acquires in the course of its life. This combination of congenital (hereditary) and acquired properties represents those internal conditions on which the possibility of the development or non-development of the disease largely depends. This fact is of great importance, since it is possible to purposefully change the reactivity of the organism in a direction that hinders the implementation of the action of potential allergens. Any stimulus has a dual effect on the body: specific and nonspecific. The first is related to the quality of the stimulus, its ability to cause the development of certain changes in the body. The specific side of the action of the allergen affects the immune system, which has the appropriate receptors for it. The immune system responds to the impact of the allergen with a certain reaction in accordance with the program that it has. The action of the program is determined by hereditary and acquired properties. It has been established that the immune response to each antigen is genetically predetermined. The class and types of antibodies formed depend on the features of the functioning of the structural genes of immunoglobulins. Immune response genes determine the intensity of the immune response by the number of antibodies formed and the severity of a delayed-type allergic reaction involving sensitized lymphocytes. Hereditary or acquired defects in the work of some parts of the immune system can contribute to the development of allergic reactions. For example, with insufficient activity of a certain subpopulation of T-suppressors, the formation of JgE increases, which can lead to the development of an atonic type of sensitization. Deficiency of secretory JgA contributes to the penetration of allergens through the mucous membranes of the respiratory tract or the gastrointestinal tract and the development of atonic, immunocomplex or other types of allergic reactions. The non-specific side is manifested in the action of the allergen (antigen) as a stressor. Therefore, in the first time after the introduction of various antigens, more or less the same type of changes in the activity of some parts of the neuroendocrine system are revealed in the form of activation of the sympathetic-adrenal, pituitary-adrenal and other systems.

The immune system, like any other system of the body, acts and is regulated in the interests of the whole organism, despite the fact that it functions according to its own internal laws and programs. The function of the immune system is influenced by the neuroendocrine system. Through this system, the body adapts to constantly changing environmental conditions, the action of its various factors. The ability to influence the immune system is ensured by the presence on its constituent cells of the appropriate receptors for mediators of the nervous system and hormones. Clinical observations show that the state of the higher parts of the central nervous system can affect the course and development of allergic diseases. The facts of exacerbations of the course of allergic diseases against the background of tension in the psycho-emotional sphere under the influence of negative emotions are well known. Cases of the appearance of these diseases after negative emotions and the development of acute allergic reactions to a number of food and other allergens after brain damage are described. The higher parts of the central nervous system have a pronounced effect on the manifestations of bronchial asthma. The autonomic nervous system plays a significant role in immune reactions and allergic processes. Activation of the sympathetic and parasympathetic divisions affects the formation of antibodies in different ways.

An analysis of the clinical picture of allergic diseases points more to the role of local rather than generalized dystonia of both parts of the autonomic nervous system. The highest parasympathetic excitability in the corresponding tissues, regardless of the state of the sympathetic, was found in bronchial asthma, urticaria, and migraine. The influence of the nervous system is realized in tissues both directly through the cholinergic and adrenergic receptors that are present on the cells, and through a change in the activity of the endocrine glands, the centers of regulation of which are located in the hypothalamus. Clinical and experimental observations have shown that changes in the hormonal balance of the body can have a significant impact on the occurrence and course of allergic processes. In turn, the allergic processes themselves disrupt the functions of the endocrine glands. Activation of the pituitary-adrenal and sympathetic-adrenal systems under stressful conditions inhibits the occurrence of inflammatory and allergic reactions in some cases. For example, in an experiment against the background of removal of the adrenal glands in animals, anaphylactic shock and a number of other allergic reactions are more severe. Allergic processes cause activation of the pituitary-adrenal system. This activation is nonspecific, secondary, and is a response to injury. At the same time, allergic processes occurring in the adrenal glands themselves block the synthesis of cortisol to varying degrees, which often enhances the formation of corticosterone. Repeated exacerbations of allergic processes lead to the depletion of this system. Therefore, in patients with long-term allergic diseases, a certain degree of adrenal insufficiency is always detected. There are also indications of a large role of sex hormones in the occurrence and course of allergic processes. It is known, for example, that in some cases the development of allergic diseases is associated with changes in the menstrual cycle or the onset of menopause. Thyroid dysfunction is a factor contributing to the development of allergies, with hyperfunction playing a more pronounced role. It is noted that against the background of hyperthyroidism, the drugs used often cause the development of drug allergies. At the same time, the introduction of a large amount of thyroid hormones inhibits the development of allergic reactions. Insulin and the closely related states of hyper- and hypoglycemia have a certain effect. It is believed that hyperglycemia inhibits delayed-type reactions, the development of anaphylactic shock, and hypoglycemia enhances them. The role of the parathyroid glands is evidenced by the development of some signs of hypoparathyroidism (short-term tetanic spasms of the limbs) in patients with bronchial asthma and the favorable therapeutic effect of parathyroid hormone in bronchial asthma and urticaria. Thus, allergic diseases play an important role in the occurrence of a number of pathological conditions of the body.

3. Drug allergy

This is a collective designation of various diseases, the etiological factor of which is drugs, and the pathogenesis is allergic. Drug allergy is a special branch of clinical allergology, therefore, the immunological principles of classification of various allergic diseases are also applicable to the classification of drug allergies. Almost any allergic disease (except pollinosis) can be caused by various drugs, at the same time, each of the nosological forms of an allergic disease can be triggered by other allergens.

There is the following classification.

1. Allergic complications and diseases associated with circulating humoral antibodies (immediate reactions):

1) system:

a) anaphylactic shock;

b) acute urticaria and angioedema;

c) serum sickness and serum-like reactions;

d) bronchial asthma, allergic rhinosinusopathy (atonic form);

e) exacerbation of the underlying disease (bronchial asthma, allergic rhinitis, urticaria and Quincke's edema, atonic dermatitis - neurodermatitis);

f) agranulocytosis, purpura, acquired hemolytic anemia;

2) local: reactions like the Artyus-Sakharov phenomenon.

2. Allergic complications associated with cellular antibodies (delayed type reactions):

1) local: contact-type complications (dermatitis, dermatoconjunctivitis, keratitis, pharyngitis, glossitis, etc.);

2) system:

a) generalized, widespread dermatitis;

b) fungal-like reactions (erythematovesicular dermatitis);

c) complications of the hyperergic type (vasculitis, erythroderma, bullous, exfoliative and hemorrhagic dermatitis, Lyell's syndrome, Stevens-Johnson syndrome, etc.);

d) exacerbation of the underlying disease (collagenoses, some forms of eczema and neurodermatitis, etc.).

Complications of the first group are distinguished by the fact that biochemically active substances of the antigen-antibody reaction are involved in their mechanism, and allergic antibodies (reagins) are found in the blood serum of patients. Positive skin or provocative tests in allergic complications with a similar mechanism occur, as a rule, within 15-20 minutes. The second group of complications is made up of reactions, in the mechanism of which the processes of irritation by allergic components of epidermal and connective tissue structures and the formation of various types of inflammation (including after skin and provocative tests) after 12-24 hours or more have a leading role. Classical biochemical substances, as a rule, do not take part in these reactions.

Anaphylactic shock

It is the most formidable allergic complication. Anaphylactic shock can be caused by almost all currently used drugs, sera and vaccines, pollen allergens during the period of incorrect provocative tests, foodstuffs, especially fish, milk, eggs and others, alcoholic beverages, bathing in cold water with cold allergies, wasp stings , bees, bumblebees, hornets. Anaphylactic shock refers to allergic complications that occur with circulating humoral antibodies, the main characteristic of which is their effect on the mechanism of biologically active substances of the antigen-antibody reaction in tissues and liquid tissue media, and as an intermediate link, the processes of excitation of the central nervous system. In the pathogenesis of anaphylactic shock (and other types of humoral, immediate type allergies), three stages are distinguished: immunological, pathochemical (biochemical) and pathophysiological. The initial stage of the immunological stage is sensitization, i.e. hypersensitivity process. Sensitization occurs within approximately 7-8 days (in the experiment), and in humans this period can last many months and years. The sensitization phase is characterized by the immunological restructuring of the body, the production of homocytotropic antibodies (or reagins). The interaction of an allergen with antibodies occurs in organs and cells where antibodies are fixed, i.e. in shock organs. These organs include skin, smooth muscles of internal organs, blood cells, nervous tissue, connective tissue. Especially important is the reaction in mast cells of the connective tissue, which are located close to small blood vessels under the mucous membranes, as well as on basophilic leukocytes. During the pathochemical stage, the allergen-antibody complex leads to suppression of the activity of inhibitors of tissue and serum enzymes, which causes intoxication and the release of some biologically active substances (histamine, serotonin, heparin, acetylcholine, etc.) and the formation of other biologically active substances (bradykinin, slow-acting substances of anaphylaxis responsible for bronchospasm, etc.). The pathophysiological stage gives a complex of pathophysiological disorders underlying the clinical picture. Characteristic are bronchospasm, spasms of smooth muscles of the intestine, bladder, uterus, impaired vascular permeability. In this phase, allergic inflammation also occurs, which develops on the skin, mucous membranes and internal organs. The pathomorphological basis of anaphylactic shock is plethora and swelling of the meninges and brain, lungs, hemorrhages in the pleura, endocardium, kidneys, adrenal glands, mucous membranes, stomach and intestines, emphysema.

The speed of the complication is from a few seconds or minutes to 2 hours. The symptoms of shock are diverse, their severity varies in different patients. The degree of severity is divided into four stages: mild, moderate, severe and extremely severe (fatal). Most patients complain of sudden weakness, shortness of breath, dry cough, dizziness, decreased vision, hearing loss, severe itching of the skin or a feeling of heat throughout the body, chills, abdominal pain, heart, nausea, vomiting, urge to stool and urination. Loss of consciousness may occur. Objectively, tachycardia, thready pulse, low or completely undetectable blood pressure, cold sweat, cyanosis or sharp redness of the skin, muffled heart sounds, dilated pupils, convulsions, foam from the mouth, sometimes a sharp swelling of the tongue, swelling of the face (angioedema), larynx, involuntary defecation, urinary retention, widespread rash. The duration of the symptoms of anaphylactic shock depends on the degree of sensitization, the correctness and timeliness of treatment for concomitant diseases, etc. In some cases, the death of patients occurs within 5-30 minutes from asphyxia, in others - after 24-48 hours or several days from severe changes in the kidneys (due to glomerulonephritis), liver (hepatitis, liver necrosis), gastrointestinal tract (profuse gastrointestinal bleeding), heart (myocarditis) and other organs. After suffering anaphylactic shock, fever, lethargy, pain in the muscles, abdomen, lower back, vomiting, diarrhea, skin itching, urticaria or Quincke's edema, attacks of bronchial asthma, etc. are observed. Complications of anaphylactic shock, in addition to those mentioned above, include a heart attack, pneumonia, hemiparesis and hemiparalysis, exacerbation of chronic colitis with prolonged intestinal bleeding. Mortality in anaphylactic shock ranges from 10 to 30%. All patients who have suffered anaphylactic shock need dispensary observation of an allergist. The most important preventive measures are the targeted collection of an allergic history, as well as the elimination of unreasonable prescriptions of drugs, especially for patients suffering from one form or another of an allergic disease. The drug, to which there was an allergic reaction of any kind, should be completely excluded from contact with the patient in any pharmacological form.

Acute urticaria and angioedema (angioneurotic edema, giant urticaria)

This is a classic allergic skin disease, which is associated with a violation of the permeability of the vascular wall and the development of edema, often accompanied by damage to the cardiovascular system and other body systems. Etiological factors that can cause Quincke's edema are many drugs, foods, household, bacterial and fungal allergens, etc. According to the pathogenesis, Quincke's edema refers to an allergic disease that occurs with humoral, circulating antibodies. The main mediator of an allergic reaction is histamine. Mediators cause capillary dilation and increased permeability of blood vessels, leading to flushing, blistering, and edema. In the clinic of acute urticaria, complaints of excruciating local or widespread pruritus, chills, nausea, abdominal pain, and vomiting predominate.

With angioedema, there is no skin itching, there is a feeling of tension in the skin, an increase in the size of the lips, eyelids, ears, tongue, scrotum, etc., with swelling of the larynx - difficulty swallowing, hoarseness of voice. Quincke's edema is considered as one of the forms of urticaria. Unlike urticaria, with angioedema, deeper sections of the skin and subcutaneous tissue are captured. Often these diseases are combined. Acute urticaria can occur with complications such as myocarditis, glomerulonephritis, and laryngeal edema, which can lead to severe asphyxia requiring urgent tracheotomy.

Serum sickness and serum-like reactions These are classic systemic allergic diseases that occur after the administration of foreign therapeutic sera and many therapeutic drugs. Diseases refer to allergic reactions that occur with humoral, circulating antibodies. In the clinical picture, an incubation period of 7 to 12 days is distinguished, which, depending on the degree of sensitization, can decrease to several hours or increase to 8 weeks or more. According to the degree of severity, mild, moderate and severe forms are distinguished. Patients complain of itching, chills, headache, sweating, abdominal pain, sometimes nausea, vomiting, joint pain. During the examination, rashes on the skin, Quincke's edema, fever from subfebrile numbers to 40 ° C, swollen lymph nodes, swelling of the joints, tachycardia, hypotension are determined. There may be swelling of the larynx with the threat of asphyxia. The duration of the course of the disease is from several days to 2-3 weeks, sometimes there is an anaphylactic form of serum sickness, which in its course resembles anaphylactic shock. Serum sickness can give complications: myocarditis, glomerulonephritis, hepatitis, polyneuritis, encephalitis. The prognosis in a significant number of cases is favorable, if there are no late severe complications from the internal organs indicated above.

Allergic reactions such as the Arthus-Sakharov phenomenon Another name for these reactions is "gluteal reactions" because they occur at the site of drug administration. The causes of these reactions are foreign sera, antibiotics, vitamins (for example, B₁), aloe, insulin and many other drugs. The pathogenetic mechanism is that there is a local interaction of the antigen (or hapten) with antibodies in the wall of small vessels, the antibody approaches the vessel wall, but does not penetrate into the tissues. The antigen-antibody complex is formed in the subendothelial layer of the blood vessel wall, in which it irritates tissues, causing necrotic changes. Histamine does not participate in these reactions. In soft tissues, a granuloma is formed, which is complex in morphological structure. The following factors indicate increased sensitivity: the primary development of necrosis according to the type of Arthus phenomenon, the rapid formation of a capsule around the focus, pronounced vascular and cell proliferative reactions around the necrosis with the formation of granulomatous structures and giant forms of macrophages. A characteristic feature of the morphological granuloma is the development of tuberculoid structures, which are very similar to the picture of the tuberculous process. The term of the reaction - from 2-3 days to 1 month or more. Patients complain of severe pain at the injection site, local skin itching. Objectively marked hyperemia, compaction, painful when touched. If injections are not stopped in a timely manner, then the infiltrates increase in size, become sharply painful, and local necrosis may form. Granuloma in soft tissues has a tendency to aseptic abscess formation and fistula formation. The prognosis is favorable in most cases.

Bronchial asthma

Bronchial asthma is an allergic disease, in the clinical course of which the central place is occupied by expiratory type asthma attacks (expiration is difficult), caused by bronchospasm, hypersecretion and swelling of the bronchial mucosa. There are many reasons why asthma can develop. They can be allergens of infectious and non-infectious origin. Of the infectious allergens, Staphylococcus aureus, Staphylococcus aureus, Klebsiella, Escherichia coli and others, that is, opportunistic and saprophytic microorganisms, are in the first place. Non-infectious include household allergens (house dust and feathers, mites), book and library dust, pollen from trees, grasses, weeds, animal hair and dander, food for aquarium fish. Food allergens - fish, cereals, milk, eggs, honey and others - are important as the cause of bronchial asthma mainly in children, and in adults - with hay fever. Allergens can be pathogenic and non-pathogenic fungi, medicinal substances. Bronchial asthma is divided into atonic (non-infectious-allergic) and infectious-allergic. According to these two forms, the pathogenesis of the disease is also considered, while the pathogenesis of the attack and the pathogenesis of the disease are taken into account. The result of an allergic reaction occurring in the tissues of the bronchial tree is always an attack of bronchial asthma. In the atonic form, an attack is the result of an allergic reaction with circulating, humoral antibodies (reagins, which are mainly related to JgE), fixed on sensitized mast cells, a large number of which are located in the connective tissue of the bronchopulmonary apparatus.

In bronchial asthma, three stages are distinguished: immunological, pathochemical and pathophysiological. In the formation of an attack, the slow-acting substance anaphylaxin, histamine, acetylcholine and other biologically active substances that are released during the formation of the antigen-antibody complex take part. In the pathophysiological stage of the atonic form of bronchial asthma, a spasm of the smooth muscles of the bronchi and bronchioles develops, the permeability of blood vessels increases, there is an increase in mucus formation in the mucous glands, and excitation of nerve cells.

Allergic mechanisms are the main link in the pathogenesis of bronchial asthma, however, at some stage of the disease, second-order mechanisms are activated, in particular, neurogenic and endocrine ones. There is also a genetic predisposition to atonic diseases (about 50%). One of the constitutional genetic features is a decrease in β-adrenergic receptor sensitivity, which causes an increase in the sensitivity of the smooth muscles of the bronchioles to the action of histamine, acetylcholine, and thereby leads to bronchospasm. In the infectious-allergic form of bronchial asthma, the pathogenesis is associated with an allergy of the cellular (delayed) type. In the mechanism of this type of allergy, the leading role is played by the processes of irritation of skin and connective tissue structures by allergens and the formation of various types of inflammation. The initial stage of a cell-type allergic reaction is the direct specific contact of sensitized lymphocytes with allergic agents on the surface of sensitized cells. In the histological picture, there are features of the proliferation of histiomonocytic elements that create structures of the tuberculoid type, massive perivascular infiltration by mononuclear cells such as medium and small lymphocytes. With the development of an allergic reaction of a cellular type, in addition to the factor of inhibition of macrophage migration, other humoral factors are distinguished (lymph node permeability, lymphotoxin, chemotaxis, skin-reactive factor, etc.). In addition to macrophages and fibroblasts, the objects of influence of humoral factors, which are biochemical mediators of an allergic reaction of a cellular type, can be epithelial cells, endothelium of the walls of blood vessels, non-cellular elements (myelin), etc. An allergic reaction of a cellular type develops as a response to antigens of microorganisms, but can also occur in relation to purified proteins and simple chemicals in combination with an autologous protein.

In the clinical picture of bronchial asthma, recurrent asthma attacks play a leading role. They usually start at night or early in the morning. A number of patients have some precursors: lethargy, itching in the nose, nasal congestion or sneezing, a feeling of tightness in the chest. An attack begins with a painful cough, usually dry (without sputum), then a typical expiratory-type dyspnea appears (expiration is difficult). From the very beginning of the attack, breathing changes, becomes noisy and whistling, audible at a distance. The patient tries to maintain a state of rest, often takes a sitting position in bed or even on his knees, reflexively trying to increase lung capacity. The number of respiratory movements is reduced to 10 or less per minute. At the height of the attack, due to the great tension, the patient is covered with sweat. The pause between inhalation and exhalation disappears. The chest is in the position of a deep breath, breathing becomes possible mainly due to the participation of the intercostal muscles. There is tension in the abdominal muscles. During an attack, the skin of the face turns pale, cyanosis is often noted. When listening over the entire surface of the lungs, dry whistling rales are determined. The attack ends most often with a cough with a separation of light, viscous or thick and purulent sputum.

Asphyxiation attacks can be mild, moderate and severe, depending on their duration, the possibility of relief (cessation) with the help of drugs, the form of bronchial asthma, the duration of its course and the presence of concomitant diseases of the bronchopulmonary apparatus. There are cases when an attack of bronchial asthma cannot be stopped within 24 hours with conventional anti-asthma drugs. Then the so-called asthmatic state, or asthmatic status, develops. In the pathogenesis of the asthmatic condition in the atonic form of bronchial asthma, the main role is played by mucosal edema and spasm of the smooth muscles of the small bronchi. In the infectious form, mechanical obstruction of the bronchial lumen with thick viscous mucus is observed.

The clinical manifestation in an asthmatic condition is severe expiratory dyspnea with very rare shallow breathing. The skin becomes moist, cyanotic, with a grayish tinge. The position of the patient forced - sitting. Respiratory noises (wheezing with wheezing) weaken until they completely disappear ("silent lung"), creating a deceptive impression of well-being. In severe status asthmaticus, hypoxic coma develops, which can be of two types: quickly and slowly advancing. A rapidly flowing coma is characterized by an early loss of consciousness, the disappearance of reflexes, cyanosis, and frequent shallow breathing. Wheezing over the lungs ceases to be heard, heart sounds become loud, the pulse is frequent, blood pressure drops. With a slowly flowing coma, all signs are extended in time. An asthmatic condition can be complicated by pneumothorax, atelectasis of the lung tissue due to blockage of the bronchi with viscous sputum. The prognosis for the atonic form is favorable. With an infectious form, it is much worse, in which case the disease often leads to disability. The causes of deaths are the abuse of certain drugs, drug allergies (anaphylactic shock), withdrawal syndrome in patients who have long received glucocorticoid hormones, strong sedatives.

Data from immunological studies in bronchial asthma. Allergic skin-sensitizing antibodies (or reagins) are various types of immunoglobulins that have the ability to specifically react with allergenic substances. They are the most important types of antibodies that are involved in the mechanisms of allergic reactions in humans. Differences of allergic antibodies from "normal" globulins are their immunological specificity and biological properties of various allergic reactions. Allergic antibodies are divided into damaging (aggressive) witness antibodies and blocking ones, which cause the transition of the state of allergy into immunity. The most reliable method for detecting reagins in the blood serum of patients with allergic diseases of the humoral type is the Prausnitz-Küstner method. In the atonic form of asthma, positive results were obtained with household, pollen, food, fungal and a number of other allergens, as well as in some cases with an infectious form with bacterial monovaccines. Reagins are immunologically heterogeneous, some of them are associated with JgA and JgJ, but the bulk are associated with the JgE type. With bronchial asthma and other allergic diseases in the blood serum, the content of JgE increases by 4-5 times. JgE is also found in very low concentrations in nasal mucus, bronchi, colostrum and urine. Complications of bronchial asthma are pulmonary emphysema, pneumosclerosis, chronic cor pulmonale, pulmonary heart failure.

Pollinosis (hay fever)

This is a classic disease that is caused by the pollen of wind-pollinated plants. It has a pronounced seasonality, i.e., it becomes aggravated during the flowering period of plants. Pollinoses are caused by pollen of trees and shrubs (such as birch, acacia, alder, hazel, maple, ash, poplar, etc.), meadow, cereal grasses (such as timothy, fescue, bluegrass, etc.), cultivated cereals (such like rye, corn, sunflower) and weeds (such as wormwood, quinoa, dandelion, etc.). Pathogenetically, hay fever is a typical allergic disease that occurs with circulating humoral antibodies. Reagins to pollen allergens are determined in blood serum, nasal mucosa, sputum, conjunctiva.

Clinical variants of pollinosis are rhinitis, conjunctivitis and asthmatic bronchitis or bronchial asthma. Other options are possible, for example, with neurodermatitis, urticaria. Patients in the period of exacerbation complain of painful and frequent bouts of sneezing with copious watery discharge from the nasal cavity, nasal congestion and itching, eyelid itching, lacrimation, pain in the eyes, itching of the mucous membranes of the nasopharynx, larynx, widespread skin itching. Pollen asthma is characterized by attacks of expiratory dyspnea, which are combined with symptoms of rhinitis and conjunctivitis. Symptoms of the so-called pollen intoxication develop: headache, weakness, sweating, chills, low-grade fever. The eyes of the patients are swollen, inflamed, watery, the nose is swollen, the voice is nasal. Breathing through the nose is difficult. The course of the disease can be relatively mild with isolated rhinitis or conjunctivitis, moderate - with a combination of these diseases and a more pronounced picture of pollen intoxication, severe - with the addition of bronchial asthma, which can even be provoked by an asthmatic condition.

In patients suffering from hay fever, short-term exacerbations may occur outside the flowering period of plants after ingestion of food products that have common antigenic properties with tree pollen (nuts, birch, cherry, apple juice and other products). Also, mild exacerbations of hay fever in patients with chronic diseases of the gastrointestinal tract are caused by eating cereals in the form of bread, various cereals, and alcoholic beverages. Also, for patients suffering from hay fever, it is considered very dangerous to use decoctions of various herbs in the winter to treat colds. Phytotherapy in such patients can contribute to a severe exacerbation of hay fever and cause attacks of bronchial asthma.

A laboratory blood test reveals eosinophilia, lymphocytosis. In the blood serum, the content of histamine, serotonin, α₂- and γ-globulins. In the sputum of patients with pollen bronchial asthma, an accumulation of eosinophils is found. In patients with pollen asthmatic bronchitis and bronchial asthma, bronchial hypersensitivity to acetylcholine and histamine was noted. With polynosis, complications are possible in the form of bacterial conjunctivitis, sinusitis, frontal sinusitis, ethmoiditis, asthmatic bronchitis and bronchial asthma. Patients with hay fever are potential asthmatics, but in general there are a sufficient number of cases of a long and rather favorable course of the disease, when the ability to work is disturbed only during the flowering period of plants, and in the rest of the year, good health is maintained. Patients with hay fever need long-term observation of an allergist.

The most severe form of drug allergy is Lyell's syndrome. The causes of this syndrome are different: taking antibiotics and sulfa drugs, as well as viral and bacterial diseases. Lyell's syndrome is called acute allergic epidermal lysis. It comes on suddenly and sharply. It is characterized by the appearance on the skin and mucous membranes of pink, red or brownish spots of various sizes, against which flaccid blisters and detachment of the surface layers of the epidermis are formed. As a result, continuous erosive surfaces are formed that resemble a second degree burn. The general condition progressively worsens, the body temperature rises to 39-40 ° C, a sharp weakness develops, disturbances in the activity of the cardiovascular system, kidneys, and liver appear. A coma may develop. The prognosis of the disease is unfavorable, approximately 30% of patients die rather quickly.

Stevens-Johnson Syndrome

This is a malignant form of exudative erythema. The process is accompanied by high temperature, the appearance of a rash on the skin and mucous membranes of the mouth, nose, genitals, in the anus. The rash often has a bullous character (in the form of blisters). Also characteristic are eye lesions in the form of conjunctivitis, keratitis. Complications in reactions of hyperergic type: pyoderma, myocarditis, hepatitis, neuritis, glomerulonephritis. With Lyell's syndrome - sepsis. Based on clinical observations, clear risk factors for allergic drug complications have been identified.

These factors are divided into two groups. The first group includes factors that depend on the patient:

1) heredity burdened with allergic diseases (the so-called allergic constitution);

2) concomitant classical allergic diseases in the past or at the time of observation;

3) prolonged and uncontrolled self-treatment of patients with a variety of drugs;

4) occupational hazards for workers in factories for the manufacture of medicines, the chemical industry, etc.;

5) prolonged fungal diseases (trichophytosis, rubrophytosis, pityriasis versicolor) creates a risk of allergy to penicillin.

The second group includes factors depending on the doctor:

1) unreasonable prescription of antibiotics and chemotherapy drugs for preventive and therapeutic purposes (especially for viral diseases);

2) improper treatment (choice of dose, route of administration). Dangerous long-term use of antibiotics in the form of aerosols, drops, ointments in patients with an allergic constitution, unjustified intravenous administration of antibiotics in the absence of vital indications (such as: sepsis, peritonitis, endocarditis, etc.);

3) repeated and repeated treatment with a drug or chemical compounds that have antigenic properties in common with it;

4) polypharmacy. It has been established that a number of drugs increase the allergic activity of other drugs (for example, sulfonamides - antibiotics used orally);

5) underestimation by the doctor of damage to the excretory organs and, accordingly, the level of excretion of drugs during drug therapy;

6) poorly collected allergic history before prescribing drugs;

7) the simultaneous use of antihistamines, which does not inhibit the occurrence of drug allergic complications, but only masks the initial symptoms that could be prevented by the timely withdrawal of the drug.

LECTURE No. 6. Ways to strengthen immunity. Preventive immunization

In human life, there are several critical stages in the development of the ability of the immune system to protect the body from foreign cells and substances. These stages are associated with age-related changes, during which the immune system behaves unpredictably when the introduction of an antigen into the body causes an incorrect paradoxical reaction. This is expressed in the fact that the immune response may be either insufficient to repel the aggression of a foreign agent, or excessive, leading to various types of allergic reactions.

The first period of increased risk is the first month after birth. The child is born practically "sterile". The microflora of the mother is not dangerous for him due to passive immunity, which consists of protective antibodies of the mother received by the child through the placenta during fetal development and with milk during breastfeeding. Microbes that are present in the maternity hospital pose a potential danger to the newborn, since he has few opportunities to resist them. His body (immune system) does not yet produce its own antibodies, phagocytes are not active enough, etc. Therefore, all objects that come into contact with a newborn child must be practically sterile. If the child was born healthy, then he should not stay long in the maternity hospital or department. At home, a newborn is literally attacked by the microflora of family members and household items. It takes at least a month for the child to adapt to it. However, by the end of the first week of life, the number of lymphocytes sharply increases in his blood.

The second period of weakening of the protective forces falls on the 3rd-6th months of the child's life. This is due to the fact that by this period the supply of maternal antibodies obtained through the placenta ends. Because of this, the body's susceptibility to influenza viruses, colds and the causative agent of childhood infections increases, which at this age proceed atypically and do not give stable immunity. During this period, it is undesirable for a child to contact children who attend kindergarten and school. Long-term natural feeding is very important, since through breast milk the lack of antibodies that can protect it from infections and protect it from the development of food allergies, which most often appear during these months, is partly compensated.

The third period falls on the 2nd year of life, when the circle of contacts of the child with the environment expands, and the local immunity of the mucous membranes of the respiratory and digestive systems is not yet fully functional, which is why there is a risk of repeated viral and bacterial infections. Hardening, walking in the fresh air, proper nutrition help to avoid them. At this age, it is necessary to avoid visiting crowded places with the child.

The fourth period is the 4th-6th years of the baby's life. This is the so-called pre-school period, when the child attends kindergarten, in which there are constant contacts with children. At this age, chronic tonsillitis often develops, adenoids increase, there are frequent respiratory infections, and a tendency to allergic reactions appears.

The fifth period is adolescence, beginning at 12–13 years of age for girls and 14–15 years of age for boys. This is a time of very rapid growth and development of the body, which the organs of the immune system do not keep up with. The “splash” of sex hormones reduces the activity of T-lymphocytes and leads to increased production of antibodies by B-lymphocytes. This leads to the activation of inflammatory, chronic and autoimmune diseases. At the same time, during this period, there is an alleviation of the course of allergic diseases, up to their complete disappearance. Sanitation of all foci of chronic infection (carious teeth, adenoids, diseased tonsils, etc.) is necessary. Also important is a proper, balanced diet in all respects. During all periods of growth and development of the child, the number of drugs used to treat various diseases should be minimal. One of the methods that strengthen the immune system and prevent certain diseases is vaccination.

Vaccination is the most effective method of protection against infectious diseases currently known. The basic principle of vaccination is that a weakened or killed disease agent is injected into the patient to stimulate the production of antibodies necessary to fight the pathogen. Vaccinations are successfully used to combat rubella, measles, mumps, hepatitis B, polio, rotavirus infection, influenza or bacteria (causative agents of tuberculosis, diphtheria, whooping cough, tetanus). The essence of vaccination is to create or enhance artificial immunity. There is a concept of "herd" immunity. The more people who are immune to the disease, the less likely the unimmunized are to get sick and the less the risk of an epidemic (i.e., with the help of vaccination, the so-called immune layer of the population is created). Vaccination can be both single (against measles, mumps) and multiple (against polio, DPT). The multiplicity shows how many times it is necessary to inject a vaccine into the body to form immunity.

Revaccination is an event aimed at maintaining the immunity that was created by previous vaccinations. Usually done a few years after vaccination. In the event of a focal outbreak of any infectious disease, mass vaccination is carried out to prevent an epidemic. It is a one-time initial vaccination used to quickly break the chain of transmission. An example of such vaccination would be mass vaccination coverage before an impending influenza epidemic. But vaccination also has disadvantages. It is carried out only against certain strains, ineffectiveness due to virus mutation is possible.

Vaccines are of various types:

1) live vaccines containing a weakened live microorganism;

2) inactivated ("killed") vaccines;

3) chemical vaccines. They contain components of the cell wall or other parts of the pathogen;

4) toxoids (contain an inactive toxin produced by bacteria);

5) combined vaccines (containing several components).

Immunocorrection also includes the use of drugs to restore impaired immunity. This is either monotherapy or the use of immunomodulators according to a certain scheme. To do this, drugs are used that replace the lost function of immunity (immunoglobulins, interferons), and drugs that stimulate a reduced immune function (interferon inducers, herbal preparations, non-specific immunostimulants). There are no universal means of increasing immunity. The immune system of the human body is very complex, therefore, the issues of strengthening and correcting immunity must be approached reasonably, comprehensively and individually, focusing primarily on promoting a healthy lifestyle. This is a complete, balanced diet, and hardening of the body, and the absence of stress, and a rational daily routine (work, rest, sleep), and an active lifestyle. All this will help to strengthen the immune system and, consequently, the health of the body.

Author: Anokhina N.V.

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