LECTURE No. 12. Malabsorption syndrome in children. Clinic, diagnosis, treatment

Enteropathy is a pathological condition that is caused by a deficiency or dysfunction of certain intestinal enzymes, caused by the absence, deficiency or disruption of the structure of certain intestinal enzymes that ensure digestive processes.

Absorption of carbohydrates: food carbohydrates consist of disaccharides:

1) sucrose (regular sugar = fructose + glucose), lactose (milk sugar = galactose + glucose);

2) monosaccharides: glucose and fructose;

3) vegetable starches (a polysaccharide consisting of glucose molecules).

The enterocyte is not capable of transporting carbohydrates larger than a monosaccharide. Therefore, carbohydrates must be broken down before absorption. Malabsorption syndrome is a syndrome of impaired intestinal absorption; malabsorption syndrome can be caused by: lack of pancreatic enzymes - a violation of the cavity phase of digestion; cholestasis, intestinal dysbiosis - disturbance of the metabolism of bile acids, lipid transport and disturbance of the biliary phase of digestion; deficiency of cavity enzymes (disaccharidases, peptidases, etc.) leads to disruption of membrane digestion; atrophy of the mucous membrane of the small intestine - to a violation of absorption, i.e., the cellular phase of digestion, while membrane digestion also suffers; pathology of intestinal lymph flow, mesenteric circulation to - deterioration of further transport of absorbed substances - the outflow phase suffers; accelerated passage of food through the intestines leads to disruption of all types of digestion.

1. Enzymopathy

Enzymopathy is a pathological condition caused by the absence, deficiency or disruption of the structure of certain cellular enzymes that ensure digestive processes.

The clinical picture is due to impaired absorption of one or more nutrients through the mucous membrane of the small intestine. Clinical manifestations of malabsorption syndrome in the form of diarrhea, weight loss, protein deficiency, signs of hypovitaminosis.

Malabsorption syndrome can be primary (hereditary) or secondary (acquired). Classification. Pathogenetic classification.

1. Exocrine pancreatic insufficiency:

1) cystic fibrosis of the pancreas;

2) chronic malnutrition with protein and calorie deficiency;

3) Shwachman-Diamond syndrome;

4) chronic pancreatitis with exocrine insufficiency;

5) specific enzyme defects (lipase, trypsinogen).

2. Insufficiency of bile acids:

1) obstruction of the biliary tract (biliary atresia, cholelithiasis, cancer of the head of the pancreas);

2) resection of the ileum;

3) cirrhosis of the liver, chronic hepatitis (decreased secretion);

4) dysbacteriosis.

3. Violations of the functions of the stomach:

1) postgastrectomy syndrome;

2) vagotomy;

3) pernicious anemia caused by vitamin B12 deficiency

4. Dysmotility:

1) hyperthyroidism;

2) diabetes mellitus;

3) scleroderma; 4 amyloidosis.

5. Pathology of the intestinal mucosa:

1) celiac disease;

2) lactase deficiency;

3) sucrase and isomaltase deficiency (combined);

4) exudative enteropathy;

5) intolerance to cow's milk protein (and/or soy);

6) insufficiency of enterokinase;

7) abetalipoproteinemia (Bassen-Kornzweig syndrome);

8) impaired transport of amino acids (tryptophan, methionine, lysine, etc.);

9) vitamin B12 malabsorption (transcobalamin-II deficiency);

10) congenital disorders of folic acid absorption processes;

11) chlorine-losing diarrhea;

12) vitamin D-dependent rickets;

13) enteropathic acrodermatitis;

14) Menkes syndrome (curly hair syndrome);

15) Crohn's disease;

16) malabsorption after suffering enteritis;

17) tropical sprue;

18) Whipple's disease;

19) chronic infections (immunodeficiency), in particular giardiasis;

20) primary immune deficiency (Wiskott-Aldrich syndrome);

21) congenital short intestine;

22) short bowel syndrome after resection (resection of the proximal part of the small intestine, resection of the ileum, resection of the ileocecal region);

23) eosinophilic gastroenteritis.

Etiology. The etiology in each specific case is different (absence or reduced activity of lactase, α-glucosidase, enterokinase). Among hereditarily caused impaired intestinal absorption, disaccharidase deficiency (sucrase, lactase, isomaltase), true celiac disease (gliadin intolerance), enterokinase deficiency, monosaccharide intolerance (glucose, fructose, galactose), impaired absorption of amino acids (cystinuria, Hartnup disease, etc.) are found. ), impaired absorption of vitamin B12 and folic acid, etc. Secondary, or acquired, malabsorption occurs in many chronic diseases of the stomach and intestines (pancreatitis, hepatitis, dysbacteriosis, dyskinesia, Crohn's disease, etc.).

Clinic. Clinical picture in children: chronic diarrhea dominates with a high content of lipids in the feces. Dystrophy gradually develops, children are stunted. Clinical manifestations of vitamin deficiency and water-electrolyte balance disorders are added (dry skin, seizures, glossitis, hypokalemia, hyponatremia, hypocalcemia, etc.) Pancreatic digestion insufficiency syndrome is characterized by (pancreatic steatorrhea): creatorrhoea with a predominance of unchanged muscle fibers, steatorrhea represented by neutral fat, amilorrhea (extracellular starch). For the syndrome, disturbances in the flow of bile are typical (hepatogenic steatorrhea): steatorrhea (with a predominance of fatty acids against the background of a smaller amount of neutral fat in the complete absence of soaps), creatorrhoea is possible (altered muscle fibers predominate).

Intestinal diarrhea is characterized by steatorrhea, mainly represented by soaps and fatty acids. Diagnostics. Methods of paraclinical examination.

1. General blood analysis.

2. General urine analysis.

3. Feces for Giardia, helminth eggs, scraping for enterobiasis.

4. Coprogram (expanded, expanded): starch, neutral fat, fatty acids, connective tissue, iodine-philic microflora are absent in normal feces.

5. Biochemical study of blood serum: proteinogram, liver function tests (ALT, AST, alkaline phosphatase, bilirubin, cholesterol), K, Fe, Ca, P, folic acid, vitamin B12, carotene).

6. Sugar curve - a flat sugar curve indicates diffuse damage to the mucous membrane. It should be noted that glucose testing is carried out on an empty stomach, after 15-30, 60-120 minutes.

7. d-xylose test. d-xylose is a pentose absorbed passively through intact mucosa. Excreted by the kidneys. In malabsorption, most of the xylose is lost in the stool and does not reach the circulatory system. At least 30% is excreted in the urine, i.e. more than 1,25 g of the administered per os (5 g), (PS According to studies, this test has a direct correlation with the glucose load test. Considering the complexity of the d-xylose test) .

8. Load tests with lactose, maltose, sucrose, starch. When loading with lactose, the rise in the lactose breakdown product in the blood after oral administration of 50 g of lactose by less than 20% indicates lactase deficiency.

9. Chromatographic identification of carbohydrates and amino acids contained in urine.

10. Hydrogen breath test: Determination of the amount of hydrogen in exhaled air after loading with sugars at a dose of 2 g/kg (maximum up to 50 g). The test is based on the fact that if sugar is not adsorbed in the upper parts of the small intestine, it reaches the distal parts, where intestinal bacteria act on it to produce hydrogen. The latter is quickly absorbed and exhaled in measurable quantities. An increased amount of exhaled hydrogen (more than 20 g/million during the first 2 hours) is considered a pathology. (PS In patients taking AB, and in approximately 2% of healthy individuals, hydrogen-producing intestinal flora is absent).

11. Sowing feces for dysbacteriosis.

12. Research of pancreatic enzymes in blood and urine.

13. Ultrasound of the pancreas, liver, gallbladder.

14. Determination of chlorine (Cl) in sweat fluid. If necessary, molecular genetic testing for cystic fibrosis.

15. X-ray of the gastrointestinal tract - information about the transit time of barium through the intestines, damage to the mucous membrane, the presence of a stricture or tumor.

16. Gastroduodenoscopy with biopsy. A biopsy of the small intestine helps in diagnosing celiac disease, but is not diagnostic for many other diseases.

17. Colonoileoscopy with biopsy.

2. Endocrine pancreatic insufficiency

Cystic fibrosis of the pancreas (cystic fibrosis) is a hereditary disease with a recessive type of inheritance. Frequency in population 2-8: 100 population. In patients with cystic fibrosis, the chloride channel on the apical part of the cell membrane “does not work”, leading to a disruption in the release of chlorine from the cell, which contributes to an increased escape of sodium ions from the lumen into the cell, followed by the aqueous component of the intercellular space. The consequence is a thickening of the secretions of the exocrine glands (bronchopulmonary system, pancreas, salivary glands, gonads). The respiratory system and pancreas are most often affected. The disease manifests itself with respiratory and intestinal syndromes already in the first year of life. The degree of interest of systems and organs varies. Paraclinical markers are: coprogram - the presence of a large amount of neutral fat and almost always its predominance over muscle fibers and polysaccharides.

Ultrasound of the pancreas - diffuse compaction of the parenchyma, and with age, a decrease in the size of the pancreas.

High sweat chlorides (60,0 or more mmol/l), repeatedly positive (at least 3 times).

Molecular genetic examination. But it should be noted that negative results of this study do not exclude the diagnosis of cystic fibrosis.

Shwachman-Diamond syndrome (congenital hypoplasia of the pancreas, combined with neutropenia, short stature and bone abnormalities).

Diagnosis based on pancreatic insufficiency syndrome in the first year of life, neutropenia, normal sweat chlorides.

Chronic pancreatitis with exocrine insufficiency - causes may be previous diseases, including mumps, trauma, medications, toxins, diseases and abnormalities of the bile and pancreatic ducts, systemic diseases.

Specific enzyme defects (lipase, trypsinogen).

1. Isolated deficiency of pancreatic lipase (Shedon-Rey syndrome) is manifested by fatty diarrhea due to neutral fats. Children have a good appetite and develop adequately physically and neuropsychically.

Diagnosis: based on fatty stool, neutral fat in feces, normal sugar curve, d-xylose test, sharp decrease or absence of lipase in pancreatic juice, absence of morphological changes in the pancreas, normal sweat chlorides.

Treatment: replacement therapy.

2. Isolated trypsin deficiency occurs with a frequency of 1: 10; the type of inheritance is autosomal recessive.

Clinically manifested shortly after birth by mushy or watery, foul-smelling stools due to natural feeding, poor development and increasing malnutrition. A large amount of protein and fat is found in the stool. Treatment: replacement therapy.

3. Amylase deficiency - diagnosis based on clinical manifestations, watery, sour-smelling stools. Coprogram (starch). Decreased or absent amylase activity. Effect against the background of an elimination (starch-free) diet.

3. Bile acid deficiency

Obstruction of the biliary tract (biliary atresia, cholelithiasis, cancer of the head of the pancreas), resection of the ileum, dysbacteriosis, cirrhosis of the liver, chronic hepatitis (decreased secretion). In a coprological study, the predominance of fatty acids against the background of a smaller amount of neutral fat in the complete absence of soaps; creativeorrhea is possible - altered muscle fibers predominate.

4. Disorders of the functions of the stomach

Postgastrectomy syndrome, vagotomy, pernicious anemia caused by vitamin B12 deficiency.

5. Dysmotility

Hyperthyroidism, increased thyroid hormone levels, increased motility, decreased food transit time, decreased digestion and absorption time of fats, diarrhea and steatorrhea. Diabetes mellitus: Diarrhea is secondary and associated with diabetic neuropathy.

Syndrome mechanisms:

1) violation of the exocrine function of the pancreas, steatorrhea;

2) decreased motility of the antrum of the stomach, impaired fat emulsification, steatorrhea;

3) violation of the autonomous autonomic regulation of the intestine, intestinal stasis, increased proliferation of bacteria, de-conjugation of bile acids, fat malabsorption. Scleroderma, decreased motility of the small intestine associated with a decrease in the number of smooth muscle cells of the intestinal wall, increased proliferation of bacteria, deconjugation of bile acids, fat malabsorption. Amyloidosis, deposition of amyloid protein in many organs, including the smooth muscle tissue of the intestinal wall, decreased motility, increased bacterial growth, deconjugation of bile acids, fat malabsorption.

6. Pathology of the intestinal mucosa

Celiac disease (celiac enteropathy, celiac disease, celiac sprue, non-tropical sprue).

Causes of development: congenital chronic disease of the small intestine, caused by the absence or decrease in the activity of peptidases of the brush border of the small intestine, which break down gliadin, a component of the protein of various cereals (wheat, rye, barley, oats).

Diagnosis of malabsorption: subtotal or total atrophy of the mucous membrane of the small intestine, clinical effect of a gluten-free diet, improvement in absorption parameters and x-ray data when gluten is excluded from the diet, improvement in the morphology of the small intestine from the use of a gluten-free diet, relapse of morphological disorders after discontinuation of a gluten-free diet.

Radiological signs: intestinal dilatation is the most constant and important symptom, it is especially pronounced in the middle and distal parts of the jejunum. Dilatation of the intestine is explained by its hypotension. Intestinal dilatation is absent in pancreatic steatorrhea and is not a consequence of increased fat content in the intestine.

Serological diagnosis is possible: determination of the content of antigliadin (AGA) antibodies, anti-endomysial (EMA) and anti-reticular (ARA) IgA antibodies in the blood serum. The presence of these antibodies is considered specific for the disease, and their study can be used for screening the closest relatives of patients, and also to establish the frequency of celiac disease in the population.

In the expanded coprogram - the presence of neutral fat and especially fatty acids and soaps, a flat sugar curve during glucose loading, indicating a violation of the absorption of di- and mono-substances.

The main treatment method is a diet excluding all foods containing gluten. Of the porridges, only rice, buckwheat, and corn are allowed, and the preparation of cakes, pastries, and cookies from soy flour, rice flour, and starch. The diet is prescribed even if the disease is asymptomatic and must be followed throughout the patient’s life. It must be remembered that even 100 mg of wheat flour taken daily causes pronounced changes in the morphological picture during biopsy.

Lactase deficiency. Lactase deficiency in children and adults has a heterogeneous molecular genetic nature.

There are two types of the enzyme: children's lactase and a more specific adult type lactase. At the age of 3-5 years, the gene regulation of enzyme synthesis switches from the child to the adult type.

There are 4 forms of lactase deficiency:

1) primary hereditary lactase deficiency: alactasia with an autosomal recessive (possibly dominant) type of inheritance;

2) transient lactase deficiency in preterm infants;

3) hypolactasia of the adult type (persistence of the child form of lactose);

4) secondary lactase deficiency (with enteritis, food allergies, celiac disease, immunodeficiency states). Clinical manifestations in the form of diarrhea after drinking milk. Diagnosis: diarrhea, in coprogram pH < 5,0. If there is no violation of cavity or membrane digestion, then no other changes in the coprogram can be found, the glycemic curves when loaded with glucose, galactose, d-xylose are normal, and when loaded with lactose - flat.

Biopsy of the small intestine - in persons with primary deficiency, morphological changes in the mucous membrane of the small intestine are usually not found, jeunoscopy - often without any features, visual endoscopic picture of the mucosa - a positive effect when withdrawing dairy products, worsening of the condition (diarrhea) after taking milk.

Treatment if lactase deficiency occurs in a breastfed child has 2 options.

1. If the child has clinical and laboratory signs of lactase deficiency, but is gaining weight, breastfeeding should be continued, but milk and dairy products, as well as beef, should be excluded from the mother’s diet.

2. If, against the background of lactase deficiency, the child’s body weight does not increase or decreases with a sufficient amount of breast milk, and therapeutic measures do not have a positive effect, it is necessary to stop breastfeeding and switch to dairy-free or low-lactose formulas. With a correct diagnosis, the clinical effect is observed already in the first 2-3 days.

Sugarase and isomaltase deficiency. Diagnosis: recurrent diarrhea, vomiting after taking sucrose, delayed physical development, onset of the disease after transferring the child to mixed or artificial feeding, improvement in general condition after eliminating sucrose and starch from the diet, flat glycemic curve after a load of sucrose, normal, as a rule, curve with glucose load, chromatography of urine sugars, coprogram, as in lactase deficiency.

Treatment: elimination diet.

Exudative enteropathy. Exudative enteropathy (protein-containing enteropathy) is characterized by increased release of protein into the intestinal lumen from the blood due to increased intestinal permeability and loss of protein in feces.

There are primary and secondary forms of exudative enteropathy.

Primary - a congenital generalized disease of the lymphatic system, selectively localized in the intestine. In foreign literature they are characterized as an independent nosological unit.

Pathogenesis: increased extravasation of protein occurs with increased pressure in the lymphatic vessels of the intestine.

Secondary causes of the development of exudative enteropathy are celiac disease, gastroenteritis, intolerance to cow's milk protein and many other diseases.

Pathogenesis: increased permeability of intestinal membranes for macromolecules.

Clinic and diagnosis: edematous syndrome; blood serum decrease in the total level of protein, g-globulins, cholesterol: in a coprogram: as in celiac disease due to impaired absorption of fat and its transport (neutral fat, fatty acids, soaps); X-ray of the intestine: X-ray changes are associated with swelling of the intestinal wall. The passage of the contrast agent is timely. With lymphangiectasia, the intestinal wall may have a cone-shaped thickening of circular folds in the form of a garland. In more severe cases, pseudopolyposis manifestations can be detected. The endoscopic picture is diverse: with preserved folding of the jejunal mucosa, its pale pink or pink color with a pronounced vascular pattern, sometimes combined with pinpoint hemorrhages, lymphofollicular hyperplasia, free hyperplasia of the mucosa in the form of numerous bulges is also observed.

Biopsy: according to Waldmann, with exudative enteropathy, changes were revealed in the lymphatic system of the mucous membrane and mesentery of the small intestine, which were called intestinal lymphangiectasia - dilatation of lymphatic vessels, interstitial edema.

Treatment.

1. A low-fat diet, the administration of triglycerides containing medium-chain fatty acids is recommended, since their absorption occurs without the participation of the intestinal lymphatic system and they can reduce pressure in the intestinal lymphatic vessels. Limit table salt.

2. In / in the introduction of protein drugs.

3. Symptomatic therapy.

Cow's milk protein intolerance. Cow's milk protein intolerance occurs most often in children, mainly under the age of 2 years, in approximately 1 in 200 young children.

Pathogenesis: immune reaction to proteins, mainly /? - lactoglobulin (this protein is not found in human milk). Clinical manifestations in the form of diarrhea.

Diagnosis: acute symptoms should be relieved within 48 hours, and chronic symptoms should be relieved within 1 week after stopping milk feeding. With endoscopy and biopsy of the jejunum: changes develop that resemble cases of untreated celiac disease, although not so pronounced; an increased titer of antibodies to cow's milk protein.

Treatment: elimination of cow's milk, and if necessary, soy.

Enterokinase deficiency. Enterokinase activates pancreatic trypsinogen, converting it into the active enzyme trypsin. Due to enterokinase deficiency, protein digestion in the intestine is impaired. Occurs only in children.

Clinical manifestations: diarrhea, edema, hypoproteinemia; enterokinase activity in the duodenal contents is practically absent, while the activity of amylase and lipase is unchanged.

Treatment: replacement therapy with pancreatic enzymes.

Abetolipoproteinemia. Abetolipoproteinemia (Bassen-Kornzweig syndrome) is a condition in which apo-B protein, necessary for the formation of chylomicrons and very low-density lipoproteins, is absent, which leads to the overcrowding of enterocytes with fats, and the absorption of fats is impaired.

Clinical manifestations in the first year of life, developmental delay is detected. The stool is profuse and discolored, the abdomen is distended. Mental development is somewhat behind. The appearance of cerebellar symptoms is typical after the age of 10. In adolescence, atypical retinitis pigmentosa develops. Diagnosis: detection of acanthocides in peripheral blood, hypocholesterolemia (200-800 mg/l), absence or minimal amount of b-, b-lipoproteins (b- or b-lipoproteinemia), pronounced accumulation of fasting lipids in the villi of enterocytes of the duodenal mucosa.

Treatment: restriction of long-chain fats, vitamins A, D, E, K, consumption of medium-chain triglycerides, disruption of amino acid transport.

Diagnosis: based on thin layer chromatography of amino acids in urine and blood serum.

Vitamin B12 malabsorption (transcobalamin-P deficiency). Deficiency of transcobalamin-II, a protein necessary for intestinal transport of vitamin B12, leads to severe megaloblastic anemia, diarrhea, and vomiting.

Treatment: vitamin B12 1000 mcg/week for transcobalamin-II deficiency and 100 mcg/month for other diseases, Congenital disorders of folic acid absorption processes.

Clinical features: megaloblastic anemia, decreased intelligence. Chloride-wasting diarrhea is a rare specific congenital disease caused by a defect in chloride transport in the ileum. Clinical manifestations: debilitating diarrhea from the moment of birth as a result of the accumulation of chlorine ions in the intestinal lumen.

Diagnosis: diarrhea, hypokalemia, hypochloremia, alkalosis. In other respects, the absorption function of the intestine is not impaired. Treatment: additionally add potassium to the diet, limit the consumption of chlorides.

Enteropathic acrodermatitis is caused by malabsorption of Zn.

Clinic: dermatitis (rash at the junction of the skin and the mucous membrane), there may be alopecia, diarrhea, developmental delay, decreased Zn in the blood serum, and alkaline phosphatase activity.

Treatment: zinc sulfate 150 mg/day.

Menkes syndrome. Menkes syndrome (curly hair syndrome) is caused by impaired transport of Cu (copper). Inherited in an autosomal recessive manner.

Clinic: growth retardation, hair anomaly, cerebellar degeneration.

Diagnosis: on the basis of the clinic and a decrease in Cu in the blood serum.

The prognosis is unfavorable.

Whipple syndrome. It almost never occurs in children.

Etiology: it is believed that they are rod-shaped microorganisms that also affect the small intestine.

Clinic: fever, diarrhea, arthralgia, polyserositis.

Diagnosis: biopsy in the duodenum reveals PAS-positive macrophages, and bacteria can be detected in the mucous membrane.

Diagnosis methods.

I stage. Identification of the syndrome of malabsorption.

According to clinical signs:

1) loss of body weight with normal or increased appetite - decreased absorption of fat, protein, carbohydrates;

2) plentiful fetid stools - reduced absorption of fat;

3) muscle weakness, edema - reduced absorption of proteins;

4) flatulence, rumbling in the stomach, excessive discharge of gases - digestion of carbohydrates by intestinal microflora;

5) parasthesia, bone pain, tetany - decreased absorption of Ca and vitamin D;

6) muscle cramps - excessive loss of K and Mg;

7) hemorrhagic syndrome - decreased absorption of vitamin K;

8) glossitis, stomatitis, cheilitis - deficiency of vitamin B12, folic acid and other B vitamins;

9) acrodermatitis - Zn deficiency.

II stage. Exclusion of infectious genesis of enteropathy.

Stage III. Establishing the type (phase) of digestive disorders (cavitary, parietal-membrane):

1) in case of disturbance of cavity digestion (preenteral mechanisms), identify its causes: dysfunction of the stomach, excretory pancreatic insufficiency, bile deficiency (decreased formation, impaired excretion or reabsorption in the intestine);

2) in case of violation of parietal digestion (enteral mechanisms), the following techniques can be used: timing (age of the patient) of manifestation of the disease, the connection between the manifestation of the disease and the child’s nutritional characteristics, and the connection between the deterioration of stool and the child’s nutritional characteristics. The prognosis with timely diagnosis and treatment is favorable.

Prevention consists of diet therapy with the exclusion of intolerable foods.

Author: Pavlova N.V.

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