Childhood diseases. Rickets, rickets-like diseases (lecture notes)

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Childhood diseases. Rickets, rickets-like diseases (lecture notes)

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LECTURE No. 6. Rickets, rickets-like diseases

Rickets is a disease of infants and young children with a disorder of bone formation and lack of bone mineralization, the leading link is the deficiency of vitamin D and its active metabolites during the period of the most intensive growth of the body.

Etiology. The main factor is hypovitaminosis D, vitamin D deficiency of exogenous or endogenous origin. Lack of sun exposure and exposure to fresh air, especially in winter and autumn in cities, since vitamin D is endogenously formed in the skin under the influence of solar radiation. Nutritional factors: improper feeding and nutritional deficiency of vitamin D, long-term artificial feeding with unadapted milk formulas.

Perinatal factors: prematurity (immaturity of enzyme systems). The rapid growth of the child, diseases accompanied by acidosis, insufficient intake of calcium and phosphorus salts.

Pathogenesis. Vitamin D is a steroid compound and is known as vitamin D₂ (ergocalciferol) and vitamin D₃ (cholecalciferol), which are similar in structure, physical, chemical properties and effect on the human body. Vitamin D supplied with food is converted in the liver and kidneys, resulting in the formation of 1,25-dihydroxy-vitamin D, which has a hormone-like effect, this compound affects the genetic apparatus of intestinal cells, increases the synthesis of a protein that binds calcium and ensures its transport in the body.

With a lack of vitamin D, the absorption and metabolism of calcium is disturbed, its concentration in the blood decreases, which causes a reaction of the parathyroid glands and an increase in the secretion of parathyroid hormone, which regulates the metabolism of calcium and phosphorus.

Increased secretion of parathyroid hormone leads to the mobilization of calcium from bone tissue, suppression of phosphate reabsorption in the renal tubules, and therefore the content of inorganic phosphates in the blood falls and the activity of alkaline phosphatase sharply increases. Violations of phosphate-calcium metabolism lead to the development of acidosis, which is accompanied by impaired excitability of the nervous system.

Clinic. The following degrees of rickets are distinguished by severity:

1) mild - small changes in the nervous and muscular systems; does not give residual effects (I degree);

2) moderate severity - pronounced changes in the bone, muscle, nervous and hematopoietic systems, moderate dysfunction of internal organs, a slight increase in the size of the liver and spleen, anemia (grade II);

3) severe - pronounced changes in the central nervous, bone and muscle systems, internal organs (III degree).

The initial period is more often noted in the second or third month, or manifests itself throughout the first year of life. From the side of the autonomic nervous system: sweating, nape baldness. From the nervous system: anxiety, irritability, tearfulness, disturbed sleep, muscular dystonia. Unsharp softening of the edges of the large fontanel and bones along the swept and lambdoid sutures.

Laboratory data. Biochemical studies: mild decrease in the amount of phosphorus, normal calcium content, increase in phosphatase activity. Increased phosphorus in daily urine. There are no radiological changes.

In the period of the height of the disease, along with the phenomena of inhibition of the nervous system, changes in the bones appear (softening of the bones of the skull, chest, limbs, pelvic bones, lower jaw) and is manifested by craniotabes, arched curvature of the forearms, deformities of the chest. Frontal and parietal tubercles, rosaries on the ribs, thickening of the epiphyses of tubular bones in the form of pearl strands, pronounced muscular hypotension of the muscles of the anterior abdominal wall with the formation of a frog belly, hypotension of the heart muscle (deafness of tones, tachycardia, gentle systolic murmur), weakness of the ligamentous apparatus, leading to spinal deformities. Bone changes, hardly noticeable with rickets of the I degree and distinct with the II degree, turn into deformation with rickets of the III degree. With rickets II and III degree, the spleen and liver are enlarged.

Biochemical studies: hypophosphatemia, hypocalcemia, increased activity of alkaline phosphatase. On radiographs, the contours of the bones are blurred, stripes are visible that correspond to zones of calcification in the metaphyses during the repair period. The epiphyses of the tubular bones are goblet, the edges of the metaphyses are fringed.

Late rickets include rare cases of the disease, when its active manifestations are observed at the age of over 4 years. Late rickets, observed in the war and the first post-war years, was characterized by the presence of common symptoms of the disease: anorexia, sweating, pain in the legs, fatigue. Bone deformities were noted only in some cases.

Convalescence period: neurological and vegetative symptoms disappear, condition improves, muscle tone increases, motor and static functions are restored, constipation disappears. The level of phosphorus, calcium is restored, decreases, and the level of alkaline phosphatase approaches the norm.

The period of residual effects: rachitic changes in the internal organs disappear, the tone of the muscles and ligamentous apparatus is restored. All biochemical parameters are normalized.

Diagnostics is carried out on the basis of clinical, laboratory data and X-ray data.

Differential diagnosis is carried out with a number of rickets-like diseases of a hereditary nature - phosphate diabetes, renal tubular acidosis, Debre - de Toni - Fanconi syndrome, as well as with congenital dislocation of the hip, chondrodystrophy, osteopathy in chronic renal failure, congenital bone fragility.

Treatment. Vegetables and fruits should be introduced into the child’s diet in a timely manner. Complementary foods should contain sufficient amounts of vitamins, salts, and foods containing natural vitamin D₃ (egg yolk, fish oil). Normalization of the regime with sufficient exposure to fresh air, massage, gymnastics. At the initial manifestations, full-term children are prescribed vitamin D supplements.₂ 300 - 800 IU per day, per course 400-000 IU; during the peak period for moderate and severe rickets, 600-000 IU per day is prescribed in 10-000 doses, for a course of 16 - 000 IU. During treatment, monitor the sensitivity of the child’s body to vitamin D using the Sulkovich test to prevent hypervitaminosis.

Ultraviolet therapy has a beneficial effect in the initial period and in the subacute course of rickets in young children. Massage and gymnastics are used at any time, but not in acute cases.

Forecast with timely treatment and elimination of the cause, it is favorable. In severe cases, psychomotor developmental delay, skeletal deformity, and posture disorders are possible.

Prevention. Rational nutrition, better natural feeding, vegetable and fruit juices, additional vitamins, sufficient insolation, sanitary and hygienic regime, hardening, therapeutic nutrition, massage, proper education. Antenatal prophylaxis in pregnant women in the last 2-3 months of pregnancy with vitamin D is advisable₂ 500-1000 IU per day. A long stay in the open air and a balanced diet are necessary. In the autumn-winter period, ultraviolet irradiation of children for preventive purposes should begin from 1-1,5 months of life. Two courses should be carried out with an interval of 2 months. The physiological requirement for vitamin D of a healthy full-term baby in the first year of life ranges from 400-500 IU per day. In cases where a child for some reason does not receive ultraviolet irradiation for prophylactic purposes, an artificial vitamin D preparation should be prescribed.₂ or D₃. For the purpose of antenatal prophylaxis in the last 3-4 months of pregnancy, Gendevit is recommended 1-2 tablets per day (250-500 IU vitamin D₂), under unfavorable conditions - 4 tablets per day. Contraindications: maternal age over 30 years, maternal illness. Postnatal prophylaxis is carried out from 2-3 weeks of age at 500 IU per day (1 drop of videohol), for a course of 150-000 IU.

Author: Gavrilova N.V.

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