Rakhitis

Rickets (from the Greek rhachis - "ridge", "spine") was known to doctors in ancient times. In 1650, the English anatomist and orthopedist Glisson described the clinical picture of rickets, which was called the "English disease", "slum disease". A significant contribution to the study of rickets was made by Russian pediatricians: N.F. Filatov, A.A. Kisel, G.N. Speransky, A.F. Tur, K.A. Svyatkina, E.M. Lukyanova.

The disturbance of bone formation is localized mainly in the area of the bone epimetaphyses (growth zones). Since bone growth and the rate of their remodeling are highest in early childhood, bone manifestations of rickets are most pronounced in children of the first 2-3 years of life. Rickets is also characterized by changes in other organs and systems, and a decrease in the child's immune reactivity.

Infantile rickets is common in children during the first years of life. Rickets was first mentioned in the works of Soranus of Ephesus (98-138 AD), who identified deformation of the lower limbs and spine in children. Galen (131-201 AD) described rickets-related changes in the skeletal system, including deformation of the chest. In the Middle Ages, rickets was called the English disease, since it was in England that its severe forms were widespread, which was associated with insufficient insolation in this climate zone. A complete clinical and pathological description of rickets was made by the English orthopedist Francis Episson in 1650. In his opinion, the main risk factors for the development of rickets in children are an adverse heredity and improper nutrition of the mother. In 1847, in the book "Pediatrics" by S.F. Khotovitsky described not only the damage to the bone system in rickets, but also changes in the gastrointestinal tract, vegetative disorders, and muscle hypotonia. In 1891, N. F. Filatov noted that rickets is a general disease of the body, although it manifests itself mainly in a peculiar change in the bones.

According to modern concepts, rickets is a disease characterized by a temporary discrepancy between the needs of a growing organism for phosphorus and calcium and the insufficiency of their transport systems in the body. This is a disease of a growing organism caused by a metabolic disorder (primarily phosphorus-calcium metabolism), the main clinical syndrome of which is damage to the skeletal system (impaired formation, proper growth and mineralization of bones), in which the pathological process is localized mainly in the area of the metaepiphyses of bones. Since the growth and rate of bone remodeling are highest in early childhood, damage to the skeletal system is most pronounced in children aged 2-3 years. Rickets is a multifactorial metabolic disease, the diagnosis, prevention and treatment of which should take into account all the factors of pathogenesis: insufficiency and imbalance of calcium and phosphorus intake with food, immaturity of the child's endocrine system, concomitant diseases, etc. In addition to the pathology of phosphorus-calcium metabolism, there are also disturbances in the metabolism of proteins and microelements (magnesium, copper, iron, etc.), polyvitamin deficiency, and activation of lipid peroxidation.

ICD-10 code

E55.0. Active rickets.

Epidemiology of rickets

Rickets occurs in all countries, but is especially common among northern peoples who live in conditions of insufficient sunlight. Children born in autumn and winter suffer from rickets more often and more severely. At the beginning of the 20th century, rickets was observed in 50-80% of young children in Western European countries. Up to 70% of children in Ukraine during these years also had rickets. According to A.I. Ryvkin (1985), rickets in children of the first year of life occurs in up to 56.5%, according to S.V. Maltsev (1987), its prevalence reaches 80%. The disease is most severe in premature babies.

Until now, classical (vitamin D-deficiency) rickets occupies a significant place in the structure of morbidity of young children. In Russia, its incidence in recent years has fluctuated from 54 to 66%. According to Moscow pediatricians, classical rickets currently occurs in 30% of young children. This figure can be considered underestimated, since only severe and moderate forms of the disease are registered. In developed countries, where specific prevention of rickets with vitamin D and vitaminization of baby food have been introduced, severe forms of rickets have become rare, but its subclinical and radiological manifestations remain widespread. Thus, in France, latent vitamin D deficiency was detected in 39%, and obvious clinical manifestations - in 3% of children admitted to hospitals for various diseases. In the northern provinces of Canada, hypovitaminosis D was detected in 43% of the examined children. In southern countries, despite sufficient intensity of ultraviolet radiation, rickets remains a very common disease. In Turkey, rickets was detected in 24% of children aged 3-6 months, although the introduction of vitamin D prophylaxis has reduced its prevalence to 4%.

Rickets, especially moderate and severe, suffered in early childhood can have an adverse effect on the subsequent development of children. Such children develop poor posture, flat feet, flattening and deformation of the pelvic bones, caries, and myopia. The role of rickets in the development of osteopenia and osteoporosis, which are widespread in adolescents, has been proven. The consequences of vitamin D deficiency in childhood are shown in Table 11-1.

Consequences of Vitamin D Deficiency

Organs	Consequences of deficiency
Bones and bone marrow	Osteoporosis, osteomalacia, myelofibrosis, anemia, myeloid dysplasia
Gastrointestinal tract	Decreased absorption of calcium, phosphorus, magnesium, hepatosplenic syndrome, gastrointestinal motility disorder
Lymphoid system	Reduced immunity, synthesis of interleukins 1, 2, phagocytosis, interferon production. Insufficient expression of the la antigen, which causes a predisposition to atopy
Muscular system	Muscle hypotonia, cramps (spasmophilia)

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ]

Causes of Rickets

The main etiological factor of rickets is vitamin D deficiency. At the same time, rickets is considered a multifactorial disease, in which there is a discrepancy between the high need of a growing child for phosphorus-calcium salts and the insufficient development of regulatory systems that ensure the supply of these salts to tissues.

There are two ways to provide the body with vitamin D: intake with food and formation in the skin under the influence of ultraviolet rays. The first way is associated with the intake of cholecalciferol (vitamin D3) with products of animal origin (cod liver, fish roe, egg yolk; to a lesser extent - human and cow's milk, butter). Ergocalciferol (vitamin D2) can be found in vegetable oils. The second way is associated with the formation of vitamin D in the skin from 7-dehydrocholesterol under the influence of ultraviolet rays with a wavelength of 280-310 μm. Previously, these two ways of providing vitamin D were considered equivalent. However, recently it has become known that more than 90% of vitamin D is synthesized by ultraviolet irradiation, and 10% comes from food. Under favorable conditions, the child's skin produces the necessary amount of vitamin D. With insufficient insolation due to climatic conditions (smoky air, cloudiness, fog), the intensity of vitamin D synthesis decreases.

[ 8 ], [ 9 ], [ 10 ], [ 11 ], [ 12 ], [ 13 ], [ 14 ], [ 15 ]

Formation of active metabolites of vitamin D

When entering the body, vitamin D is converted into more active metabolites through complex transformations in the liver and kidneys.

The first stage of activation is associated with the fact that vitamin D entering the digestive tract or formed in the skin is transported to the liver, where, under the influence of the enzyme 25-hydroxylase, it is converted into 25-hydroxycholecalciferol, or calcidiol, the main form of vitamin D circulating in the blood. In healthy children, the content of 25-hydroxycholecalciferol in the blood serum is about 20-40 ng/ml.

The second stage of vitamin D metabolism is repeated hydroxylation in the kidneys, where 25-hydroxycholecalciferol is transported by the vitamin D-binding protein (transcalciferin). At the level of the kidney mitochondria, the most active metabolite is formed - 1,25-dihydroxycholecalciferol, or calcitriol, as well as 24,25-dihydroxycholecalciferol. The formation of the main metabolite - calcitriol - occurs with the participation of the renal enzyme 1-a-hydroxylase. The concentration of calcitriol in blood plasma is about 20-40 pg/ml.

The content of vitamin D metabolites in the blood serves as an objective criterion for a child’s provision with vitamin D.

[ 16 ], [ 17 ], [ 18 ], [ 19 ], [ 20 ], [ 21 ]

The main physiological function of vitamin D

The main physiological function of vitamin D is to control the transport of calcium ions in the body (hence the name "calciferol" - "carrying calcium") - it is carried out by regulating the absorption of calcium ions in the intestine and increasing reabsorption in the renal tubules, as well as stimulating the mineralization of bone tissue. With a decrease in the level of calcium and inorganic phosphates in the blood or with an increase in the secretion of parathyroid hormone, the activity of renal 1-a-hydroxylase and the synthesis of 1,25-dihydroxycholecalciferol a sharply increase.

At normal and elevated levels of calcium and phosphorus in the plasma, another renal enzyme, 24-hydroxylase, is activated, with the participation of which 24,25-dihydroxycholecalciferol is synthesized, which promotes the deposition of calcium and phosphates in bone tissue and suppresses the secretion of parathyroid hormone.

In recent years, the ideas about the role of vitamin D have been significantly expanded by data on the transformation of this vitamin in the body, which has led to a change in views on vitamin D as a typical vitamin. According to modern concepts, vitamin D should be considered a powerful hormonally active compound, since, like hormones, it affects specific receptors. It is known that the metabolite of vitamin D (1,25-dihydroxycholecalciferol) transmits a signal to the gene apparatus (DNA) of cells and activates genes that control the synthesis of functional transport proteins for calcium ions. The target organs for this metabolite are the intestines, kidneys, and bones. In the intestine, vitamin D stimulates the absorption of calcium and equivalent amounts of inorganic phosphates. In the kidneys, with its participation, active reabsorption of calcium and inorganic phosphates occurs. Vitamin D regulates the mineralization of cartilage tissue and bone apatites. It is believed that the metabolite plays an important role in the embryogenesis of bone tissue.

Vitamin D is involved in regulating the activity of enzymes of the main bioenergetic cycle of Krebs, enhances the synthesis of citric acid. It is known that citrates are part of bone tissue.

Vitamin D and its active metabolites affect the cells of the immune system, therefore, with vitamin D deficiency in infants, secondary immune deficiency occurs (the activity of phagocytosis, the synthesis of interleukins 1 and 2, and the production of interferon decrease).

Neuroendocrine regulation of phosphorus-calcium metabolism is carried out by secretion of parathyroid hormone. A decrease in the level of ionized calcium associated with vitamin D deficiency serves as a signal for an increase in the level of parathyroid hormone. Under the influence of parathyroid hormone, calcium in bone apatites passes into a soluble form, due to which the level of ionized calcium can be restored. The antagonist of parathyroid hormone is calcitonin. Under its influence, the content of ionized calcium in the blood serum decreases, and bone mineralization processes intensify.

What causes rickets?

Pathogenesis of rickets

The process of rickets formation is complex and depends on many factors, but primarily on the factors regulating the phosphorus-calcium balance. In the complex picture of rickets pathogenesis, cause and effect constantly change places, so it is difficult to determine what is primary and what is secondary in rickets. Conventionally, several stages can be distinguished in the development of the disease.

First stage

Vitamin D deficiency changes the permeability of intestinal cell membranes, which leads to impaired calcium absorption. In response to hypocalcemia, the activity of the parathyroid glands is activated. Parathyroid hormone slows down the reabsorption of phosphates in the kidneys. In addition, with vitamin D deficiency, inorganic phosphorus is not split off from organic compounds contained in food. All this leads to a decrease in phosphorus levels. Hypophosphatemia is one of the first biochemical manifestations of rickets. The calcium level during this period is normal, since parathyroid hormone enhances the formation of 1, 25-dihydroxycholecalciferol and temporarily increases bone resorption, and simultaneously increases the intake of calcium from the intestine.

[ 22 ], [ 23 ], [ 24 ], [ 25 ], [ 26 ], [ 27 ], [ 28 ], [ 29 ]

Second stage

As calcium deficiency in the body increases, not only is calcium absorption in the intestine impaired, but its mobilization from the skeleton also becomes clearly insufficient, which leads to a decrease in the level of calcium and phosphorus in the blood serum. As a result, the synthesis of the organic matrix of bone tissue, bone growth, and mineralization are impaired, osteoporosis (uniform decrease in bone volume and other signs) and osteomalacia (bones soften and bend easily) develop. Growth of defective osteoid tissue may occur due to the accumulation of osteoclasts in different areas, since parathyroid hormone stimulates their formation. The activity of alkaline phosphatase produced by osteoclasts increases.

Rickets is characterized by impaired muscle tone, which contributes to the development of diffuse rachitic muscle hypotonia. In addition, electrolyte imbalance leads to disruption of the relationship between the sympathetic and parasympathetic divisions of the autonomic nervous system and the development of autonomic dysfunction.

Third stage

Hypophosphatemia causes a decrease in the alkaline reserve of the blood and the development of acidosis, which is accompanied by a disorder of the metabolism of proteins, fats and carbohydrates. There is a decrease in the level of citrates in the blood due to their insufficient formation from pyruvic acid in the tricarboxylic acid cycle. With rickets, the metabolism of not only calcium and phosphorus is disrupted, but also other microelements (magnesium, potassium, iron, zinc, etc.), therefore rickets is a disease accompanied by a disorder of not only phosphorus-calcium, but also all other types of metabolism.

Pathogenesis of rickets

Symptoms of Rickets

The first symptoms of rickets appear at the age of 1-2 months, and the full clinical picture is usually observed at the age of 3-6 months. The initial clinical signs of the disease (sweating, loss of appetite, persistent red dermographism, increased excitability) occur due to a violation of the functional state of the autonomic nervous system. Sleep may soon worsen, the child begins to turn his head, and "baldness" of the back of the head appears. It is important to emphasize that the detection of only symptoms of autonomic nervous system disorder is not a basis for establishing a diagnosis of "rickets". To establish a diagnosis, changes in the skeletal system are required: softening along the cranial sutures (craniotabes), pain when pressing on the bones of the skull, pliability of the edges of the large fontanelle, flattening of the back of the head. Due to osteoid tissue hyperplasia in rickets, hypertrophied parietal and frontal tubercles, "rickety beads", thickening of the forearm bone epiphyses ("rickety bracelets") may form. In severe rickets, an overhanging "Olympic forehead" and a sunken bridge of the nose may be observed. The anterior part of the chest together with the sternum protrudes forward, resembling a chicken breast. An arcuate curvature of the lumbar spine appears - pathological kyphosis (rickety hump). The ribs become soft, pliable, the chest is deformed, flattened from the sides, its lower aperture widens. At the site of attachment of the diaphragm, a retraction of the ribs appears - the so-called Harrison groove. Hypotonia of the muscles of the anterior abdominal wall leads to the formation of a characteristic "frog belly". In addition to muscle hypotonia, weakness of the ligamentous apparatus is observed (joint laxity, the “gutta-percha boy” phenomenon).

When the child begins to stand up, an O- or X-shaped curvature of the legs develops (depending on the predominance of the tone of the flexor or extensor muscles).

In patients with rickets, delayed closure of fontanelles and sutures, delayed eruption of teeth, defects in tooth enamel are observed, and the development of early caries is characteristic.

In addition to bone and muscle disorders, this disease may cause functional changes in the respiratory system (due to weakness of the respiratory muscles and deformation of the chest). In some cases, due to pronounced muscle hypotension, a slight expansion of the heart borders is possible. The ECG shows prolongation of the QT, PQ intervals, and, less often, repolarization disorders.

Symptoms of Rickets

Classification of Rickets

In Russia, it is common to use the classification of rickets proposed by S. O. Dulitsky (1947). According to this classification, there are different degrees of rickets severity (mild, moderate, severe), periods of the disease (initial, peak, convalescence, residual effects), as well as the nature of the course (acute, subacute, recurrent). In 1990, E. M. Lukyanova et al. proposed adding three clinical variants of rickets to the classification, taking into account the leading mineral deficiency (calcipenic, phosphoropenic, without deviations in the content of calcium and inorganic phosphorus in the blood serum).

The severity of rickets is assessed taking into account the severity of disorders in the skeletal system, as well as vegetative changes, muscle hypotonia, and changes in other organs. Mild rickets is characterized by changes in the skeletal system against the background of pathological changes in the functional state of the autonomic nervous system. With moderate rickets, changes in the skeletal system are more pronounced, and muscle hypotonia develops. With severe rickets, along with pronounced bone changes and diffuse muscle hypotonia, there is a delay in the development of motor and static functions, as well as dysfunction of many internal organs and systems (lung damage, cardiovascular system, etc.).

Acute rickets is most often observed in children in the first six months of life, born with a weight of more than 4 kg, or in children with a large monthly gain. Subacute rickets is typical for children with intrauterine or postnatal hypotrophy, as well as for premature babies. In subacute rickets, signs of osteoid hyperplasia prevail over signs of osteomalacia, in addition, all symptoms develop more slowly than in acute rickets. Recurrent rickets is characterized by periods of clinical improvement and deterioration.

In the calcipenic variant of rickets in children, the level of total and ionized calcium in the blood is reduced. With the leading role of calcium deficiency, bone deformations with a predominance of osteomalacia processes and increased neuromuscular excitability are expressed. In the phosphoropenic variant of rickets, a decrease in the level of inorganic phosphorus in the blood serum is observed. Bone changes are more pronounced due to osteoid hyperplasia and weakness of the ligamentous apparatus. Rickets with minor deviations in the content of calcium and inorganic phosphorus in the blood is characterized by a subacute course, moderate hyperplasia of osteoid tissue, and the absence of distinct changes in the nervous and muscular systems.

[ 30 ], [ 31 ], [ 32 ]

Diagnosis of rickets

Laboratory criteria for active rickets

• reduction of the content of inorganic phosphates in the blood serum to 0.6-0.8 mmol/l;
• reduction of total calcium concentration in the blood to 2.0 mmol/l;
• decrease in the content of ionized calcium to less than 1.0 mmol/l;
• increase in alkaline phosphatase activity in blood serum by 1.5-2.0 times;
• reduction of 25-hydroxycholecalciferol levels in blood serum to 20 ng/ml and below;
• reduction of the level of 1, 25-dihydroxycholecalciferol in the blood serum to 10-15 pg/ml;
• compensated metabolic hyperchloremic acidosis with base deficit up to 5.0-10.0 mmol/l.

Radiological criteria for rickets

On radiographs, the violation of bone tissue mineralization is manifested by the following signs:

• changes in the clarity of the boundaries between the epiphysis and metaphysis (i.e. in areas of preliminary calcification the boundary becomes uneven, blurred, fringed);
• progressive osteoporosis in areas of maximum bone growth, an increase in the distance between the epiphysis and diaphysis due to increasing metaphyses;
• disruption of the contours and structure of the epiphyses ("saucer-shaped epiphyses"). Radiographic signs change as the disease progresses.

Differential diagnostics of rickets is carried out with other diseases that have similar clinical symptoms: renal tubular acidosis, vitamin D-dependent rickets, phosphate diabetes, Debre-de-Tony-Fanconi disease, hypophosphatasia, cystinosis.

Diagnosis of rickets

[ 33 ], [ 34 ], [ 35 ], [ 36 ], [ 37 ], [ 38 ]

Treatment of rickets

Treatment of rickets should be comprehensive, it is necessary to prescribe therapeutic doses of vitamin D, as well as use therapeutic and health-improving measures. Depending on the severity, therapeutic doses of vitamin D are 2000-5000 IU/day for 30-45 days. At the beginning of treatment, vitamin D is prescribed in a minimum dose - 2000 IU for 3-5 days, if well tolerated, the dose is increased to an individual therapeutic dose. After achieving a therapeutic effect, the therapeutic dose is replaced by a prophylactic dose (400-500 IU/day), which the child receives during the first 2 years of life and in the winter period in the third year of life.

Vitamin D preparations (ergocalciferol or cholecalciferol solutions) have been used for many years to treat and prevent rickets. The forms of many drugs cause certain problems due to the complexity of dosing. Thus, in recent years, an alcohol solution of vitamin D2 has practically not been produced due to the risk of overdose. For the treatment and prevention of rickets, you can use vigantol - an oil solution of vitamin D3 (one drop contains 600 IU) and domestic oil solutions of vitamin D2 (one drop contains 700 IU). However, oil forms of vitamin D are not always well absorbed, therefore, in case of intestinal malabsorption syndrome (celiac disease, exudative enteropathy, etc.), oil solutions of vitamin D are used sparingly. In recent years, an aqueous form of vitamin D3 - aquadetrim, which has a convenient dosage form and a clear dosage, has been widely used for the prevention and treatment of rickets. One drop of cholecalciferol solution (aquadetrim) contains 500 IU of vitamin D3. The advantage of the aqueous solution is rapid absorption from the digestive tract. The solution is well absorbed and does not cause dyspeptic disorders.

If children with rickets have concomitant acute diseases (ARI, pneumonia, etc.), vitamin D should be discontinued for the period of high temperature (2-3 days), and then re-prescribed in a therapeutic dose.

In addition to vitamin D, calcium preparations are prescribed for the treatment of rickets: calcium glycerophosphate (0.05-0.1 g/day), calcium gluconate (0.25-0.75 g/day), etc. To increase calcium absorption in the intestine, a citrate mixture, lemon juice or grapefruit juice are prescribed. To normalize the function of the central and autonomic nervous system, magnesium and potassium aspartate (asparkam, panangin), as well as glycine, are prescribed. If rickets occurs against the background of hypotrophy, a 20% aqueous solution of carnitine (carnitine chloride) can be prescribed at a rate of 50 mg / (kg x day) for 20-30 days. Carnitine chloride helps to normalize metabolic processes, under its influence, physical development indicators improve. In addition, orotic acid (potassium orotate) can be used at a rate of 20 mg / (kg x day). It is known that orotic acid enhances the synthesis of calcium-binding protein in intestinal enterocytes. Of particular importance is the use of antioxidants: tocopherol acetate (vitamin D) in combination with ascorbic acid (vitamin D), glutamic acid, beta-carotene. After 2 weeks from the start of drug therapy, therapeutic exercise and massage are added to the complex of therapeutic measures for all children. After the end of drug treatment, children over six months are prescribed therapeutic baths (salt, pine).

Treatment of rickets

Prevention of rickets

A distinction is made between antenatal and postnatal prophylaxis. It can be non-specific and specific (using vitamin D).

Antenatal prevention of rickets

Antenatal prevention of rickets begins even before the birth of the child. When patronizing pregnant women, the expectant mother's attention is drawn to following a daily routine, spending enough time in the fresh air, and eating a balanced diet. Pregnant women should consume at least 200 g of meat, 100 g of fish, 150 g of cottage cheese, 30 g of cheese, 0.5 l of milk or kefir, fruits, and vegetables daily. In the last 2 months of pregnancy, a woman should receive 500 IU of vitamin D daily, and 1000 IU in the autumn-winter period. Pregnant women from risk groups (nephropathy, chronic extragenital pathology, diabetes mellitus, hypertension) should be prescribed vitamin D in a dose of 1000-1500 IU from the 28th-32nd week of pregnancy.

[ 39 ], [ 40 ], [ 41 ], [ 42 ], [ 43 ], [ 44 ], [ 45 ], [ 46 ], [ 47 ]

Postnatal prevention

The main components of postnatal prevention of rickets in children are: walks in the fresh air, massage, gymnastics, breastfeeding, timely introduction of yolk and other types of complementary feeding. In the absence of breast milk, it is recommended to use modern adapted formulas.

Postnatal specific prevention of rickets is carried out with the help of vitamin D. According to WHO experts, for healthy full-term infants the minimum dose is up to 500 IU/day. In the conditions of central Russia this dose is prescribed in the spring, autumn and winter periods starting from the age of 3 or 4 weeks. With sufficient insolation of the child from June to September, specific prevention using vitamin D is not carried out, however, in case of a cloudy summer, especially in the northern regions, specific prevention of rickets is carried out in the summer months. Preventive administration of vitamin D is carried out during the first and second years of life.

Specific prevention of rickets in premature infants has its own characteristics. Rickets in premature infants is osteopenia associated with calcium and phosphorus deficiency, immaturity of the child, hypoplasia of bone tissue, insufficient mineralization and rapid bone growth in the postnatal period. Children with stage I prematurity are prescribed vitamin D from 10-14 days of life at a dose of 400-1000 IU/day daily during the first 2 years, excluding the summer months. With stage II-III prematurity, vitamin D is prescribed at a dose of 1000-2000 IU/day daily during the first year of life, and in the second year - at a dose of 500-1000 IU/day, excluding the summer months. Higher doses and early administration of vitamin D used in premature infants can be explained by the fact that breast milk does not provide the calcium and phosphorus needs of these children.

Contraindications for prophylactic administration of vitamin D: idiopathic hypercalciuria, organic CNS lesions with craniosynostosis and microcephaly, hypophosphatasia. Relative contraindications: small fontanelle or its early closure. Such children need delayed rickets prophylaxis from 3-4 months of age. In such cases, an alternative may also be the administration of suberythemal doses of UFO (1/2 biodose) 15-20 procedures every other day, at least 2 courses per year during the first 2 years of life.

How to prevent rickets?

Prognosis for rickets

With early diagnosis of rickets and appropriate treatment, the disease proceeds favorably and without consequences. Without treatment, moderate and severe rickets can adversely affect the subsequent development of children. Flattening and deformation of the pelvis, flat feet, myopia occur, and multiple dental lesions (caries) may appear. Infants suffering from rickets are prone to frequent acute respiratory diseases, pneumonia, etc.

Children who have had moderate to severe rickets should be under dispensary observation (quarterly examination) for 3 years. Specific prophylaxis is carried out during the second year of life in the autumn, winter and spring periods, and in the third year of life - only in winter.

In case of rickets, vaccination is not contraindicated. The planned preventive vaccination can be done 2 weeks after the prescription of vitamin D.

References

Korovina NA et al. Prevention and treatment of rickets in children (lecture for doctors) / NA Korovina, AV Cheburkin, I.N. Zakharova. - M., 1998. - 28 p.

Novikov P.V. Rickets and hereditary rickets-like diseases in children. - M., 2006. - 336 p.

Novikov P.V., Kazi-Akhmetov E.A., Safonov A.V. New (water-soluble) form of vitamin D for the treatment of children with vitamin D-deficiency and hereditary D-resistant rickets // Russian Bulletin of Perinatology and Pediatrics. - 1997. - No. 6. - P. 56-59.

Prevention and treatment of rickets in young children: Methodological recommendations / Edited by E.M. Lukyanova et al. - M.: M3 USSR, 1990. - 34 p.

Strukov V.I. Rickets in premature infants (lecture for doctors). - Penza, 1990. - P. 29.

Fox A.T., Du Toil G., Lang A., Lack G. Food allergy as a risk factor for nutritional rickets // Pediatr Allergy Immunol. - 2004. - Vol. 15 (6). - P. 566-569.

PettiforJ.M. Nutritional Rickets: deficiency of vitamin D, calcium or both?// Am. J. Clin. Nutr. - 2004. - Vol. 80 (6 Suppl.). - P.I725SH729S.

Robinson PD, Hogler W, Craig ME et al. The reemerging burden of rickets: A decade of experience from Sidney // Arch. Dis. Child. - 2005. - Vol. 90 (6). - P. 1203-1204.

Zaprudnov A.M., Grigoriev K.I. Rickets in children. - M., 1997. - 58 p.

[ 48 ], [ 49 ], [ 50 ], [ 51 ]