Rickets: small residents of large cities are at risk. A modern view on the pathogenesis and prevention of rickets in children An individual approach to prescribing vitamin D preparations

This information intended for healthcare and pharmaceutical professionals. Patients should not use this information as medical advice or recommendations.

Modern approaches to the prevention and treatment of rickets in children

Rickets is widespread in children in the first two years of life. This disease has been known for a very long time, the first mention of rickets is found in the writings of Soranus of Ephesus (98-138 AD) and Galen (131-211 AD). A complete clinical and pathological description of rickets was made by the English orthopedist F. Glisson in 1650. For some time, rickets was called the “English disease”, since its prevalence was high in England. The English name rickets comes from the Old English wrickken, which means “to bend,” and Glisson changed it to the Greek rhachitis (spine), since in rickets it is significantly deformed. At the beginning of the twentieth century, our compatriot I. Shabad discovered that cod fish oil is quite effective in the prevention and treatment of rickets, and the American researcher Mellanby in 1920 found that it is active active principle Fish oil is a fat-soluble vitamin. Vitamin D was discovered and obtained by McCollum in 1922, after which it became possible to study its specific effect on bones, muscles, intestines and renal tubules.

Rickets occurs in all countries, but especially often among those northern peoples who live in conditions of lack of sunlight. Children born in autumn and winter suffer from rickets more often and more severely. At the beginning of the twentieth century, rickets occurred in approximately 50-80% of children in Austria and England. In the first half of the twentieth century in Russia, rickets was detected in 46-68% of children in the first two years of life. In Bulgaria, where there are many sunny days throughout the year, the prevalence of rickets among children under one year of age is about 20%. In Russia, the incidence of rickets in recent years among children early age ranges from 54 to 66%. Currently, the incidence of rickets among infants in the city of Moscow, according to the reports of district pediatricians, does not exceed 30%. However, this indicator is underestimated at least twice, since the diagnosis of rickets is registered in the case of moderate forms, and its mild forms are not statistically taken into account.

Back in 1891, N. F. Filatov emphasized that rickets is a general disease of the body, manifested mainly by a peculiar change in the bones. In recent decades, rickets has been considered as a disease caused by a temporary discrepancy between the needs of a growing organism for calcium and phosphorus and the insufficiency of systems that ensure their delivery to the child's body. And although rickets can be classified as a metabolic disease with predominant violation phosphorus-calcium metabolism, it is characterized by disturbances in protein metabolism, activation of lipid peroxidation processes, metabolism of microelements (magnesium, copper, iron, etc.), multivitamin deficiency.

Infant rickets is not only a pediatric, but also a medical and social problem, as it has serious consequences that lead to a high morbidity rate in children. Immunity dysfunctions detected during rickets in the form of decreased synthesis of interleukins I and II, phagocytosis, interferon production, as well as muscle hypotension predispose to frequent respiratory diseases. Osteoporosis, osteomalacia, osteopenia, observed with rickets, contribute to the formation of postural disorders, multiple dental caries, and anemia. Due to a decrease in the absorption of calcium, phosphorus, and magnesium, the consequences of rickets are often autonomic dysfunction and impaired motor skills gastrointestinal tract in the form of simple constipation, dyskinesia of the biliary tract and duodenum. Rickets suffered at an early age can have an adverse effect on the further growth and development of children, and its consequences can persist throughout the child’s life.

The most significant factors determining the development of rickets are:

• insufficient formation of cholecalciferol in the skin;
• violation of phosphorus-calcium metabolism in the liver, kidneys, intestines;
• insufficient intake of vitamin D from food.

The main link in the pathogenesis of D-deficiency rickets should be considered endogenous or exogenous deficiency of vitamin D and its metabolites with a subsequent decrease in calcium intake from the intestine. However, vitamin D metabolites affect the functions of not only enterocytes, but also cells of other organs, which expands our understanding of the biological significance of vitamin D and the consequences of disorders of its metabolism. The amount of vitamin D produced in the skin depends on the condition of the child’s skin and the dose of ultraviolet radiation. Vitamin D deficiency due to insufficient insolation among residents of the North is apparently not fully compensated by the intake of the vitamin from traditional food, which is evolutionarily and genetically fixed in the form of structural features of the skeleton (short stature, curvature of the limbs). On the other hand, high levels of sun exposure can lead to the formation of toxic levels of vitamin D. Therefore, in order to achieve optimal effects of vitamin D on the body, there are adaptation mechanisms that broadly correspond to the cascade mechanisms of other biological systems. However, the vitamin D regulatory system is more susceptible to dysfunction as a result of exposure to environmental factors (atmospheric, nutritional, social). All these features, including genetic polymorphisms in the structure and function of receptors for vitamin D metabolites, as well as different conditions interactions with other regulatory systems mineral metabolism create the prerequisites for selecting individual doses of vitamin D preparations in the treatment of rickets.

The incidence of rickets is higher in the autumn and winter seasons. Rickets is especially common among children living in regions with insufficient insolation, cloudiness, frequent fogs and unfavorable environmental conditions (smoke). atmospheric air). Most often, rickets develops in children born either to young mothers or to women over 35 years of age. Of great importance for the formation of phosphorus-calcium metabolism disorders in young children is an unbalanced diet of a pregnant woman in terms of basic food nutrients (deficiency of protein, calcium, phosphorus, vitamins D, B1, B2, B6). Rickets most often affects children whose mothers did not get enough exposure to the sun during pregnancy, did not move much, or had extragenital diseases.

In recent years, the role of perinatal risk factors for the development of rickets has increased. Among the children we examined with mild and moderate forms of rickets, 27% were born from the 3rd–5th pregnancy. Rapid, induced or operative labor was observed in 73% of mothers. In 63% of women, a combination of the pathological course of pregnancy and childbirth was observed. At the time of birth, 8% of mothers were 17-18 years old. Rickets was diagnosed in 10% of children born prematurely at a gestational age of 32-34 weeks with an average weight of 2323 g (minimum 1880, maximum 3110). At the time of the study, only 7.9% of children were breastfed, and 23.8% of children who were bottle-fed and had Clinical signs rickets, received diluted and undiluted cow's milk, kefir, and unadapted milk formulas. Among full-term patients, 46% of children had excess weight (an average of 13.4%), and 6.9% of patients had an excess weight (an average of 12.6%). It should be noted that all children with rickets and malnutrition had signs perinatal encephalopathy. Among children with rickets, 79.3% suffered from repeated bronchopulmonary diseases, 27% from urinary tract infections, 15.9% from atopic dermatitis, 7,9% - iron deficiency anemia, 6.3% - malnutrition. Convulsive syndrome was detected in 6.3%.

It should be noted that under equal conditions of nutrition, care and prevention, it is possible to state different in severity variants of the course of rickets - from minimal to severe. It is possible to establish the predisposition of children to disorders of phosphorus-calcium metabolism only on the basis of an analysis of numerous individual predisposing factors.

Prevention of rickets is divided into antenatal and postnatal, nonspecific and specific.

Antenatal prevention of rickets

It is necessary to observe the daily routine of a pregnant woman, including a sufficiently long sleep day and night. Outdoor walks are recommended for at least 2-4 hours daily, in any weather. It is extremely important to organize a balanced diet for a pregnant woman (daily consume at least 180 g of meat, 100 g of fish - 3 times a week, 100-150 g of cottage cheese, 30-50 g of cheese, 300 g of bread, 500 g of vegetables, 0.5 l of milk or fermented milk products). Instead of milk, you can use special milk drinks intended for pregnant and lactating women (“Dumil Mama Plus”) and capable of preventing disturbances in phosphorus-calcium metabolism in the fetus and mother during pregnancy and lactation. "Dumil Mama Plus" contains high-quality whey proteins with high nutritional value, carbohydrates that stimulate the growth of normal intestinal microflora, as well as the absorption of calcium and magnesium in the intestine. In the absence of these special milk drinks, it is possible to recommend taking multivitamin preparations throughout the entire period of lactation. Regular appointment multivitamin preparations can prevent disturbances in phosphorus-calcium metabolism in the body of a pregnant woman and thereby provide the developing fetus with calcium, phosphorus, and vitamin D.

Pregnant women at risk (nephropathy, diabetes, hypertension, rheumatism, etc.) starting from the 28–32nd week of pregnancy, it is necessary to additionally prescribe vitamin D in a dose of 500-1000 IU for 8 weeks, regardless of the time of year. Instead of vitamin D preparations, in the winter and spring periods of the year, and especially in the northern regions, ultraviolet irradiation can be used, which promotes the endogenous synthesis of cholecalciferol. It is necessary to start irradiation with 1/4 biodose, gradually increasing it to 2 biodoses. The minimum distance is 1 meter. Course - 20-30 sessions daily or every other day.

Postnatal prevention of rickets

It is necessary to comply with the conditions for proper feeding of the child. Breast milk is the best for a baby in the first year of life, provided the nursing woman is properly fed. A woman’s daily diet during lactation should be varied and include required amount protein, including animal origin; fat enriched with polyunsaturated fatty acids, carbohydrates that provide the body with energy, as well as vitamins and microelements.

When artificially feeding a child, it is necessary to select a milk formula that is as close as possible to human milk, containing 100% lactose, which enhances the absorption of calcium, cholecalciferol and has a calcium to phosphorus ratio of 2. In infant formula, a calcium to phosphorus ratio of 1.2-2 is allowed, but in breast milk it is 2.0.

Therapeutic exercise and massage should be carried out systematically, regularly, for a long time, with a gradual and uniform increase in load.

Postnatal specific prevention of rickets is carried out with vitamin D, the minimum prophylactic dose of which for healthy full-term infants is 400-500 IU per day. This dose is prescribed starting from the 4-5th week of life in the autumn-winter-spring period, taking into account the child’s living conditions and risk factors for the development of the disease. In the summer, with insufficient insolation (cloudy, rainy summer), especially in the northern regions of Russia, when feeding with unadapted milk formulas, it is advisable to prescribe a prophylactic dose of vitamin D. Specific prevention of rickets in full-term children is carried out in the autumn-winter-spring period in the first and second year life. Children at risk for rickets in the autumn-winter-spring period during the first two years of life should receive vitamin D daily in a dose of 1000 IU.

Premature babies with stage I prematurity are prescribed vitamin D from the 10th to 14th day of life, 400-1000 IU daily for 2 years, excluding summer. According to the methodological recommendations of the USSR Ministry of Health in 1990, in case of stage II prematurity, vitamin D is prescribed in a dose of 1000-2000 IU daily for a year, excluding the summer period; in the second year of life, the dose of vitamin D is reduced to 400-1000 IU. However, this dose of vitamin D may be excessive. Therefore, it is necessary to focus on the child’s health status after weight restoration.

Equivalents:
1 IU = 0.025 mcg cholecalciferol;
1 mcg cholecalciferol = 40 IU vitamin D3.

Contraindications to prescribing a prophylactic dose of vitamin D:

• idiopathic calciuria (Williams-Bourne disease);
• hypophosphatasia;
• organic damage to the central nervous system with symptoms of microcephaly and craniostenosis.

Children with small fontanel sizes have only relative contraindications to the administration of vitamin D. Specific prevention of rickets in them is carried out starting from 3-4 months under the control of the size of the large fontanel and head circumference.

Therapeutic measures for rickets include restoration of phosphorus-calcium metabolism, normalization of lipid peroxidation processes, elimination of metabolic acidosis, hypokalemia, and elimination of vitamin D deficiency.

Treatment for rickets usually includes:

• organization correct mode child's day. Children should be in the fresh air for at least 2-3 hours every day, and the room where the child is located should be regularly ventilated;
• proper nutrition of the child, adapted according to his age;
• hygienic baths and rubdowns, douches, massage, physical therapy (after the activity of rickets subsides);
• drug therapy.

Treatment of rickets involves the administration of vitamin D preparations. Depending on the severity of rickets, it is recommended to use from 2000 to 5000 IU of vitamin D per day for 30-45 days. Next, the dose of vitamin D is reduced to a preventive dose (500 IU) daily for 2 years (except for the summer months) and in the third year of life in winter. Most often, we recommend starting treatment with a dose of 2000 IU for 3-5 days, with a gradual increase if the drug is well tolerated to individual treatment dose(from 3 to 5 thousand IU). A dose of 5000 IU is prescribed for severe bone changes. Children at risk 3 months after the end of the first course can be given anti-relapse treatment with vitamin D3 at a dose of 2000-5000 IU for 3-4 weeks.

The daily requirement for vitamin D depends on:

• child's age;
• genetic characteristics;
• the nature of the child's feeding;
• features of child care;
• time of year;
• severity of phosphorus-calcium metabolism disorder;
• children's health status;
• the nature of the concomitant pathology;
• climatic conditions of the area where the child lives.

The oil forms of vitamin D that exist so far are not always well absorbed.

The causes of impaired absorption of vitamin D oil solution are:

• syndrome of impaired absorption in the small intestine (celiac disease, food allergy, exudative enteropathy, etc.);
• chronic pancreatitis;
• cystic fibrosis;
• dysembryogenesis of enterocytes;
• chronic enterocolitis;
• nonspecific ulcerative colitis, Crohn's disease.

In recent years, the aqueous form of vitamin D3 - aquadetrim (Terpol, Poland) - has been widely used for the prevention and treatment of rickets.

The benefits of vitamin D3 aqueous solution are:

• rapid absorption from the gastrointestinal tract;
• optimal dose selection - one drop contains 500 IU;
• rapid onset of clinical effect;
• high efficiency for rickets and rickets-like diseases, as well as for pathologies of the gastrointestinal tract.

Employees of the Research Institute of Pediatrics and Pediatric Surgery of the Ministry of Health of the Russian Federation have shown the high therapeutic effectiveness of the water-soluble form of vitamin D3 in all patients with acute and subacute rickets in a daily dose of about 5000 IU. The drug also proved effective in treating children with vitamin D-resistant rickets at a daily dose of 30,000 IU. Aquadetrim is well tolerated; no side effects or adverse events have been identified during its use.

Currently, an alcohol solution of vitamin D2 should not be used due to the high dose (about 4000 IU in 1 drop) and the possibility of overdose due to the evaporation of alcohol and an increase in the concentration of the solution.

Thus, the selection of doses of vitamin D is carried out in accordance with the characteristics of the clinical picture of rickets and the dynamics of the disease. Doses and duration of therapy for rickets are very different, their selection depends on many factors, including the individual characteristics of the organism.

Detection in a child, especially with aggravated heredity for urolithiasis, tubulointerstitial nephritis against the background of metabolic disorders, during treatment with vitamin D, a decrease in the anti-crystal-forming ability of urine, a positive Sulkovich test, oxalate and (or) phosphate, calcium crystalluria serves as the basis for adjusting the dose of vitamin D.

Along with vitamin D, calcium preparations are prescribed for rickets, especially for children who are bottle-fed, born prematurely, underweight, with signs of morphofunctional immaturity.

The smallest amount of calcium is found in calcium gluconate. The traditional use of eggshell powder (calcide) along with lemon juice or a citrate mixture solution, which improves the absorption of calcium salts in the intestines, remains traditional.

The calcium requirement for a healthy baby during the first 6-12 months is 500-600 mg.

Our experience shows that in children with severe rickets and hypocalcemia, it is advisable to perform calcium electrophoresis on the chest and legs.

Calcium preparations are prescribed orally in the first and second half of life for 3 weeks in age-appropriate doses.

Of particular importance is the use of antioxidants in acute period rickets and during intercurrent illnesses. The most justified is the use of tocopherol or its combination with vitamin C, beta-carotene and (or) glutamic acid. To reduce autonomic disorders and muscle hypotension, carnitine, panangin, asparkam, and glycine are prescribed for 3-4 weeks.

In order to correct violations of physical development in the second year of life, children with rickets can be prescribed Acti-5, which is a syrup containing lysine, a complex of phosphoric acid and organic calcium salts necessary for the formation of the bone skeleton and muscle development. In children from 2.5 to 6 years old, Akti-5 is prescribed 1 teaspoon 2-3 times a day, over 6 years old - 2 teaspoons 2-3 times a day. When taking the drug in children with functional disorders of the gastrointestinal tract, abdominal pain and loose stools can rarely occur.

At severe course rickets, potassium orotate, carnitine hydrochloride (el-car, carnitene), ATP are used to restore metabolic processes.

Restorative therapy includes massage and exercise therapy, which are prescribed 2 weeks after the start of drug therapy, balneotherapy (pine, salt baths for a course of treatment of 10-15 baths). Balneotherapy is carried out 2-3 times a year. The volume of drug therapy should be determined not only by the severity of rickets, but also by the age of the patients. To exclude polypharmacy, it may be recommended medicinal products, assigned in a certain sequence.

Clinical laboratory, ultrasound and densitometric studies indicate the need for long-term observation (at least 3 years) of children who have suffered rickets. They are subject to quarterly inspection. X-rays of bones are performed only when indicated.

Rickets is not a contraindication for preventive vaccinations. After 3-4 weeks from the start of therapy, vaccination is possible.

Statistics on the incidence of rickets in children

Rickets is not common in all countries of the world. In African countries, this disease is very rare. It is practically unknown in China and Japan. In countries where fishing is developed, rickets is also extremely rare (due to the content of fish oil). These are countries such as Greenland, Denmark, Norway, Iceland. The abundance of sunlight also does not create conditions for the spread of rickets. Therefore, this disease is unknown in Turkey and Greece. Statistics also show that the incidence of rickets in rural areas is much lower than in cities.

Rickets is especially common among northern peoples who live in conditions of lack of sunlight. According to W. Osler (1928), at the beginning of the 20th century, rickets occurred in approximately 50-80% of children in Austria and England. In Bulgaria, where there are many sunny days a year, the prevalence of rickets among children under one year old is about 20%. Up to 70% of children in Russia also had rickets in these years. According to A.I. Ryvkina (1985), rickets in children of the first year of life occurs in up to 56.5%, according to SV. Maltsev (1987), its prevalence reaches 80%.

On the territory of Russia, rickets of mild and moderate severity are diagnosed mainly. So, in infants in St. Petersburg, approximately 10-15%, in Moscow, in 30%, in Krasnoyarsk, in 54.8% of the examined. According to statistical analysis Ministry of Health and Social Development of the Russian Federation, the incidence rate of children with rickets in Russia in recent years exceeds 50%.

According to the statistical analysis of the Ministry of Health and Social Development, the incidence rate of children with rickets for 2012, 2013, 2014 in the city of Achinsk is 33%.

Analysis of medical documentation (form No. 112) on cases of rickets in health care facilities of the city of Achinsk for 2011-2013

A set of child development stories was carried out on the basis of the children's city hospital in Achinsk. The present study included 300 stories of child development (form No. 112) aged from birth to one year for 2011, 2012, 2013 (100 stories of child development for each year). We identified patients with a history of symptoms of rickets and compared them with a number of healthy children. Symptoms mentioned referred to the manifestation of rickets, if they were absent from the child from birth, appeared at the age of 2 - 4 months against the background of active growth and preceded or were combined with characteristic bone changes. An additional criterion that made it possible to classify symptoms of autonomic dysfunction as manifestations of rickets in infants was a decrease in their severity or disappearance when the child was given additional vitamin D.

The incidence of the disease for 2011-2013 is shown in Table 4.

Table 4

Prevalence of the disease

From the data presented, we see that the incidence of the disease for 2012, 2013 and 2014 is approximately the same and amounts to 42%. Of the 300 analyzed histories of the development of a child with symptoms of rickets over three years, 127 children were identified.

In a further study, we used the history of the development of a child with manifestations of the disease. After analyzing them, we identified the clinical symptoms of the disease. The most common of them were: changes in the child's behavior (anxiety, irritability, "anxious" sleep), increased sweating with sour smell, baldness of the back of the head, delay in the psychomotor and physical development of the child, muscle hypotonia, costal “rosary”, “bracelets” on the wrists, “strings of pearls” on the fingers.

Table 5 shows the frequency of clinical symptoms in children.

Table 5

Frequency of clinical symptoms of rickets in children

We derived the average number of symptoms of the disease for each system. From Figure 1 it is clear that in sick children, symptoms of damage to the muscular and skeletal systems predominate.

Picture 1

Frequency of clinical symptoms in children

We distributed children with manifestations of rickets depending on the stage and severity of the disease. From Figure 2 it can be seen that initial manifestations were recorded in 50 children, the peak period in 65, and convalescence in 12 children.

Mild severity was recorded in 50 children, moderate in 55, severe in 10 children.

Acute course in 55, subacute in 60 children.

Figure 2

Distribution of children depending on the stage and severity of the disease

We also found that the initial manifestations occurred at the age of 2 - 3 months, the peak period at the age of 6 months, and convalescence at the age of 1 year. The data is presented in Table 6.

Table 6

Distribution of children depending on age and stage of disease

", March 2012, p. 34-40

I.N. Zakharova, N.A. Korovina, Yu.A. Dmitrieva, GBOU DPO "Russian medical Academy Postgraduate Education" Ministry of Health and Social Development of the Russian Federation

The problem of rickets today receives rather modest attention. Majority scientific research regarding metabolic features bone tissue and mineral metabolism, is devoted mainly to the problem of osteoporosis. Some pediatricians continue to regard rickets as a physiological condition that does not require correction.

However, for a number of reasons we cannot agree with this view. Infantile rickets is not only a pediatric, but also a medical and social problem, as it has serious consequences that cause a high incidence of children in older age. Early childhood rickets and the associated impairment of peak bone mass accumulation may predispose to the development of osteoporosis later in life. Osteopenia and osteomalacia, observed in rickets, contribute to the formation of posture disorders, multiple dental caries. The consequences of impaired absorption of calcium, phosphorus, magnesium may be muscle hypotonia, autonomic dysfunction, gastrointestinal motility disorders. Immune dysfunctions detected in rickets in the form of a decrease in the level of interleukins, interferon, and phagocytosis indicators predispose to frequent infectious diseases, disrupting the social adaptation of the child.

According to the statistical analysis of the Ministry of Health and Social Development of the Russian Federation, the incidence rate of children with rickets in Russia over the past 5 years has exceeded 50%. High frequency diseases, despite active prevention, requires a revision of existing views on the etiology and pathogenesis of rickets, methods of its prevention and therapy.

Etiology

Main etiological factor the development of rickets in children is considered vitamin D deficiency in organism. It is known that vitamin D enters the human body in two ways: with food and as a result of synthesis in the skin under the influence of ultraviolet rays. The richest sources of vitamin D are cod liver, tuna, fish oil, to a lesser extent - butter, egg yolk, milk. Herbal products contain its analogue - ergocalciferol (vitamin D2). Vitamin D absorption occurs mainly in the duodenum and jejunum in the presence of bile acids.

Photosynthesis of vitamin D in the skin is carried out by converting 7-dehydrocholesterol (provitamin D3) into cholecalciferol (vitamin D3) under the influence of solar radiation and skin temperature. The rate of photosynthesis of cholecalciferol in the skin is about 15-18 IU / cm2 / h, which allows most people to fully satisfy the need for it due to endogenous synthesis in the skin with adequate insolation. However, it should be borne in mind that the efficiency of vitamin D synthesis in human skin is significantly affected by climatic conditions, geographic latitude of the area, the level of air pollution, as well as the degree of skin pigmentation. In particular, it has been shown that in the zone near 55° north latitude, where Moscow, Nizhny Novgorod, Kazan and a number of other cities of Russia are located, solar radiation is able to ensure the formation of an adequate amount of vitamin D in the skin only during 4 months of the year (from mid-April until mid-August). Thus, under certain conditions important role in the prevention of hypovitaminosis D, cholecalciferol, obtained from food or as part of vitamin preparations, plays.

Pathogenesis

Formed in the skin and received from the intestine, cholecalciferol binds to a specific vitamin D-binding protein that transports it to places of further metabolism. Part of vitamin D is transported to adipose and muscle tissues, where it is fixed, representing a reserve form. Its main amount is transferred to the liver, where the first stage of transformation occurs - hydroxylation with the formation of calcidiol - 25(OH)D3, which is the main transport form of vitamin D and a marker characterizing the supply of the body with it. Synthesis of 25(OH)D3 depends only on the amount of the initial substrate, i.e. vitamin D, supplied with food or formed in the skin. Formed in the liver, 25-hydroxycholecalciferol is transported via a D-binding protein to the kidneys, where the second stage of its transformation occurs in the proximal convoluted tubules, leading to the formation of the hormonally active form of vitamin D - calcitriol (1,25(OH)2D3) or an alternative metabolite 24 .25(OH)2D3. Under conditions of calcium and phosphorus deficiency in the body, the metabolism of 25(OH)D3 follows the path of formation of 1,25(OH)2D3, the main effect of which is to increase the serum concentration of calcium by enhancing its absorption from the intestine and reabsorption in the kidneys, as well as through resorption calcium from bones. The process of formation of calcitriol is catalyzed by the enzyme alpha-1-hydroxylase, which is present in the mitochondria of renal tubular cells. At normal or elevated concentrations of calcium and phosphorus in the blood serum, the activity of the 24-hydroxylase enzyme increases, under the action of which an alternative metabolite 25(OH)D3 - 24.25(OH)2D3 is formed, which ensures the fixation of calcium and phosphorus in bone tissue.

In conditions of vitamin D deficiency, the synthesis of calcitriol decreases, resulting in a decrease in calcium absorption in the intestine. The resulting hypocalcemia activates the synthesis of parathyroid hormone. Under conditions of secondary hyperparathyroidism, bone resorption increases to maintain normocalcemia, and renal calcium reabsorption and phosphate excretion also increase (Fig.). The increase in calcium absorption in the intestine is temporary, since this process is carried out through the activation of 1,25(OH)2D3 synthesis in the kidneys by parathyroid hormone, however, under conditions of deficiency of the original substrate (25(OH)D3), the process of calcitriol formation will also be disrupted.

Pathogenesis of vitamin D deficiency rickets

Deficiency of calcium, phosphates and increased bone tissue resorption in conditions of secondary hyperparathyroidism are the key pathogenetic moments in the formation of bone changes typical of rickets. In the distal parts of the growth zones during rickets, significant changes are observed, expressed in the inability of the newly formed osteoid to adequately mineralize. Proliferation and hypertrophy of cartilage cells leads to the proliferation of metaphyseal plates, which manifests itself in the form of deformations of the skull bones typical for rickets, the appearance of “rickets rosaries”. Thus, under conditions of hypovitaminosis D in the structure of bone metabolism, there is a predominance of resorption processes over new formation of bone tissue, leading to the deposition of osteoid in the absence of its adequate mineralization. With continued deficiency of vitamin D, the bones of the skeleton lose their strength and undergo deformation due to muscle contraction and the weight of one’s own body.

Clinical manifestations of vitamin D deficiency rickets are usually combined with characteristic biochemical changes in the form of hypocalcemia, hypophosphatemia, increased alkaline phosphatase activity, as well as a pronounced decrease in the level of 25(OH)D3 up to its complete absence in blood .

Considering the role of hypovitaminosis D in the pathogenesis of rickets, it is recommended that young children undergo specific prevention diseases with vitamin D preparations at a dose of 500 IU daily during the autumn-winter-spring period. At the same time, despite the prevention carried out almost everywhere, the frequency of rickets in Russia remains high. Along with this, recently there is evidence that the symptoms of rickets in young children do not always correlate with the level of vitamin D in the body, and in some cases the disease develops even with normal levels of 25(OH)D3 in the blood serum. This requires an active search for additional factors involved in the development of the rachitic process in order to optimize the prevention and treatment of the disease in children.

The high intensity of osteogenesis processes at an early age puts the child’s bone tissue in a critical position in relation to any adverse effects of the external environment and, first of all, to the deficiency of various macro and micronutrients in the diet. Currently, in the pathogenesis of rickets, a large role is given to calcium deficiency. The results of modern research suggest that when there is a calcium deficiency in a child’s diet, the need for vitamin D increases significantly, which predisposes children with the development of the disease. normal level 25(OH)D3. The pathogenesis of rickets with calcium deficiency in the diet may be based on the acceleration of the metabolism of 25-hydroxycholecalciferol in order to increase the level of 1,25(OH)2D3. In this situation, the need for vitamin D sharply increases, and, in the absence of additional intake of cholecalciferol into the body, the content of 25(OH)D3 decreases to a level corresponding to hypovitaminosis. Thus, a violation of bone mineralization in a growing body can occur both in the case of vitamin D deficiency with adequate calcium intake, and in case of calcium deficiency in conditions of sufficient supply of cholecalciferol to the body.

A significant role in the occurrence of rickets belongs to deficiency or imbalance of the protein component of nutrition. There is evidence that qualitative and quantitative protein deficiency, deficiency of essential amino acids and hypovitaminosis D lead to unidirectional changes in the metabolism of calcium and phosphorus, as well as in the structure of bone tissue. Against the background of these conditions, there is a decrease in the content of vitamin D-dependent calcium-binding protein in the mucosa of the small intestine, a decrease in the rate of absorption of macro- and microelements in digestive tract and mineralization of bone tissue.

Disorders of phosphorus-calcium metabolism can also occur in conditions changes lipid composition diet, affecting the secretion of bile, which plays an important role in the absorption of calcium, phosphorus and vitamin D. Moreover, some fatty acid are capable of forming insoluble salts with calcium and excreting them in feces, which can also lead to hypocalcemia and disruption of mineralization processes with excess fat consumption.

Inferiority of carbohydrate composition of food also significantly affects phosphorus-calcium metabolism and the chemical structure of the skeleton. The works of domestic researchers previously indicated that rickets occurs more easily and is more severe in children who receive an excessive amount of monotonous, carbohydrate-rich foods. This is due to the fact that phytic acid contained in cereals forms insoluble salts with calcium, which disrupts the process of absorption of the mineral.

In addition to hypovitaminosis D, a major role in the disruption of bone metabolism plays deficiency of a number of vitamins and microelements, in particular ascorbic acid, retinol, B vitamins, magnesium, manganese, zinc, silicon. These micronutrients take an active part in the mechanisms of bone remodeling, bone matrix formation, influence the activity of parathyroid hormone synthesis, and determine the structure of nuclear receptors for calcitriol.

Risk factors

Most domestic researchers indicate the existence of certain risk factors, the presence of which may predispose to the development of the rachitic process. A significant component in the pathogenesis of the disease is the unfavorable socio-economic living conditions of the mother, insufficient exposure of the pregnant woman and child to the fresh air, and deterioration of environmental conditions in large cities. An important role in the development of rickets is played by frequent infectious diseases, contributing to the emergence of nutritional deficiencies against the background of decreased appetite and increased endogenous costs. In addition, the occurrence of metabolic acidosis against the background of the disease increases the solubility of phosphorus-calcium salts and prevents normal mineralization of bone tissue.

Unfavorable course of pregnancy in the mother, delay prenatal development fetus, prematurity, morphofunctional immaturity can cause a slowdown in the maturation of enzymatic systems, which will ultimately lead to disruption of phosphorus-calcium metabolism, vitamin D metabolism and the development of clinical rickets even in conditions of adequate specific prevention. Pathology of the organs involved in the metabolism of cholecalciferol in the baby’s body (biliary tract, liver, kidneys, intestines, skin) can contribute to the development of rickets. It is known that the predisposition to rickets is higher in infants who have high rates of growth and weight gain in the first months of life. In such a situation, a high need for calcium can only be met with an adequate level of calcitriol in the serum, the increased formation of which requires acceleration of the metabolism of the original substrate - 25(OH)D3, which, in turn, leads to rapid depletion of the metabolite in tissue depots and blood serum . These risk factors can contribute to the development of endogenous hypovitaminosis D even with sufficient intake of cholecalciferol in the child’s body.

It should be noted that in modern conditions certain features of maternal and infant history can be identified in most children, but rickets does not develop in all cases. In this regard, it is of particular interest to identify the most significant risk factors for the development of rickets at the present time with the aim of their timely identification and correction during preventive and therapeutic measures. In the course of analyzing the anamnestic data of 117 children with rickets and 62 healthy infants, we found that among the described factors, the most significant at the present stage are accelerated rates of weight gain and growth in the first year of life, and also accompanying illnesses on the part of the organs involved in the metabolism of vitamin D. These factors were identified in more than 50% of children with rickets, and were detected significantly more often in them (p<0,05) по сравнению со здоровыми младенцами.

Thus, at present, the attitude towards rickets as a disease caused exclusively or predominantly by exogenous vitamin D deficiency cannot be considered correct. Rickets is a multifactorial disease, in the pathogenesis of which the significance of vitamin D deficiency should be considered not so much from the position of its insufficient intake into the child’s body, but rather taking into account the characteristics of its metabolism under the influence of a combination of exo- and endogenous factors that contribute to the development of disorders of various types of metabolism and pathological changes in many organs and systems.

Prevention

Taking into account modern ideas about the mechanisms of regulation of phosphorus-calcium metabolism and the pathogenesis of rickets, prevention of the disease should include:

• ensuring sufficient intake of vitamin D in the body;
• creating conditions for its adequate metabolism.

The main reserves of calcium and vitamin D in the fetal body are formed in the last trimester of pregnancy. It is during this period that the transplacental transport of cholecalciferol and 25(OH)D3 becomes most active, and the rate of calcium deposition in the child’s body is about 130 mg per day. There is no doubt that adequate formation of endogenous reserves of vitamins and minerals by the time the baby is born can only occur if there is sufficient supply of them into the body of the expectant mother. Accordingly, an extremely important task of preventing rickets in a child is organization of rational nutrition and regimen of the expectant mother.

The need to sufficiently provide a pregnant woman with vitamin D is determined by the fact that the fetus is completely dependent on the amount of cholecalciferol and 25(OH)D3 coming from the mother. Moreover, only in conditions of a sufficient amount of 25-hydroxycholecalciferol can calcitriol be synthesized by the placenta and fetal kidneys to meet the needs of the growing organism. Studies have shown that there is a clear relationship between the level of 25-hydroxycholecalciferol in the mother’s body and in the umbilical cord blood. Based on the results of numerous observations, it is justified to recommend that pregnant women take multivitamin preparations, containing in their composition 400–500 IU vitamin D, especially in the third trimester of pregnancy, when the transport of cholecalciferol into the fetus is most active. Women from risk groups - with insufficient insolation, the presence of somatic pathology (nephropathy, diabetes mellitus) - may be recommended to take additional vitamin D in a daily dose 1000 IU. It should be noted that the correlation between the level of 25(OH)D3 in the mother and child is observed only during the first 8 weeks of the infant’s life. Subsequently, endogenous reserves do not satisfy the child’s need for vitamin D, which determines the need for its additional administration.

Postnatal prevention of rickets can be divided into nonspecific and specific. Nonspecific prevention includes the correct formation of a child’s daily routine, sufficient exposure to fresh air, daily massage and gymnastics, and wide swaddling to ensure sufficient physical activity. It is necessary to carry out adequate correction of functional disorders of the gastrointestinal tract, treatment of malabsorption syndrome, pathology of the biliary tract and kidneys.

Specific prevention of rickets is to adequately provide the child with vitamin D. The main sources of cholecalciferol in the postnatal period for breastfed children are breast milk and solar radiation. As mentioned above, the majority of Russian residents may experience a deficiency of solar radiation due to the peculiarities of their geographical location. In addition, exposure to direct sunlight is currently not recommended due to the increased risk of developing skin cancer, which depends not so much on the total duration of sun exposure, but on the age at which the most intense exposure was observed. Accordingly, exposure to direct sunlight is not recommended for children in the first half of life, and therefore, insolation cannot be regarded as an adequate prevention of the development of hypovitaminosis D and rickets in young children.

The most important thing for preventing rickets is proper nutrition of the child. Currently, prolonged breastfeeding in Europe and North America is regarded as one of the main risk factors for the development of rickets in children. This situation is due to the fact that the vitamin D content in human milk is insufficient (no more than 50–60 IU/l) to prevent the development of the disease in an exclusively breastfed infant. However, it should be noted that with a rather low vitamin D content in human milk, a balanced mineral composition of human milk plays an important role in the prevention of rickets in breast-fed children. Breast milk contains 300 mg/l calcium and 140 mg/l phosphorus, with optimal digestibility of the elements and their optimal ratio (2:1), corresponding to that in the child’s bone tissue. In addition, the important role of the optimal protein and fat composition of human milk and the presence of certain biologically active substances in it, in particular a peptide related to parathyroid hormone, which increases the absorption of calcium in the intestine, should be taken into account.

Modern adapted formulas for feeding infants contain an average of 400 IU/l. Therefore, formula-fed children receiving up to 1 liter of formula per day often do not require additional prophylactic administration of vitamin D. The ratio of Ca and P in the composition of milk formulas becomes important, which should approach 2:1, corresponding to that in breast milk and ensuring maximum absorption of these elements. The fat composition of milk formulas has a particular effect on the absorption of calcium. In particular, there is evidence that the inclusion of beta-palmitate (triglycerides containing palmitic acid in the middle (beta) position) in the mixture prevents the formation of insoluble fatty acid salts with calcium in the intestine, thereby ensuring complete absorption of the mineral. Thus, in a study by Litmanovitz I. et al. Feeding a high-beta palmitate formula has been shown to have a positive effect on bone conduction velocity in infants during the first three months of life. On the Russian market, an example of an infant formula for artificial feeding containing beta palmitate is the Nutrilon ® Comfort mixture. Considering the advantages of modern milk formulas, it should still be noted that the daily amount of nutrition that provides the child’s physiological need for vitamin D is achieved only by 5–6 months of age, and the clinical picture of rickets develops at the beginning of the first half of the child’s life. Thus, in conditions of insufficient insolation, low vitamin D content in breast milk and insufficient intake of it into the baby’s body in the early stages of artificial feeding for the prevention of rickets and hypovitaminosis D great importance has the additional purpose of cholecalciferol.

According to the methodological recommendations of the Ministry of Health of 1990, the optimal preventive dose of vitamin D for young children is currently 500 IU, which is prescribed starting from 4–5 weeks of age in the autumn-winter-spring period for breastfed children during the first and second year of life. For children at risk for developing the disease (in the presence of concomitant pathology from the kidneys or gastrointestinal tract or accelerated growth rates of the child), in accordance with these recommendations, the administration of cholecalciferol in a dose of 1000 IU for a month, followed by a transition to 500 IU per day.

The list of references is in the editorial office.

Information about authors:
Irina Nikolaevna Zakharova , Head of the Department of Pediatrics, Russian Medical Academy of Postgraduate Education, Ministry of Health and Social Development of the Russian Federation, Professor, Dr. med. Sciences
Nina Alekseevna Korovina , Professor of the Department of Pediatrics, Russian Medical Academy of Postgraduate Education, Ministry of Health and Social Development of the Russian Federation, Dr. med. Sciences
Yulia Andreevna Dmitrieva , Assistant, Department of Pediatrics, State Budgetary Educational Institution of Further Professional Education "Russian Medical Academy of Postgraduate Education" of the Ministry of Health and Social Development of the Russian Federation

In the minds of most people, pathologies of the skeletal system are associated primarily with old age - the imagination immediately pictures a bent old woman leaning on a stick, or a gray-haired grandfather confined to a wheelchair. However, these stereotypes are destroyed by the terrible disease rickets, which affects the smallest and most defenseless - children in the first years of life.

Infancy and early childhood are the time when a person’s foundations for the rest of his life are laid. and skeleton, which are intensively formed in the first months and years, are no exception here. About the danger of rickets, one of the most common diseases of the skeletal system in children, all parents who are responsible for the future of their children need to know.

What is rickets disease?

Name diseases rickets is of Greek origin: ῥάχις means “spine,” although deformities affect more than just the spinal column. Rickets is a pathology that develops in early childhood, causing disturbances in bone formation with reduced mineralization of bone tissue.

As a result of the shortage and disorders of calcium-phosphorus metabolism rapidly growing bones form incorrectly, soften and bend. Following mineral metabolism, other types of metabolism are also disrupted, which leads to disruptions in the functioning of the muscular, nervous, immune, digestive and endocrine systems. Internal organs may also suffer: liver, spleen, lungs, heart and etc.

Rickets can be called a growth disease, since it is based on a deficiency of calcium and phosphorus salts, vitamin D and a number of other nutrients that play a key role in osteogenesis ( bone formation) an extremely fast growing organism. Indeed, during the first year of life, the baby’s weight increases three times!

Due to a lack of awareness among poorly educated groups of the population, there is a myth that rickets is not a particularly terrible disease, but a natural age-related phenomenon that goes away on its own after two years, when the child’s growth rate slows down. Therefore, it is supposedly not necessary to treat it at all. This is a deeply erroneous position!

Although in a couple of years calcium-phosphorus metabolism indeed usually returns to normal even without treatment, and the bone matrix is ​​mineralized and the skeleton acquires sufficient strength, consequences of rickets can darken the rest of your life. This includes an ugly figure (scoliosis, hunchback, flat feet, crooked legs, ugly and diseased teeth, poor posture), and developmental delays, myopia, weakened immunity, anemia, etc.

Yes, yes, an incorrectly formed skeleton will lead to a lot of seemingly unrelated “sores”! And years later, rickets, suffered at a tender age, will make itself felt by another most dangerous ailment of the skeletal system - osteoporosis, which we will talk about in the section “How are they related?” rickets and osteoporosis?. So prevention and treatment of osteoporosis is the direct responsibility of all parents.

Level incidence of rickets yesterday and today

Rickets is not a new disease for humanity - it has been known since ancient times. However, the level incidence of rickets changed with the course of historical time.

Characteristic descriptions of the signs of rickets are found in the works of ancient Greek doctors who worked in Rome, Soranus of Ephesus and Galen. Later, European artists of the Renaissance often recorded on their canvases the features of rickets (enlarged abdomen, protruding forehead, deformed limbs and chest) in small models. It is likely that such body changes were considered normal features of childhood anatomy.

In connection with urbanization and the development of industry in the 17th century, rickets affected an increasing number of children, especially residents of dusty, smog-drowning, cramped working-class neighborhoods of English cities. It even received the name "English (fog) disease." By the way, prevalence of rickets and today it is much lower in rural areas, where babies receive more sunlight.

Russian statistics

The discovery of the causes of the disease and ways to prevent it radically changed the situation in the twentieth century. If at the turn of the last century its signs were noted in the overwhelming majority of children - 96% in the northern capital of Russia and 80% in Moscow, then today the level incidence of rickets in Russia it ranges from 30 to 66% depending on the region.

In areas with low levels of insolation (of which there are many in our country), this disease is more common. Also, its frequency depends on the efforts of pediatricians conducting conversations with parents about the need to prevent rickets. Thus, in Moscow, where medical care for the population is excellent, no more than 30% of children are susceptible to rickets.

Interestingly, the Russian for rickets differs significantly from data from other developed countries of the world, indicating only 5–9 children with rickets per million. Moreover, these are predominantly representatives of the Negroid race, which is genetically most predisposed to rickets.

Such an impressive discrepancy in statistics incidence of rickets associated with the approach to diagnosis. In the West, only clearly expressed, advanced cases of the disease are taken into account. When making a diagnosis, Russian pediatricians rely not on blood tests and x-rays of bones, but on symptoms such as increased sweating with a specific sour odor, baldness, high nervous excitability, poor dream and decreased appetite. Prescribing vitamin D and other preventive measures for first signs of rickets is a widespread pediatric practice in Russia, minimizing the risk of developing severe pathology.

Pathogenetic causes of rickets

Main pathogenetic (related to the mechanism of occurrence and development of the disease) cause of rickets is a violation of mineral, primarily phosphorus-calcium metabolism against the background lack of vitamin in the bodyD.

Calcium– the most important biologically active substance, macronutrient, involved in the functioning of the nervous system, cardiac activity, blood clotting, and muscle relaxation. But most of all (99%) of this mineral is concentrated in the human skeleton, without it it is impossible bone formation.

But for good absorption of calcium in the intestines and its entry into bone tissue is necessary sufficient amount of vitamin D , without which this essential mineral, even with a high content in food, will simply pass through the digestive system and be released into the external environment.

The situation with vitamin D is also not easy. Scientists divide it into exogenous and endogenous types. First in uniform ergocalciferol (vitamin D 2 ) And cholecalciferol ( D 3 ) enters the body with food. Endogenous (mainly cholecalciferol) is produced in the body itself, namely in the skin, under the influence of ultraviolet rays, for which it is called the sun vitamin. Cholecalciferol, or , is the more important, bioavailable form.

It is important to note that endogenous hypovitaminosisD can develop even with an excess of exogenous vitamin supplied with food. The fact is that the path of transformation ergocalciferol and cholecalciferol into active metabolites, similar in their functions to, is complex. It converts to liver and kidneys. As a result, the resulting hormone-like substance calcitriol regulates phosphorus-calcium metabolism, growth and mineralization of bones.

Thus, reasons for the development of rickets may be related to insufficient vitamin intakeD, calcium, phosphorus from the external environment, and from dysfunction of the gastrointestinal tract, kidneys, liver.

Factors and groups risk of developing rickets

Let's consider the factors and their corresponding groups risk of developing rickets.Some of them are due to mother's health and lifestyle during pregnancy and breastfeeding:

• too early (before 17 years) or late (after 35) pregnancy;
• short interval between pregnancies;
• toxicosis during pregnancy;
• non-gynecological pathologies and complications in a pregnant woman: metabolic diseases, diseases of the digestive, urinary and other systems;
• a small amount of time a pregnant woman spends in the sun, as well as physical inactivity, which slows down metabolic transformations in the body;
• depleted of useful substances, irrational for pregnant and lactating women, vegetarianism. Lack of protein products, calcium, phosphorus, magnesium, vitamins D, B 1,2,6, etc. in the diet;
• childbirth with complications;
• living in poor social and living conditions.

IN child's health condition crucial for the occurrence of rickets have:

• time of birth from late summer to December, when solar activity is low;
• prematurity, low body weight and bone tissue. The saturation of the fetus with minerals occurs especially intensively in the last months, which is why birth at 9 months is so important;
• the weight of the newborn is more than 4 kg, as well as intensive weight gain in the first months. Let us remember that rickets - rapid growth disease, and the more rapidly the baby grows, the more difficult it is for the body to adjust mineral metabolism according to new needs and manage to saturate the skeleton with minerals;
• transition to artificial feeding, early mixed nutrition, as well as receiving expressed milk, but kept for a long time breast milk. Late introduction of complementary foods, as well as a lack of animal proteins in complementary foods, increases the likelihood mineral imbalance;
• insufficient time outdoors, lack of sunlight. You should not wrap your baby up too much. In cool weather, if possible, it is necessary to provide access to ultraviolet radiation during walking hours at least to the skin of the face and hands. You should know that glass absorbs ultraviolet rays, so sunbathing at home will not add vitamin D to your child;
• low motor activity of the baby, which may be associated with too tight swaddling, lack of necessary massage and physical therapy;
• a number of diseases, functional disorders: diseases of the skin, gastrointestinal tract, liver and kidneys (malabsorption, celiac disease, cystic fibrosis, intestinal dysbiosis, food allergies, intestinal infections, frequent acute respiratory viral infections, chronic infections, etc.), due to which the absorption and metabolism of vitamin D is impaired, calcium and other and minerals;
• perinatal encephalopathy (damage to the central nervous system that occurs during intrauterine development) with damage to the third ventricle;
• taking anticonvulsants;
• genetic predisposition to metabolic disorders and rickets;
• increased functioning of the parathyroid or thyroid glands.

Ecology

From environmental factors One should mention the pollution of the atmosphere with smog, soil and water, and food with metals (zinc, lead, strontium, etc.), which can partially displace calcium from the bones.

An important role is played by climate. Residents of northern latitudes, areas where damp, cool, cloudy weather prevails, do not receive enough cholecalciferol due to lack of sunlight. The same applies to residents of megacities, where in areas of high-rise buildings, access to ultraviolet radiation in courtyards is limited.

A separate danger is drug therapy pregnant (nursing) mother or baby with drugs that negatively affect tissue. These are glucocorticoids, phenobarbital, anticonvulsants, radiation and chemotherapy, antacids, tetracycline, heparin, cyclosporine, etc.

Thus, in group risk of developing rickets includes the following categories of children:

• premature;
• born too small or large;
• twins and triplets;
• not receiving breast milk or balanced artificial nutrition, complementary foods;
• having hereditary ;
• lacking sufficient mobility.
• These are also children who have diseases that directly or indirectly disrupt mineral metabolism, as well as those receiving medications that have a bad effect on the mineralization of bone tissue. Let's add here children from socially disadvantaged families and regions with low levels of insolation.

The climatic-geographical factor makes it possible to classify group at risk of rickets most of the children in our country.

How avoid rickets?

All conscious parents cannot help but be concerned with the question: “How avoid rickets The child has?" Firstly, this is the elimination or weakening of the influence of the risk factors listed above. Secondly, this is a number of special antirachitic measures

Before the baby is born

• Prevention of rickets starts long ago before the baby is born. The expectant mother should walk more, especially in sunny weather, experience moderate physical activity(for example, do a set of exercises recommended by your doctor or attend yoga classes for pregnant women). Her the diet should be balanced by the composition of proteins, carbohydrates, fats, vitamins and minerals.

Introduction to the pregnant woman's menu foods containing vitaminDand calcium, – good prevention of rickets. VitaminDwith food can be obtained by eating egg yolks, fatty varieties of sea fish, parsley, potatoes, seeds and nuts, oatmeal, butter and dairy products. And cheese and other dairy products, poppy seeds and sesame seeds, beans and beans, sardines, cabbage, are rich in calcium. nettle and rose hips, parsley, almonds, pistachios and hazelnuts.

Observation in the antenatal clinic, following the doctor’s recommendations and carrying out all prescribed examinations reduces the risk of developing various diseases and complications of pregnancy, which also serves as the key to the birth of a healthy child.

In the last trimester of pregnancy, specialized vitamin and mineral complexes including vitamin D and calcium. Women with diagnosed hypovitaminosisD It is recommended to take it in an additional amount of 2–4 thousand IU per day.

After the baby is born

• After the birth of the childmeasures to prevent rickets will serve breastfeeding, day walks, sunbathing, massage and physical therapy, compliance with hygienic standards for baby care, as well as hardening. If the mother’s milk is insufficient or breastfeeding has been canceled for some reason, then only adapted formulas that include vitamin D should be used. The timely introduction of all types of complementary foods should not be ignored.

Prophylactic use after 3 weeks from birth (from the second week in case of prematurity) of drugs vitamin preparations D – standard practice in domestic pediatrics. But the dosage and duration of the course should be determined by the doctor, since both a shortage and an excess of the “sunshine vitamin” are equally dangerous, which in case of overdose exhibits a toxic effect - primarily on the kidneys and liver.

Usually, for the purpose of prevention, babies are prescribed an aqueous or oily solution of cholecalciferol (vitamin D 3) in the amount of 400 IU before six months, 400–600 IU from 6 months to a year and 600 IU after a year. The aqueous solution is more easily absorbed by the body. Exceeding the indicated dosages is possible if symptoms of the disease appear. In this case, we will be talking about 2000–5000 IU.

To find out the real content level vitamin in the bloodD, you can take a blood test, which will give accurate information about the presence of hypo- or hypervitaminosisD, which will help the doctor choose the appropriate dosage or decide to discontinue the drug. However, unfortunately, such an analysis is not included in the services provided under the medical policy, and you will have to pay for it.

Taking vitaminD may alternate with course of the Ural Federal District (ultraviolet irradiation). 10–20 sessions 2 times a year will contribute to the intensive production of cholecalciferol in the skin and its accumulation in the body.

The attention of modern pediatrics and parents themselves to the problem vitamin deficiencyD will help and taking preventive measures helps in most cases avoid rickets or its serious manifestations, even when the child is at risk for this pathology.

Signs of rickets

Many parents are concerned that signs of rickets at an early stage they are often hidden. That is, outwardly the baby may look quite well, but in fact experience lack of vitaminD and have disturbances of phosphorus-calcium metabolism. That is why it is very important to attend all scheduled examinations with different specialists: pediatrician, neurologist, orthopedist and others. They may suspect rickets based on indirect signs, without waiting for its severe consequences in the form of curvature, deformation of bones and the development of accompanying organ and systemic pathologies.

First symptoms

The first symptoms of rickets may appear at 2–3 months of age and will be neurological abnormalities. Parents may be alerted to changes in behavior such as increased excitability, anxiety, restlessness, sleep disturbance, fear, flinching from sharp sounds or turning on bright lights. When crying, there is a tremor of the chin. No appetite. Muscle tone decreases, and the child turns from active and mobile to sluggish and weakened. The edges and seams of the fontanel become pliable. Constipation and delayed teething are noted. The liver and spleen enlarge.

There is usually excessive baby sweating, while sweat has a sour odor and an irritating effect on the skin. Itching causes constant rubbing of the head against the pillow and baldness of the back of the head. The urine also becomes acidic and caustic, which serves as an additional irritant.

Disease progression

By 6 months in the absence of proper treatment, the disease progresses noticeably. There is a developmental delay on the part of the nervous and muscular-ligamentous systems. The baby has difficulty turning from back to stomach and vice versa, and does not sit down when pulled by the arms. Babbling and babbling are rare, and subsequently there is a delay in speech development.

Lack of proper mineralization leads to softening of bone tissue(osteomalacia), especially noticeable in the flat bones of the skull. There is a flattening of the back of the head, depression of the lower part of the chest (“cobbler’s chest” or its protrusion (“chicken/rooster chest”), expansion of the tubular bones at the ends, curvature of the spine, narrowing of the pelvis. Protrusion abdomen is associated with muscle hypotonia. If bone mineralization is not restored by the start of walking, then O- or X-shaped leg deformity. Overgrowth of non-mineralized tissue leads to an increase in the volume of the head, hyperplasia (bulging) of the frontal and parietal tubercles, “rosary beads” - thickenings on the ribs and “bracelets” on the arms.

Changes in the skeleton are dangerous by disrupting the functioning of internal organs. Due to the deformation of the chest, the preconditions are created for pulmonary diseases (tuberculosis and pneumonia), breathing problems, and frequent respiratory tract infections. The contractility of the heart muscle may deteriorate and tachycardia may appear. Transformation of the skull is fraught with mental retardation. Pelvic narrowing in girls can complicate childbirth in the future. It is likely that intestinal hypotonicity will develop, causing constant constipation.

On the background disturbances of phosphorus-calcium metabolism hemoglobin drops, iron deficiency anemia develops, which may be indicated by pallor, marbling of the skin - also characteristic sign of rickets.

Classification of rickets

There are several parameters on the basis of which rickets classification.

• By etiology(cause of the disease) are distinguished:

1. classic rickets, conditioned vitamin deficiencyD, this is a disease of intensive growth, widespread among children under one year old;
2. secondary rickets resulting from other diseases that impair vitamin metabolismD and minerals in the body. Its cause may be malabsorption (impaired absorption of nutrients in the small intestine), pathologies of the kidneys and gallbladder, metabolic diseases, as well as long-term therapy with glucocorticoids, diuretics, anticonvulsants, etc.;
3. vitaminD-dependent rickets two types is a genetic pathology when both parents have a defective one. A quarter of cases of this type of rickets are associated with consanguinity between father and mother;
4. vitaminD-resistant rickets occurs against the background of phosphate diabetes (renal diabetes insipidus) and other hereditary disorders of kidney function that cause rickets-like conditions.

• Classic rickets subdivided depending on the clinical picture And calcium to phosphorus ratio in the blood into 3 subtypes:

1. calciumpenic when signs of calcium deficiency prevail: softening of bone tissue, abnormalities in the functioning of the autonomic nervous system and impaired neuromuscular excitability;
2. phosphopenic when signs come to the fore phosphorus deficiency: muscle hypotonicity, weakness and lethargy, dysfunction of ligaments and joints;
3. without obvious deviations in the proportions of calcium and phosphorus, but with hyperplasia (overgrowth) of bone tissue.

• With the flow highlight:

1. spicy when processes predominate softening bones and changes in the nervous system;
2. subacute when the disease progresses more slowly, making itself known first bone hyperplasia;
3. recurrent, flowing in waves, now calming down, now intensifying. Transitions to the acute phase may be associated with acute respiratory infections, weakened immunity and other factors.

• By severity demarcate 3 forms of rickets:

1. light, with which first signs of rickets do not develop into serious changes in the skeleton, organs and systems;
2. moderate severity when the disease affects the skeletal system and organs, but the changes are moderate;
3. heavy When several parts of the skeleton are severely deformed, internal organs and systems suffer. The child has a delay in physical and mental development. Consequences of rickets may remain for life.

• In addition, standard rickets cycle includes 4 stages:

1. onset of the disease(from 2 weeks – 3 months from birth);
2. height, peak of rickets(at the age of 4–6 months);
3. convalescence, or gradual disappearance of mineral imbalance (after a year, symptoms begin to decrease, usually the recovery period begins in 2–3 years);
4. manifestation of residual effects(only for I and II degrees of disease severity).

Consequences of rickets

The severity of the disease, the presence or absence of proper prevention and therapy determine how severe the disease will be. consequences of rickets.

Rickets, which occurred in a mild form, did not lead to skeletal deformities and disruption of organ function, does not leave dangerous consequences. Otherwise, the following long-term complications of rickets:

• irreversible bone deformities , short stature, incorrect posture, narrow pelvis, crooked legs, flat feet, too large and angular head, flat back of the head, curvature of the spine and even a hump;
• disruption of internal organs and due to compression and trauma by their deformed bones. As a result curvature of the chest the lungs suffer, their ventilation is impaired. The risk of chronic bronchitis and pneumonia increases;
• girls are possible in the future problems with pregnancy and natural birth of a child due to a narrow pelvis, there is a need to do C-section;
• retardation in physical and mental development , severe forms of mental retardation are possible;
• fragility of bones and laxity of the joint-ligamentous apparatus, with age - development of osteoporosis, arthrosis and arthritis;
• anemia and myopia, weakened immunity at school age. Due to deterioration of respiratory functions and immunity, the child’s incidence of acute respiratory infections and infectious diseases is higher;
• thin, weak tooth enamel, chronic caries and malocclusion. Deformation of the jaw can externally manifest itself in a skewed line of the mouth and distortion of facial features. There may be defects in chewing food and speech, diction, and external respiration. Probably with age development.

As we see, consequences of rickets are by no means harmless, so at the slightest suspicion you should quickly contact specialists in order to stop the disease at an early, relatively safe stage.

Diagnosis of rickets

Originating from parents suspicion of rickets should not serve as a reason for self-medication with shock doses of vitaminD, as this can lead to toxic damage to the kidneys and other organs. Diagnosis of rickets should be entrusted to a pediatrician, who, based on the clinical picture and a series of examinations, should prescribe adequate therapy.

The results of urine tests and blood for rickets indicate:

• low levels of total and ionized calcium in the body;
• low phosphorus;
• a significantly increased level of alkaline phosphatase, an enzyme involved in phosphorus transport, an important factor in phosphorus-calcium metabolism;
• negative or weakly positive reaction of a urine sample according to Sulkovich - an analysis that determines the quality and quantity of calcium in the urine.

X-ray and ultrasound- informative methods for determining the state of the osteoarticular system.

On x-rays in the case of rickets, reduced mineralization of the bone tissue of the tubular and flat bones, changes in growth zones - thickening at the ends of long bones, curvature of the ribs, sternum, legs. X-rays are done for diagnosis in complex cases, as well as to monitor the course of severe forms of rickets. Due to the potential danger of radiation exposure to the baby, they are usually limited to images of the wrist joint and the distal forearm.

Ultrasound examination can be subjected (with diagnosis of rickets a), the brain (neurosonography can indicate rickets and a number of other pathologies of newborns), internal organs (with severe forms of rickets– to assess their deformation).

Which doctor treats rickets?

Many parents are wondering what doctor treats rickets. In most cases, the diagnosis and treatment of this disease is carried out by pediatrician. It is he who prescribes the main treatment and determines what the baby needs. vitamin dosageD, monitors the dynamics of clinical manifestations. But due to the fact that the disease is fraught with a variety of complications, consultations with specialized specialists are necessary.

Neurologist (neurologist) will be able to assess in detail the nature of neurological changes in the child’s condition and give parents recommendations for their targeted correction. A neurologist will be able to distinguish between rickets, hydrocephalic syndrome and other possible developmental abnormalities.

Orthopedist will help fix it bone deformities, will prescribe massage and physical therapy, corrective shoes for flat feet, orthopedic products for weakness of the joint-ligamentous apparatus. If a child has suffered a serious a form of rickets, That observation by an orthopedist should become permanent.

Consultation hematologist may be useful in cases of severe iron deficiency anemia as consequences of rickets.

Nutritionist will help you choose the right menu for a nursing mother and a growing baby, taking into account his metabolic disorders.

visit gastroenterologist will be necessary if cause of rickets gastrointestinal diseases appear.

Methods rickets therapy

Rickets is a systemic disease that primarily affects bone tissue, and also affects the nervous, immune, digestive, respiratory and other systems. That's why rickets therapy should be comprehensive and combine specific and nonspecific treatment.

Specific treatment

Under specific treatment refers to the use of medications, primarily vitamin AD, preferably an aqueous solution of cholecalciferol. It is prescribed in amounts from 2000 to 5000 IU (depending on the severity of the disease) daily for a month - 45 days, depending on the severity of the disease.

To clarify the required dose and prevent vitamin D poisoning, it is possible to conduct an analysis for vitamin levelD(25-OH vitamin D) in the child’s body. However, it will most likely have to be done for a fee, moreover, this is an unpleasant test for the baby, and nurses do not always cope with collecting venous blood from infants.

After the drums doses of vitaminD, when the doctor notes a decrease in the symptoms of rickets, up to 2-3 years it can be prescribed in preventive doses - 400-600 IU per day.

Some pediatricians prescribe a vitaminD not as a single drug, but as part of children's vitamin complexes , since children develop rickets against the background of polyhypovitaminosis.

It is usually not prescribed to breastfed babies, since mother's milk is usually rich in these macronutrients. But the mother herself should adhere to calcium-rich diet, she may be recommended calcium-containing pharmacological agents.

For artificially born, low birth weight and premature babies, calcium can be prescribed if severe hypocalcemia is detected during examinations. Indications for taking calcium are serious changes in the bones with their slow formation, demineralization, osteomalacia.

The same applies to phosphorus preparations- a substance that also plays a critical role in osteogenesis.

In drug therapy acute rickets may also be included antioxidants (tocopherol, beta-carotene, vitamin C, glutamic acid). To improve the functioning of the autonomic nervous and muscular systems, a monthly course of drugs such as glycine, carnitine, asparkam, panangin or at a young age (up to 3 years) you can inhale the smell from the jar "Valerian P" and over 3 years - select the dosage with your doctor.

Nonspecific treatment

Let's not forget about nonspecific treatment rickets. It includes the following measures:

• balanced maternal and child nutrition, breastfeeding, the timely introduction of all types of complementary foods. When artificial feeding - the use of specialized adapted mixtures containing vitamin D and other essential vitamins, as well as minerals;
• walks in the open air(2–3 hours daily), sunbathing, however, overheating can be dangerous for the baby; it should be covered from direct sunlight with gauze or translucent fabric;
• daily restorative massage and course therapeutic massage from a professional massage therapist;
• physiotherapy, will help improve metabolic processes, increase muscle tone. It should be remembered that a child weakened by rickets is prone to rapid fatigue and nervous overexcitation, and if you overdo it with exercise therapy, this can be harmful. Complexes of exercises, as well as massage loads, are selected according to the age of the child and the stage of the disease. It is advisable to introduce exercise therapy and therapeutic massage a couple of weeks after starting medication;
• physiotherapeutic UFO courses (from 10 to 20 sessions twice a year) are especially relevant in the autumn-winter period, when natural sunlight is low. When they are carried out, vitamin D is canceled or its dosage is reduced in order to avoid excess and toxic action of the vitaminD. Do not overdo it with ultraviolet radiation due to the potential carcinogenic effect of radiation;
• 2–3 times a year can be carried out courses balneological procedures : up to 15 bath sessions with the addition of pine needle extract (2 teaspoons per 10 liters, duration - up to 10 minutes) or salt (2 tablespoons per 10 liters, 3-5 minutes).

Nutrition for rickets

Special attention should be paid nutrition for rickets. Let us once again emphasize the most important the role of mother's milk in the prevention and nonspecific therapy of this disease. Only in a mother’s breast milk, provided she is well-nourished, all the nutrients the baby needs, including vitamin D, B vitamins, calcium and phosphorus, are in ideal proportions. Incidence of rickets Among children receiving breast milk, it is significantly lower, and in those who are sick, it proceeds more easily and faster than in those who are breastfed.

If the child is on artificial nutrition or he has to be fed additionally due to a lack of milk from the mother, you should select adapted milk formulas that include vitamin D, phosphorus, and magnesium. Fermented milk mixtures are also recommended.

Already from 3 weeks, the gradual introduction of juices and decoctions of hypoallergenic fruits into the baby’s menu begins, and from the age of one month - fruit purees. At 3 months, the diet includes a hard-boiled egg yolk; at 3 and a half to 4 months, vegetable purees from pumpkin, zucchini, and cabbage are used; from 5 months – chicken liver, pureed to a homogeneous mass. At six months, children's cottage cheese enriched with calcium is introduced, as well as milk porridges and meat purees. You can boil and chop white lean meat and chicken.

It should be borne in mind that all complementary foods are introduced into the diet of artificial babies earlier than during breastfeeding.

Massage for rickets

Intensity and Duration massage for rickets determined by the age of the baby and the severity of the disease. For example, during an exacerbation of rickets, the effects should be extremely careful and light. Massage will help improve metabolic processes and psychomotor functions, strengthen muscles, and stop negative changes in the osteochondral system.

At the onset of the disease it is recommended restorative massage, and due to the weakened condition of the baby and rapid fatigue, massage loads recommended for this age at acute rickets should be halved.

Produced with care flexion and extension limbs in joints.

Breathing exercises stimulated by light pressure with one hand on the chest. As the child grows, these influences intensify. If deformations of the chest bones are expected, then special attention should be paid to the sternum, the area between the shoulder blades, and the intercostal muscles. Sharp, shock massage movements are not advisable. It is necessary to give preference to stroking and rubbing, since the baby is extremely sensitive and excitable during the “heyday” of rickets.

At O-shaped bowed legs When forming a flat-valgus foot, a strengthening massage is performed on the outer side of the thighs, and a relaxing massage on their inner surface. At X-shaped curvature- vice versa.

Often with rickets, coxavara develops due to low muscle tone of the buttocks, or varus deformity of the femoral neck. To correct this defect, you need to stroke and knead the buttocks and the hip joint area.

It is useful to stimulate the reflex flexion-extension of toes, pressing on the area under 2-3 fingers, and then pressing down to the middle of the heel with your thumb.

At bulging rickety tummy you need to focus your efforts on strengthening the abdominal muscles, stroking it in a circular motion in a clockwise direction. Then perform simultaneous multidirectional (up and down) stroking with two palms; stroking from the chest down.

Back massage will consist of stroking from bottom to top and to the side, along the edge of the shoulder blades to the armpit.

It is advisable for a specialist to show young parents techniques massage for rickets, or you can use the training videos from the Internet.

Does it happen rickets in adults?

Many people are interested in the question: is it possible rickets in adults? Strictly speaking, no. This is a specific disease of children of the first – second, less often third years of life. Although similar phenomena (demineralization, loss of density and strength, bone curvature) also occur in adult patients. And here the following topic deserves a separate discussion: rickets and osteoporosis .

How are they connected? rickets and osteoporosis?

These are interconnected, related pathologies of the skeletal system, having a metabolic nature, that is, caused by metabolic disorders. The difference between them is as follows. With rickets, insufficient mineralization and softening (osteomalacia) take place in the process growth and skeletal formation, while the osteoid tissue itself is formed in sufficient quantities. A occur in osteoporosis leaching of minerals and loss of strength in formed bones, while osteogenesis is slowed down and predominates destruction of bone cells.

Previously, osteoporosis was considered exclusively a problem for older people. However, today in medical practice we also talk about childhood and adolescent osteoporosis. Even more common in young patients osteopenia– a precursor to osteoporosis, the initial stage of a decrease in bone density.

Childhood and adolescent osteoporosis

Examinations of the younger generation indicate the presence of osteopenia in approximately half of children aged 10–16 years.

Lack of mineral density and bone mass is usually detected in adolescence in connection with fractures, pain in the spine and limbs. Unpleasant sensations when staying in one position for a long time, short stature, incorrect posture, asymmetric folds of skin on the body may indicate osteopenia or osteoporosis.

During adolescence disorders of bone metabolism, mineral metabolism is promoted by too intense growth and restructuring of the body, significantly increasing the need for vitamins, microelements and other nutrients. Poisoning of a growing body by smoking, alcohol or drugs is an increasing factor risk of developing osteoporosis.

Parents of those teenagers who have suffered from moderate or severe rickets should be especially vigilant. After all, the more thoroughly the skeleton is formed in early childhood, the more dense bone tissue formed in the body, the less likely development of osteoporosis after years. On the connection between rickets and osteoporosis Today many researchers point out pathologies of the skeletal system.

Prevention of osteoporosis should begin in childhood

One of the first to address this problem was Doctor of Medical Sciences, Professor, who has studied rickets for more than four decades, osteopenia and osteoporosis, disorders of calcium and phosphorus metabolism and others bone pathologies. He came to the conclusion that osteoporosis in adults is a pediatrically determined disease, that is, caused by the consequences of rickets suffered in infancy. And we need to start preventing osteoporosis from childhood!

So, a significant disturbance in the mineralization of bone tissue in early childhood, even after removal diagnosis of rickets has long-term negative consequences for child's skeletal system, and then an adult. To minimize them, it is worth giving your child pharmacological agents to strengthen bones after 3–4 years, of course, after coordinating your actions with your doctor.

Decrease consequences of rickets!

Decrease consequences of rickets a drug developed by Professor Villoriy Strukov will help "Osteomed", widely used in pediatrics. Its advantage is that it promotes the deposition of calcium in the bones, and not in soft tissues, and does not cause hypercalcemia or calcification. This is due to the fact that Osteomed improves bone metabolism, restores bone remodeling processes, increasing the activity of osteoblasts - bone tissue building cells.

"Osteomed" improves osteogenesis (the formation of new bone tissue) due to the content of a unique bee product - drone-brood homogenate, or drone milk. Present in this substance phytohormones(testosterone, prolactin, progesterone, estradiol) have a powerful stimulating effect on bone and muscle anabolism, and without those dangerous ones that synthetic analogues of hormones have.

And mineralization of bone tissue is ensured in the composition of “Osteomed”:

• vitaminD, which is much more abundant in drone jelly than in the classic antirachitic agent - fish oil;
• the most bioavailable form of calcium -.

"Osteomed" - an effective natural remedy treatment and prevention of osteoporosis, as well as therapies, the healing of which it significantly accelerates.

Also, you can’t ignore the drug "Osteo-Vit", which is a source of vitamin D. In addition, this dietary supplement contains vitamin B6, which is also important for normal calcium metabolism in the body. This drug is an excellent remedy for the prevention of rickets and other bone diseases.

From history of rickets

It's interesting to look into history of rickets as a characteristic mirror of the development of scientific and medical thought. Listings of clinical manifestations of rickets The doctors of antiquity (Soranus of Ephesus and Galen) left us with it, and the disease was described in even more detail by European doctors of the 17th century (Guilmot, Weistler and Butis).

In the 19th century, scientists (Kassovitz, Kuttner, Khotovitsky) drew attention to the seasonal nature of exacerbation of rickets and associated this with lack of sunlight. Also in the treatment of the disease, an important place was given to a balanced, nutritious diet. Korsakov pointed to a lack of calcium (lime) as the cause of rickets, Wegner and Kassovitz - to a deficiency of phosphorus. By the way, it was originally prescribed to patients precisely as a source of phosphorus.

At the beginning of the twentieth century, the domestic researcher Shabad emphasized the role of the phosphorus-calcium balance in rickets, and also suggested that it was not phosphorus, but something else that had a healing effect in fish oil.

The social and everyday condition of rickets was noted by Bystrov and Kisel.

In 1919, Huldshinsky discovered the healing effect quartz lamp for rickets.

A little earlier, in 1918, Mellanby proved the healing effect of cod oil in experiments on dogs with artificially induced rickets. He linked this to the presence of a certain vitamin in fat. The scientific community assumed that this was vitamin A. However, McCollum, in his experiment, made vitamin A in fish oil inactive with the help of oxygen and found that this did not deprive the substance of its healing power. This means that some other vitamin had an antirachitic effect, which was called vitamin D. The structural formula of vitamins D 2 and D 3 was derived by Windaus only in 1936.

Our days

Although from now on treatment and prevention of rickets gained a scientific basis, history of rickets didn't end. And today, the attention of many scientists continues to be focused on the problem of rickets, minimizing its risks and consequences. Much in the fight against rickets also depends on the awareness and consciousness of the broad masses of the population, primarily parents. By adhering to a healthy lifestyle, timely carrying out preventive and therapeutic measures, and mitigating the effects of rickets, parents save their baby from many lifelong health problems, including such a dangerous disease as osteoporosis.