Rachit - description, reasons, symptoms (signs), diagnosis. Rahit: Signs, Symptoms

04.01.2021 Analyzes

Rickets- Multifactorial disease, which relates to metabolic disorders. One of their main pathogenetic factors is insufficient consumption of calcium food, less often phosphates, vitaminad, as well as other velitamine elements necessary for the formation of hormonal forms, especially copper and zinc and vitamins of group B and ascorbic acid. In addition to an alimentary factor, the immaturity and heterochrony of the development (dysfunction) of endocrine glands, various somatic diseases flowing with maldigesty and Malabsorption, contribute to the development of bone tissue. An important link of Rakhita pathogenesis is a violation of the formation of secopalcyferol in the skin, a violation of the regulation of phosphorus-calcium exchange in the liver, kidneys.

Disruption of bone metabolism can cause or exacerbate various drugs. Most often, the development of osteopyhenia / osteoporosis cause glucocorticoids. In second place in terms of frequency, osteopathy are on the background of the use of anticonvulsants, in particular, phenobarbital. The development of violations of phosphate-calcium metabolism is possible when using thyroid hormones, long-term use of heparin (more than 3 months), antacids containing aluminum, cyclosporine, tetracycline, gonadotropin, derivatives of phenothiazine. Somatotropic hormone, glucagon, androgens and estrogens, insulin, prolactin, also contribute to the reduction of calcium calcium in the blood, which indicates the participation of many endocrine bodies in the development of Rakhit and Osteoporosis.

The serious consequences of Rahita is osteopyia / osteoporosis, dispensing of posture, multiple caries of teeth, vegetative dysfunction, resulting in violation of the work of many organs and organism systems.

Clinical manifestationrachet is more often found in spring and winter season, especially in children living in regions with insolation, cloudiness, frequent fogs or in the areas of environmental disadvantage.

Most often, Rahit develops in children born either in young mothers (younger than 17 years old), or in women over the age of 35. Of great importance for the formation of violations of phosphate-calcium exchange in the child has unbalanced nutrition of a pregnant woman: calcium deficiency, zinc, protein, phosphorus, vitamins D, 1, 2, in 6. Rahitis more often develops in children, whose mother during pregnancy was not enough in the sun, moved little, had extragnenitial diseases.

Antenatal prevention Rakhita

The antenatal prevention of Rahita provides for: compliance with the mode of the day of pregnant woman with a sufficient sleep day and night, walking in the fresh air at least 2-4 hours daily, in any weather, rational food of a pregnant woman (daily use of at least 170 g meat, 70 g of fish, 50 g Cottage cheese, 15 g of cheese, 220 g of bread, 500 g of vegetables, 300 g of fresh fruit, 150 ml of juice, 500 ml of milk or fermented milk products). The best food source of calcium is dairy products (cheeses, milk, kefir, cottage cheese).

Instead of milk, it is advisable to use special dairy drinks designed for women during breastfeeding and breastfeeding, capable of preventing phosphate-calcium exchange disorders in a woman, fetus and baby. In case of their absence, it is possible to recommend a course reception of polyvitamin preparations and calcium preparations.

Infant Rahit is widespread in children of the first years of life. The first mention of Rahit is found in the works of Senna Efesse (98-138 AD), which revealed the deformation of the lower extremities and the spine in children. Galen (131-201 AD) gave a description of the richite changes of the bone system, including the deformation of the chest. In the Middle Ages, Rakhit called English disease, since it was in England that it was the prevalence of its heavy forms, which was associated with insolation in this climatic zone. A complete clinical and pathologist of Rakhita made the English orthopedist Francis Glisson in 1650 in his opinion, the main risk factors for rickets in children are burdened heredity and improper nutrition of the mother. In 1847, in the book "Pediyatrika" S.F. Hotovitsky described not only the defeat of the bone system during rickets, but also changes in the gastrointestinal tract, vegetative disorders, muscle hypotension. In 1891 N.F. Filatov noted that Rakhit is a common disease of the body, although manifests, mainly a kind of bone change.

According to modern ideas, Rahit is a disease characterized by a temporary inconsistency between the needs of the growing organism in phosphorus and calcium and the insufficiency of the systems of their transportation in the body. This disease of the growing organism, due to disruption of methasophilic methasis, the main clinical syndrome of which is the defeat of the bone system (violation of the formation, proper growth and mineralization of bones), in which the pathological process is localized mainly in the field of metaepyyphysis. bones. Since the growth and speed of restructuring the bones are highest in early childhood, the bone lesions are most pronounced in children 2-3 years. Rahit is a polyfactory metablastic disease, in the diagnosis, prevention and treatment of which all the factors of pathogenesis should be taken into account: Insufficiency and imbalance of calcium and phosphorus with food, the immaturity of the endocrine system of the child, concomitant diseases, etc. In addition to the pathology of phosphorous calcium metabolism, protein exchange violations and trace elements (magnesium, copper, iron, etc.), multivitamin failure, activation of lipid peroxidation.

Code of the ICD-10

E55.0. Rahit active.

EPIDEMIOLOGY

Rahit is found in all countries, but especially often among the northern peoples who live in conditions of lack of sunlight. Children, born in the fall and winter, are getting rickets more often and harder. At the beginning of the XX century. Rakhit was noted in 50-80% of young children in Western Europe. Up to 70% of children in Russia these years also had Rahit. According to A.I. Ruffle (1985), Rickets in children of the first year of life meets up to 56.5%, according to S.V. Maltseva (1987), its prevalence reaches 80%. The most difficult disease occurs in premature babies.

To date, classic (vitamin D-deficient) Rahit occupies a significant place in the structure of the morbidity of young children. In Russia, its frequency in recent years ranges from 54 to 66%. According to pediatricians of Moscow, the classic Rahit is currently found in 30% of young children. This indicator can be considered understated, since only heavy and medium-sized forms of the disease are recorded. In developed countries, which introduced the specific prophylaxis of rickets with vitamin D and the vitaminization of baby food products, heavy forms of rickets have become a rarity, but subclinical and radiological manifestations remain widespread. So, in France, the hidden deficiency of vitamin D was revealed in 39%, and explicit clinical manifestations - in 3% of children who came to hospitals about various diseases. In the northern provinces of Canada, hypovitaminosis D was found in 43% of children surveys. In southern countries, despite the sufficient intensity of ultraviolet irradiation, Rahit remains a very common disease. In Turkey, Rahit was detected in 24% of children aged 3-6 months, although the introduction of prevention by vitamin D made it possible to reduce its prevalence up to 4%.

Information: RICKETS. Etiology. One of the main factors is hypovitaminosis D, vitamin D deficiency of exogenous or endogenous origin. In addition to the wrong feeding and alimentary insufficiency of vitamin D, it can lead to a violation of the formation of its active forms in the body with a lack of ultraviolet rays (in winter and autumn, in cities), liver and kidney disease (they are formation of active forms of vitamin). A certain role is played by presence (immaturity of enzyme systems), the rapid growth of the child, diseases accompanied by acidosis, the insufficient flow of calcium and phosphorus salts. Pathogenesis. Vitamin D is a steroid compound and is known in the form of vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol), which are very close in structure, physicochemical properties and influence on the human body. The vitamin D coming with food is transformed into liver and kidneys, resulting in 1.25-dihydroxy-vitamin D, which has a hormone-like action. This compound affects the genetic apparatus of the intestinal cells, thereby increasing the synthesis of protein, specifically binding calcium and providing its transport in the body. With a lack of vitamin D, the absorption and exchange of calcium is disrupted, its blood concentration falls, which causes the reaction of the parachitoid glands and increase the secretion of the pararathgamon regulating the exchange of calcium and phosphorus. The over-secretion of the parathgamon leads to mobilization of calcium from bone tissue, suppressing phosphate reabsorption in renal channels, and therefore the content of inorganic phosphates in the blood drops. At the same time, alkaline phosphatase activity sharply increases. The phosphate-calcium exchange disorders lead to the development of acidosis, which is accompanied by a violation of the excitability of the nervous system. Clinical picture. In gravity, the following degrees of Rahita distinguish: 1 degree (light) - small changes from the nervous and muscle systems; residual phenomena does not give; II degree (moderate severity) - pronounced changes in bone, muscular, nervous and hematopoietic systems, moderate disruption of the function of the internal organs, a slight increase in the size of the liver and spleen, anemia; III degree (severe) - sharply pronounced changes from the central nervous, bone and muscular systems, internal organs. Frequent complications. The initial period is more often noted in 2-3 months, but can manifest itself throughout the first year of life. Sweating, baldness of the head, anxiety, muscular dystonia; The unaware softening of the edges of a large springs. Duration 2-3 weeks. Biochemical studies: a reduced amount of phosphorus, an increase in phosphatase activity. No radiographic changes. In the period of sickness of the disease, along with the phenomena of braking the nervous system, changes in the bones appear; Craniotabes, changes in the bones of the skull, chest, limbs. The bone changes, unobthered with rickets) degrees and distinct at the II degree, are transferred to deformation with rickets of III degree. Disruption of static functions, internal organ functions, muscle hypotension, anemia is joined. When Rahute II and III degrees of the spleen and the liver are increased. On radiographs, the contours of bones are lubricated. Epiphysis of tubular bones of glassoid, edges of metaphistes are fringeless. On the 2-3rd year of life there are only consequences in the form of bone deformations, sometimes anemia. In acute flow, the rashita symptoms are noted. In the initial period - severe concern, sharp sweating, biochemical shifts in the blood, in the midst of the disease, a significant softening of bones, pronounced muscle hypotension. The acute course is observed more often in the first months of life, especially in premature and rapidly growing children. The subacute flow is characterized by a slower development of the process. It is observed more often in children over 6-9 months, as well as in children with hypotrophy. The phenomena of softening bones are expressed significantly less. Osteoid hyperplasia prevails over osteomation, frontal and dark bugs, rosary on ribs, thickening of epiphesis of tubular bones are noted. The recurrent flow is accompanied by intermittent states: usually improving summer and worsening in winter. Radiographs are visible on radiographs that correspond to observation zones in metaphyshs during the reparation. Late Rickets include rare cases of the disease, when active manifestations are noted over the age of 4. Late Rahit, observed in the military and the first postwar years, was characterized by the presence of general symptoms of the disease (anorexia, sweating, pain in the legs, fatigue). Bone deformations are marked only in terms of cases. Of particular importance are such signs as hypophosphatemia, and from the bones - osteoporosis and changes in occasion zones. The diagnosis in addition to clinical symptoms is confirmed by the study of the blood content of calcium, phosphorus, alkaline phosphatase, the data of x-ray research is important. Differential diagnosis. Rachitis differentiate from a number of ricket-like diseases of hereditary natural phosphate-diabetes, renal tubular acidosis, Debre's syndrome - de Tony Fanconi (see ), as well as from the congenital dislocation of hips, hondodroodstrophy, osteopathy in chronic renal failure, congenital bone fragility. Treatment. An important role is played by rational nutrition, normalization of a regime with sufficient stay in the fresh air, massage, gymnastics. In the initial manifestations of docking children prescribe vitamin D2 preparations of 300-800 IU / day, for the rate of 400,000-600,000 me; During the ranking period, 10,000-16,000 IU / day are prescribed in 2-3 receptions, for a course of 600,000-800,000 ME. The impact dose method used in severe complicated formas of rickets is currently not used. Vitamin D drugs should be given during meals. Sometimes the purpose of vitamin D2 is combined with a 25% solution of citric acid, a 20% sodium citrate solution (in the intestine, an easily soluble and well suused calcium citrate complex is formed) inside 20 ml per day. During treatment, it is necessary to carry out the simplest control over the sensitivity of the children's body to vitamin D with the help of Sulkovich sample for the prevention of hypervitaminosis. Ultraviolet therapy has a beneficial effect in the initial period and at a subacute of Rahita in young children. The method and dosage of irradiation depend on the age of the child, its physical condition, the conditions of the external environment, phase and the severity of Rakhita. It is recommended to carry out ultraviolet irradiation with a course, including 15-20 sessions appointed in a day, with a gradual increase in exposure. The first session of children up to 3 months begin with 1/8 biodozes, children over 3 months - with 1/4 biodoz. With subsequent treatment, after each 2 session, the exposure is increased by 1/8, or 1/4 biodoz. With insufficient stay in the open air, artificial feeding, the recurrent course of Rakhit, the course of treatment is lengthened to 25 sessions and repeated after 2 months. With the initial phase of Rakhita, irradiation is often limited to one course consisting of 15-20 sessions, in the middle phase, the course after 2-3 months increases. In the intervals between irradiation courses, specific prevention of vitamin D2 or fish oil are carried out. Massage and gymnastics are used in any period, but not in acute flow. The forecast for the timely treatment and elimination of the cause is favorable. With severe flow, psychomotor development delay, skeletal deformation and posture disturbance. Prevention. Rational nutrition, sufficient insolation, sanitary and hygienic regime, hardening, proper education. Advocative antenatal prevention in pregnant women in the last 2-3 months of pregnancy vitamin D, 5,500-1000 me / day. For the antenatal prevention, you can use ultraviolet irradiation of pregnant women. It is necessary for a long stay outdoors, rational food. In the diet of the child, vegetables, fruits should be in time. The lore must contain a sufficient amount of vitamins, salts. Important products containing natural vitamin D3 (egg yolk, fish oil) are important. The addition of a citric acid is artificially fed to nutrition (25% solution of 1 teaspoon 3 times a day) contributes to the formation of an easily absorbed Citrate calcium, and therefore the absorption of phosphorus. Flour dishes, porridges contain phosphorus in a poorly digestible child form and can contribute to the development of Rakhita, so it is desirable that the number of them in the daily diet of the child of the 1st year of life exceeded 180-200 g. In the autumn-winter period, ultraviolet radiation of children with a preventive purpose It is necessary to start with 1-1.5 months of life. Two courses should be held with intervals 2 months. The physiological need for a vitamin D of a healthy ditching child in the 1st year of life ranges within 400-500 IU / day. In cases where the child for any reason does not receive ultraviolet irradiation with the preventive purpose, the artificial drug of vitamin D2 or D3 should be prescribed for the purpose of the antenatal prophylaxis in the last 3-4 months of pregnancy, gendests are recommended for 1-2 dragey per day (250- 500 ME vitamin D2), a under adverse conditions - 4 dragey per day. Contraindications - Mother's age for over 30 years, Mother's disease. Postnatal prevention is carried out from a 2-3-non-sex age of 500 me per day (1 drop of video khol), for course 150,000-200 000 ME.

Initial period.
The first signs of the disease usually arise on 2-3 months of life. The behavior of the child changes: anxiety, bugness, increased excitability, shuddering with external stimuli (loud noise, sudden flasher of light). Sleep becomes superficial and alarming. Potting, especially on the skin of the scalp and face, the resistant red dermographism is noted. Sweat has a sour smell and irritates the skin, causing itching. The child rubs his head about the pillow, the bald sections appear on the back of the head. Physiological muscle hypertonus characteristic of this age is replaced by muscle hypotension. There appears the fuels of the seams of the skull and the edges of the Big Springs, they are planned thickening on the edges in the fields of Röbel-cartilaginous articulations ("Rachitical kits").
On the radiograph of the bones of the wrist, a slight resolution of bone tissue is detected. With a biochemical study of blood, a normal or even increased calcium concentration and a decrease in phosphate concentration are detected; It is possible to increase the activity of alkaline phosphatase. In the analysis of urine, phosphatine is detected, an increase in the amount of ammonia and amino acids.
Period of patch.
The period of the right is most often at the end of the first half of life and is characterized by even more significant disorders from the nervous system and the musculoskeletal system. Osteomalysis processes, especially pronounced in the acute course of Rahita, lead to the softening of flat bones of the skull (Craniotabes), followed, often one-sided slaughter. There are flexibility and deformation of the chest with a pressing in the lower third of the sternum ("chest of a shoemaker) or its esteem (" chicken ", or" cylinder ", chest). Characteristic of the O-shaped (less often x-shaped) curvature of long tubular bones. Formed a narrowed plane stuffed pelvis. As a result of a pronounced softening, the Röber arises a deepening along the attachment line of the diaphragm (Harrison of Borozda). The osteoidal tissue hyperplasia, prevailing at a substrate of rickets, is manifested by the formation of hypertrophied frontal and dark bugs, thickening in the field of wrists, the robe-cartilaginous joints and the interfalance joints of the fingertips of the hands with the formation of the so-called "bracelets", "richitetics", "pearl threads".
On radiographs of long tubular bones, glass-shaped expansions of metaphysis, blur and fuzziness of preliminary obscurity zones are visible.
The hypophosphatemia, moderate hypocalcemia, alkaline phosphatase is increased.
Reconvocation period.
For this period, the improvement in the well-being and condition of the child is characteristic. Static functions are improved or normalized. On radiographs, changes are detected in the form of uneven seal of growth zones. The phosphorus content in the blood reaches the norm or somewhat exceeds it. Small hypocalcemia can be maintained, and sometimes even intensify.
Period of residual phenomena.
Normalization of biochemical indicators and the disappearance of the symptoms of active rickets indicate the transition of the disease from the active phase into inactive - the period of residual phenomena. Signs of transferred Rahita (residual deformations of the skeleton and muscle hypotension) can be kept for a long time.
The degree of gravity and the course of Rahita.
For the acute flow of Rakhit, the rapid development of all symptoms, severe neurological disorders, significant hypophosphatems, the predominance of osteomalysis processes is characteristic. Moderately pronounced or almost inconspicuous neurological disorders, minor changes in the biochemical composition of blood, prevailing the processes of osteoid hyperplasia are peculiar to the flow of the flow. The existence of a recurrent flow of Rakhit is currently questioned.

Rahit in children is the exchange disease of children of the first two years of life with a predominant violation of phosphorous calcium exchange due to the temporary inconsistency of the high needs of the body in calcium and phosphorus and the impossibility of their satisfaction in connection with the deficiency of vitamin D and its active metabolites during the period of the most intensive growth of the body.

The deficiency of mineralization and softening of tubular bones in older children and adults associated with hypovitaminosis D is called osteomalysis.

Osteoporosis - The permission of the structure of bone tissue and its demineralization.

An obvious sign of rickets in a child

Rahit in children. Etiology.

The most ancient object, carrying signs of Rakhita - Mummy of the Sacred Monkey, whose age of 4000, described by LORA - Geyar. Obviously, the monkey had a genetic violation of the exchange of vitamin D, since Rakhit was extremely rare in Egypt and other ancient foci of civilization. Fossil prehistoric skeletons and remains of ancient Egyptians, Cubans, Greeks, Indians, Chinese, Incans and Babylonians did not have signs of suffered Rahita. Obviously, the tropical and subtropical location of the ancient centers of culture and the natural diet of our ancestors affected. Rakhit - the undigested industrial society, became known in Europe as " english disease"Since I acquired distribution in the cities of Britain in the XVII-XIX centuries. And he was first described by the English doctor F. Glisson in 1650. The name Rickets comes from English Ricks - Wops, Skirds, Bugry. Already then, it was noticed that Rakhit is a disease of citizens conducting life in the premises. He did not meet in a pre-industrial era. This assumption is confirmed by the fact that Rahit is striking wild animals in captivity, but not with free content.

Medical geography Rahita is a certain interest:

most often, this disease occurs in moderate latitudes, between 40 and 60 ° of northern latitude;
not observed in highland areas (above 1000 m above sea level);
it is found in blacks more often than those who live on the same territory representatives of other races;
in cities, especially large industrial centers, there is a cup than in rural areas.

Children of low-income families are most striking. After opening in the XIX century. Chemist A. Villaus Vitamin D, and the beginning of using it with a prophylactic goal, rickets as the result of dietary defects ceased to be massive in developed countries. At the same time, the problem of pathogenic consequences of hypervitaminosis D. The prevalence of Rakhita, according to a number of authors, is currently in various regions of the European part of the continent from 10 to 50%.

Factors predisposing to rickets are as follows.

Rahit in children, factors from the mother:

mother's age over 35 years old;
toxicosis of pregnant women;
extgazenital pathology (exchange diseases, diseases of the kidneys, skin, gastrointestinal tract, liver);
power defects during pregnancy and lactation with the development of hypovitaminosis D, C, E, group vitamins B, protein, calcium microelements and phosphorus;
insolation and hypodymna;
complicated childbirth;
long-term intake of glucocorticoids, thyroid hormones, antacids, tetracycline, gonadotropin, derivatives of phenothiazine, heparin, chemotherapy, radiation therapy.

Rahit in children, factors from the child:

birth time (second half of the year);
prematurity and immaturity;
body body weight at birth;
stormy gain in body weight during the first 3 months of life;
breastfeeding breast milk under the age of 35;
early translation to artificial feeding by non-adaptive milk mixtures;
hypodynamics and insufficient insolation;
diseases of the skin, liver, kidneys, perinatal encephalopathy, impaired intestinal feed syndrome;
frequent Ori and intestinal infections;
long use of anticonvulsant drugs.

Rahit in children. Pathogenesis.

The view of the bones of the pelvis is normal and when rickets

The main pathogenetic link of Rakhita is violation of phosphorous calcium exchange. The physiological content of calcium in the blood in children ranges from 2 to 2.8 mmol / l, phosphorus - from 1 to 1.4 mmol / l (calcium ratio and blood phosphorus must be 2: 1). The regulation of phosphorous calcium homeostasis is carried out mainly vitamin D., parathgormonand Calcithonin. Vitamin D enters the human body in the form of cholecalciferol (D 3) through the skin and ergocalciferol (D 2) with food. Under normal conditions up to 80% of the required amount of vitamin D, the body can be synthesized in the skin of 7-dehydroholesterol (provitamin D)) under the influence of ultraviolet rays. The process occurs in the macrophage cells of the actual dermis, in the basal layer of the epidermis and adipocytes of subcutaneous-fatty fiber. It is weakened with age, at cachexia and when skin darkening. Hyperkeratosis due to avitaminosis A shields actually to the dermis and contributes to the development of hypovitaminosis D. Sun and ordinary glass deprive the sunlight of anti-oscillatic activity. Freamed photochemical activity in cases where the sun stands low above the horizon vitamin D penetrates the blood vessels of the skin and is transferred with the participation of vitamin-o-binding protein into the liver, kidney, bones, cartilage, delicious intestines, placenta and possibly some lymphocytes, where By hydroxylation turns into its metabolites. The most active of them are formed in the liver and proximal kidney channels. Hydroxylated in the liver and kidneys is necessary for activation of food vitamin D 2, which is absorbed with lipils in the small intestine (mainly in Jejunum) and gets first in the composition of chylomicrons. Subsequently, with a blood current, it is transferred to the liver and fatty tissue in a complex with D-binding A, -Globulin. The main depot of vitamin is located in the adipocytes of subcutaneous fatty fiber.

Basic functions of vitamin D in the human body:

promotes the active absorption of calcium and phosphorus salts in the small intestine due to the effect on the synthesis of calcium binding protein;
activates the activities of Osteoblasts, stimulating the synthesis of osteocalcin bone protein by osteocalcin;
regulates bone mineralization processes;
increases the reabsorption of calcium and phosphorus salts in the renal tubules;
activates muscle reductions by activating calcium receptors in the muscles;
it has immunomodulatory and antiproliferative effect, increasing the activity of phagocytosis, the synthesis of interleukinov-1 and -2, interferon.

Deficiency of vitamin D. The body leads to calcium failure. The low level of calcium in the blood stimulates the increased production of pararathgamon with parathyroid glands.

Paranthmone functions:

contributes to the flushing of calcium salts from bones in blood;
stimulates the function of osteoclasts and bone resorption;
inhibits collagen synthesis in the active osteoblasts of the bone;
stimulates the reabsorption of calcium and magnesium in the renal tubules;
increases the excretion of phosphates and bicarbonates with urine,
Causeing metabolic acidosis.

The accumulation in the blood serum of acidic metabolic products simultaneously with a decrease in phosphorus level disrupts the function of the central and vegetative nervous system and increases their excitability. With hypophosphatemia, when rickets are softened by bones and the development of Motonia.

The third main regulator of phosphorous calcium metabolism is thyreocalcitonin - thyroid hormone.