Diagnosis of rickets, presentation on pediatrics. Rickets-like diseases in children

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Vitamin D deficiency decreases the synthesis of Ca-binding protein, which ensures the transport of Ca through the intestinal wall; decreases the absorption of Ca in the intestine; increases the excretion of P in the urine in the blood; decreases the content of Ca and P; acidosis; metabolic disorders, the appearance of muscle hypotension, dysfunction of the central nervous system and internal organs, leaching of Ca from bones, disruption of skeletal formation: bones become soft, easily deformed, and defective (demineralized) bone tissue grows in growth zones.

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The clinical course of rickets is divided into four periods: Initial period: The first symptoms of the disease appear at the age of 3-4 months, with calcium deficiency - 1.5-2 months.

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Changes in the nervous autonomic system: the child becomes restless, fearful, flinches at sudden sounds and falls asleep; the child’s sleep is restless and shallow; severe sweating, especially of the face and head, when sucking, during sleep, as a result of which prickly heat often appears on the skin; sweat causes irritation and itching of the skin, the child constantly tosses and turns on the pillow in his sleep and wipes the hair on the back of his head - baldness of the back of the head appears.

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Changes in the muscular system: General muscular hypotension; Changes in the skeletal system: Softness and pliability of the edges of the large fontanel and the sutures of the skull. The duration of the initial period is from 1.5 weeks to 1 month.

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The height of the period: If rickets is not diagnosed in a timely manner and there is no treatment, rapid progression of bone changes, dysfunction of the nervous and muscular systems occurs, and changes in internal organs appear.

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Changes in the skeletal system: skull: the edges of the large fontanel become soft, areas of softening appear along the sutures, softening of the bones of the skull (craniotabes), flattening of the back of the head and its asymmetry are noted, almost simultaneously there is a proliferation of demineralized tissue and the appearance of frontal and parietal tubercles that give the head square shape. The large fontanelle closes late (by 1.5-2 years).

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teeth: appear late, the order of their eruption is disrupted, there is a tendency to caries due to enamel defects; chest: at the junction of the bone and cartilaginous parts of the ribs, thickenings (costal beads) are formed, the softness of the ribs contributes to the appearance of lateral compression of the chest, the curvature of the collarbones increases, the upper part of the chest narrows, and the lower part expands; in the places of attachment of the diaphragm, a recess is determined (Harrison's groove), the anterior part of the chest, together with the sternum, can protrude forward (“chicken breast”) or recess (“shoemaker’s chest”).

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spine: kyphosis (rachitic hump), lordosis, and somewhat later scoliosis appear;

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limbs: the epiphyses of the bones of the forearm (“rachitic bracelets”), the phalanges of the fingers (“strings of pearls”) thicken, deformation of the softened diaphyses of the femur and tibia leads to an X-shaped or O-shaped curvature of the legs, flat feet develops.

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pelvic bones: deformations of the pelvis caused by delayed bone growth, while the entrance to the pelvic cavity narrows, the sacrum and coccyx move forward, the anteroposterior size decreases (flat rachitic pelvis).

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Changes in the muscular system: pronounced hypotension of all muscle groups; weakness and flabbiness of the abdominal wall muscles leads to an increase in the size of the abdomen (“frog belly”);

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weakness of the ligamentous apparatus appears, as a result of which joint laxity appears, the range of movements increases (symptom of a “penknife” or “jackknife”); delayed motor development appears (the child later begins to sit, stand, and walk).

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Changes in internal organs: respiratory organs: impaired breathing efficiency due to chest deformation, muscle hypotonia, decreased contractility of the diaphragm (shortness of breath, pneumonia); cardiovascular system: weakening of heart sounds, tachycardia, systolic murmur, hypotension;

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digestive organs: intestinal atony (flatulence, constipation, formation of “fecal stones”), dyspeptic disorders, liver dysfunction; hematopoietic organs: hypochromic anemia develops, disturbance of homeostasis, etc.

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The period of convalescence: neurological and autonomic symptoms disappear, the child’s general condition improves, and his motor activity increases. The normalization of muscle tone and the restoration of static skills occur much more slowly. The level of phosphorus in the blood is restored, but the level of calcium remains noticeably reduced due to its active deposition in the bones.

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Period of residual effects: By the age of 2-3 years, the child still has bone deformations, functional changes in internal organs, and biochemical blood parameters gradually normalize.

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According to the severity of rickets, there are: I degree (mild) - symptoms are present only in the initial period; II degree (moderate) – the peak period is moderately pronounced; III degree (severe rickets) - pronounced musculoskeletal changes, severe damage to the central nervous system and internal organs, delayed physical and psychomotor development, anemia.

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Complications:

enamel defects and early caries of primary and permanent teeth; rachitic narrow pelvis, especially in girls; development of persistent bone deformities, poor posture; high risk of infectious diseases.

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Additional methods for diagnosing rickets:

biochemical blood test (hypocalcemia, hypophosphatemia, increased alkaline phosphatase activity); radiography of the wrists (osteoparosis); Ultrasound (thickening of the epiphyses of tubular bones).

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Basic principles of treatment of rickets

Rational nutrition of the child: maximum duration of natural feeding, in the absence of breast milk - feed the child with adapted formulas, introduction of juices, cottage cheese, egg yolk, vegetable puree, buckwheat or oatmeal, and meat supplements according to age. Rational daily routine: sufficient time in the fresh air, sleeping in the fresh air, walks in any weather.

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3. Specific therapy: - vitamin D preparations (cholecalciferol - D3 and ergocalciferol - D2). In the initial period of rickets, the daily dose is 1500-2000 IU, in the peak period - 3000-4000 IU. The course of treatment is from 30 to 45 days. The criterion for completing the course of treatment is the normalization of clinical manifestations of rickets and laboratory parameters. For children at risk (premature, often ill, with malnutrition), the dose of the drug is selected individually. To avoid an overdose of vitamin D, it is necessary to periodically examine the urine using the Sulkovich test.

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Physiotherapy: UV irradiation 15-20 procedures are prescribed in case of malabsorption in the intestine, in case of impaired absorption of vitamin “D” or after completing a course of treatment with vitamin “D” preparations. Treatment with vitamin D and ultraviolet radiation cannot be carried out simultaneously.

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4. Nonspecific treatment: vitamin therapy: B vitamins, ascorbic acid; Calcium glycerophosphate during breastfeeding can be prescribed to the mother 0.5*3 times a day for 7-10 days a month; citrate mixture 1 teaspoon 3 times a day for 1-1.5 months (especially with large doses of vitamin D, since its use allows you to reduce the dose of the drug);

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dibazol, proserin – for severe muscle hypotension; Exercise therapy, massage, therapeutic baths with decoctions of valerian, motherwort (in the initial period and at its height), salt-coniferous baths (in the period of convalescence).

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Spasmophilia

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Spasmophilia is a disease based on hypocalcemia, which causes an increased readiness of the body for tonic and clonic convulsions.

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Occurs in children from 3 months to 2 years.

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Risk factors for the development of the disease: treatment of rickets with large doses of vitamin D (for severe rickets or feeding with unadapted formulas); hyperproduction of vitamin D in the skin of a child in early spring with increased insolation.

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Prevention of spasmophilia consists of timely detection and adequate treatment of rickets.

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Mechanism of the pathological process

Vitamin “D” increased deposition of Ca in the bones and its insignificant absorption in the intestines, a critical decrease in the level of Ca in the blood serum (hypocalcemia), hyperphosphatemia develops, a violation of mineral metabolism and acid-base balance (alkalosis), the cause of increased neuromuscular excitability and the occurrence of convulsions.

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The main clinical manifestations of spasmophilia

2 forms of infantile tetany: hidden (latent) form; explicit form.

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The latent form of the disease often precedes the overt form and can last from several weeks to several months.

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Symptoms: Khvostek's symptom - when lightly tapping with a finger in the cheek area between the zygomatic arch and the corner of the mouth (fossa caninae), the facial muscles of the corresponding side contract; Lyust's symptom - when there is a blow below the head of the fibula, rapid abduction of the foot occurs;

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Trousseau's sign - when the neurovascular bundle in the middle third of the shoulder is compressed, after 3-5 minutes the hand convulsively contracts, taking the position of the “obstetrician’s hand”; Maslov's symptom - under the influence of painful stimulation (injection), a short-term cessation of breathing occurs.

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An obvious form of infantile tetany: Laryngospasm occurs paroxysmally in the form of a slight spasm of the glottis or its complete, short-term closure, accompanied by cyanosis (the child is frightened, covered in sticky sweat), a short-term spasm is followed by a noisy inhalation, reminiscent of a “rooster crow.” The attack lasts from a few seconds to 1-2 minutes, and can be repeated throughout the day.

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Carpopedal spasm is a tonic contraction of the muscles of the feet and hands; the hands are bent as much as possible. The thumb is brought to the palm, the remaining fingers are bent at right angles at the metacarpophalangeal joints, and straightened at the interphalangeal joints (“obstetrician’s hand”); the feet are in a state of sharp plantar flexion.

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Eclampsia is the rarest, but most severe form of overt tetany, which is a general attack of tonic-clonic convulsions, which begin with numbness, lethargy, twitching of facial muscles, convulsions spread to other muscle groups, the child’s breathing becomes intermittent, sobbing, cyanosis appears, the child loses consciousness, involuntary urination and defecation occur. After an attack, the child usually falls asleep. The duration of the attack is from several to 20-30 seconds.

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Complications:

during an attack of eclampsia, respiratory and cardiac arrest may occur; with laryngospasm, breathing may sometimes stop (fatal); spasms of the respiratory muscles during carpopedal spasm.

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Diagnostic methods

Biochemical blood test: hypocalcemia, hyperphosphatemia, alkalosis in the blood.

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Basic principles of tetany treatment

An obvious form of infantile tetany requires urgent measures: create a calm environment around the child; free him from restrictive clothing; provide sufficient aeration;

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Apply methods of tactile stimulation of breathing (to create a dominant focus in the brain): pat the cheeks and buttocks, sprinkle cold water on the face, irritate the root of the tongue (Ca gluconate solution per os on the root of the tongue), pressing on it with a spatula, bring a cotton ball soaked in ammonia to your nose.

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as prescribed by a doctor, administer an anticonvulsant (secuxene, GHB, magnesium sulfate, calcium gluconate); if ineffective, artificial ventilation of the lungs and inhalation of 100% oxygen are used.

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Prescribed: drink plenty of fluids (tea, berry or fruit juices); a course of treatment with calcium preparations (5% calcium chloride solution or calcium gluconate); 5% ammonium chloride solution; 3-4 days after the seizures, a course of antirachitic treatment with vitamin D preparations

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Hypervitaminosis D

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Hypervitaminosis D (D-vitamin intoxication) is a condition caused by an overdose of vitamin D or increased sensitivity of the body to vitamin D preparations with the subsequent development of hypercalcemia and toxic changes in organs and tissues.

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Risk factors for developing the disease: uncontrolled intake of vitamin D supplements; overdose of vitamin D preparations; prescribing vitamin D in the summer;

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the use of vitamin D preparations simultaneously with adapted milk formulas, without taking into account the calciferol content in them; individual hypersensitivity to vitamin D preparations.

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Prevention of hypervitaminosis D

Compliance with the rules for using vitamin D. Individual approach to prescribing vitamin D preparations. Systematic monitoring of calcium levels in urine during treatment with vitamin D using the Sulkovich test at least once every 2 weeks.

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Mechanism of disease development

Hypercalcemia, hypercalciuria, calcium deposition in the walls of blood vessels, followed by irreversible calcification of internal organs, affects the organs involved in the activation and excretion of vitamin D (liver, kidneys and cardiovascular system), impaired mineral metabolism (hypophosphatemia), negative nitrogen balance and acidosis.

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II clinical forms of hypervitaminosis D: Acute D-vitamin intoxication: develops in children of the 1st year of life with uncontrolled intake of vitamin D.

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Leading symptoms: symptoms of intestinal toxicosis; neurotoxicosis; dysfunction of vital organs.

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Clinical symptoms of intestinal toxicosis: loss of appetite up to complete anorexia, thirst; persistent vomiting, rapid loss of body weight; development of symptoms of dehydration (dry skin, sharpened facial features, large fontanel sunken, decreased tissue turgor and muscle tone).

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Clinical symptoms of neurotoxicosis: increased excitability, followed by lethargy and drowsiness; autonomic disorders (sweating, red dermographism); confusion of consciousness up to the development of coma; convulsions.

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From other organs: changes in cardiovascular activity; renal failure; liver dysfunction; changes in blood parameters (anemia, hypercalcemia, azotemia, acetonemia); bone changes (excessive calcium deposition in the growth zones of long bones).

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Chronic D-vitamin intoxication occurs against the background of long-term use of the drug in moderate doses and is characterized by: decreased appetite, vomiting is rare; the weight curve is flattened; there is restless sleep, irritability; rapid fusion of the sutures of the skull and early closure of the large fontanel; on the part of other organs and systems, changes are insignificantly expressed.

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Complications:

acute renal failure, toxic hepatitis, acute myocarditis; early closure of bone growth zones with impaired skeletal development; early development of vascular sclerosis of internal organs, gradual lag in physical and mental development.

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Diagnostic methods:

biochemical blood test: hypercalcemia, azotemia, acetonemia; urinalysis: hypercalciuria, hyperphosphaturia; sharply positive Sulkovich test.

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Basic principles of treatment of hypervitaminosis D

Stop taking vitamin D and calcium supplements. Detoxification therapy: parenteral administration of hemodez, 5% glucose solution, rheopolyglucin, albumin, Ringer's solution. Administration of vitamin D antagonists: vitamins A and E.

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4. Hormonal therapy (prednisolone to reduce the toxic effect of vitamin D). 5. Combating acidosis (humidified oxygen, parenteral administration of sodium bicarbonate). 6. Removal of calcium preparations (drugs that bind calcium in the intestines - almagel, xidifon, cholestyramine and drugs that remove calcium from the intestines - Trilon B). 7.Symptomatic therapy.

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Nursing process for vitamin metabolism disorders

Possible patient problems: malnutrition due to poor feeding, delayed teeth; risk of disruption of skin integrity due to hyperhidrosis (risk of developing prickly heat, etc.); violation of the sleep formula; high risk of infections;

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psycho-emotional lability, retardation in neuropsychic development; decreased motor activity due to muscle hypotonia; decrease in weight and height indicators, lag in physical development; change in appearance due to deformation of skeletal bones; risk of developing seizures, eclampsia; lack of attention and communication with parents

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Possible problems for parents: lack of information about the disease; lack of knowledge about rational feeding and child care; concerns about the child's appearance; fear for the child, uncertainty about the successful outcome of the disease; Fear of vitamin D overdose due to lack of knowledge of the rules for vitamin D prophylaxis; feeling of guilt before the child.

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Nursing intervention

Clinic nurse: 1. Help parents see the prospects for the development of a healthy child, fill their lack of knowledge about the causes, characteristics of the course, prevention, treatment and prognosis of the disease.

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2. Consult parents on the organization of rational feeding in accordance with the age and needs of the child: convince the mother to continue breastfeeding the child for as long as possible; when introducing complementary foods, use products containing vitamin D (buckwheat porridge, egg yolk, butter and vegetable oil, fish, caviar); from the second half of the year - meat, minced liver;

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For children with rickets, it is advisable to cook porridge with vegetable broth; when artificial feeding, preference is given to adapted lactic acid formulas, while taking into account the dose of vitamin D contained in them; limit as much as possible whole cow's milk in the child's diet due to the high content of calcium and phosphates; from 4 months, start introducing freshly prepared juices, fruit and vegetable purees in optimal quantities.

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3. Organize sufficient time for the child to spend time in the fresh air at any time of the year, try to avoid walks in direct sunlight in the spring, and avoid restrictions on the child’s physical activity. 4. Recommend sleeping on open verandas (protected from the wind) and in the shade of trees.

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5. During the waking period, stimulate the child’s mental and motor activity, encourage play activities, and select toys and games in accordance with age. 6. Recommend that parents regularly conduct courses of therapeutic exercises and massage, teach them basic techniques in accordance with the age and condition of the child.

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7. Train parents to conduct therapeutic baths with decoctions of valerian, motherwort in the initial period of rickets and when the child is restless, salt and pine baths. 8. Consult parents on the method and technique of giving vitamin D: explain the features of the action and use of oil and alcohol preparations, teach the rules for calculating a single and daily dose in drops, warn against overdose (use only a special pipette, count the drops correctly), vitamin Before use, it is preferable to dilute “D” in breast milk and store it in a cool place, protected from light.

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9. Help parents correctly assess the child’s condition and promptly consult a doctor if he or she develops dyspeptic disorders or changes in behavior. 10. Convince parents of the need for dynamic monitoring of the child by a pediatrician.

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Hospital nurse: Perform all manipulations carefully and, if possible, exclude invasive interventions. Independent interventions: compliance with SER and child care rules; monitoring compliance with the child’s balanced diet; organizing the child's leisure time; creating a positive emotional mood; eliminating the lack of parental knowledge about the disease.

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Dependent interventions: giving the child therapeutic doses of vitamin D and other medications as prescribed by the doctor; interdependent massage, exercise therapy, therapeutic baths.

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Sources of information: Textbook by Ezhova N.V., pp. 201-212. Textbook of Svyatkina K.A., pp. 39, 99-115. Textbook by Sevostyanova N.G., pp. 302-318. Textbook by Tulchinskaya V.D., pp. 54-66.

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Thank you for your attention!

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Rickets is a disease of young children in which calcium-phosphorus metabolism is disrupted as a result of vitamin D deficiency. Rickets is the most common disease in children. According to various researchers, rickets occurs in 20-60% of children. Reliable data are unknown, since mild forms of the disease and initial manifestations are often missed.

Slide 3: Factors contributing to the development of rickets in children

Artificial feeding Prematurity of children (multivitaminosis, including hypovitaminosis D, increased need for vitamin D₃, immaturity of morphological and functional systems). High rates of skeletal growth, rapid remodulation of bone tissue. Poor child care.

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Exogenous factors: Insufficient supply of vitamin D, phosphates, calcium, magnesium, zinc and other microelements, vitamins, amino acids. Insufficient exposure of the child to fresh air and insufficient insolation, which leads to disruption of the formation of vitamin D₃ from 7-dehydrocholesterol in the epidermis under the influence of ultraviolet rays.

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Endogenous: Disruption of the absorption of vitamin D₃ in the intestines. Disruption of the processes of hydroxylation of inactive forms of vitamin D into active forms (D₃) in the liver and kidneys. Impaired absorption of phosphorus and calcium in the intestine, their increased excretion in the urine, impaired utilization of bone tissue. Impaired functional activity of vitamin D₃ receptors.

Slide 6: Classification of rickets

Degree of severity Period of illness Nature of course 1st - mild Initial Acute 2nd - moderate severity Heightened period Subacute 3rd - severe Convalescence Recurrent Residual effects

Slide 7: Working classification of Lukyanova E.M. (1988) highlight:

Classic vitamin D deficiency is rickets. Vitamin D-dependent rickets is associated with a genetic defect in the synthesis of 1,25(OH)₂D₃ in the kidneys or with resistance of target organs to it. Vitamin D-resistant rickets (tubulopathies, hypophosphatasia). Secondary rickets in liver diseases, malabsorption syndrome, etc.

Slide 8: Diagnosis of rickets

Clinical data. Biochemical blood test: Decrease in phosphorus concentration; Increased alkaline phosphatase activity; Calcium content – ​​N or hypocalcemia; Decreased citric acid content (hypocitremia). X-ray of skeletal bones – osteoporosis.

Slide 9: Clinical manifestations of rickets

I degree The first symptoms of rickets are autonomic disorders: sleep disturbances; irritability; tearfulness; increased sweating: most of the face, scalp; “sour” sweat → rubbing the head into the pillow → baldness of the back of the head; Red dermographism. Bone compliance - edges of the greater fontanelle → lesser fontanelle → sagittal suture (minor osteoporosis).

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Slide 11: II degree

Head: craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone); deformation of the bones of the skull; late closure of the large fontanel, impaired teething (untimely, incorrect) Chest: deformation of the clavicles (increased curvature); “costal rosary” (hemispherical thickening at the point of transition of the cartilaginous part of the rib into the bone); expansion of the lower aperture and narrowing of the upper, compression of the chest from the sides; deformation of the sternum (“keeled”, “lake-shaped” chest). Spine: kyphosis in the lower thoracic vertebrae, kyphosis or lordosis in the lumbar region, scoliosis in the thoracic region, flat pelvis.

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Slide 13: III degree

Deformation of the bones of the skull, chest, spine + various changes in the tubular bones: upper limbs: curvature of the humerus and forearm bones; Deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers). b) lower limbs: curvature of the hips forward and outward; various curvatures of the lower extremities (O- or X-shaped deformities); deformities in the joint area.

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Slide 16: Treatment of rickets

It is necessary to eliminate the causes that led to the development of the disease; pathological changes that have occurred in the body. Treatment is divided into nonspecific and specific. Nonspecific treatment: rational nutrition; correct child routine; sufficient exposure to fresh air; daily hygienic, periodically medicinal coniferous and with sea salt.

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Slide 17: Specific treatment

Specific treatment depends on the period of the disease and its course. In the initial period of the disease during the subacute course in full-term children, general ultraviolet radiation is prescribed every day or every other day, 15-25 sessions. Start UV treatment with 1/8 biodose and increase to 1.5 biodose. Prescribe vitamin D 2000 IU per day for 3-4 weeks. At the height of the disease, vitamin D is prescribed at 5000 IU per day for 3-4 weeks. An aqueous solution of vitamin D₃ (cholecalciferol) is mainly used; 1 drop contains 500 IU. During treatment with vitamin D, it is advisable to perform a Sulkovich test (determining the level of calcium in the urine) once a week. After achieving a therapeutic effect, they switch to a prophylactic dose (500 IU per day), which is prescribed to the child for 2 years.

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Dispensary observation is carried out up to 3 years of age; inspection quarterly; Vaccination is allowed 3 weeks after the start of vitamin D3 therapy.

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Slide 19: Prevention

Antenatal and postnatal prevention is carried out. Antenatal prevention Nonspecific measures: Rational nutrition of the pregnant woman, adequate lifestyle, sufficient exposure to fresh air. Prevention of viral-bacterial and other diseases in a pregnant woman. Timely treatment of gestosis in pregnant women. Prevention of miscarriage. Specific prevention: Carried out in the last 2-3 months of pregnancy in the autumn-winter period of the year. Prescribe vitamin D 500 IU every day or ultraviolet radiation, 10-15 sessions every day or every other day (start with ¼ biodose and increase to 2.5-3 biodoses).

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Slide 20: Postnatal prevention

Nonspecific: Breastfeeding, timely introduction of supplements and complementary foods. Carrying out massage and gymnastics (30-40 minutes a day). Sufficient exposure to fresh air, air baths.

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Specific prevention: Starts from 3-4 weeks (in premature infants from 10-14 days of life). Every day the child is given 500 IU of vitamin D₃ until he is 1.5 years old. In the summer months (3 months), vitamin D is not given due to intense sun exposure. For premature babies and children with increased skin pigmentation, the daily dose of vitamin D is increased to 1000 IU and given for 2 years, excluding the summer months. If children are fed with adapted formulas, vitamin D is not prescribed. To prevent hypervitaminosis D, it is necessary to perform a Sulkovich test once every 2-7 weeks.

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Slide captions:

• prof. MAKEEVA N.I.

• Rickets in children. Spasmophilia. Hypervitaminosis D.

• KHARKIV NATIONAL MEDICAL UNIVERSITY
• (Rector – Prof. V.N. Lesovoy)
• DEPARTMENT OF PEDIATRICS No. 2
• (Head of the department - Prof. N.I. Makeeva)

• Rickets is mentioned in the works:
• Herodotus of Halicarnassus
• (484 – 425 BC)
• Saran of Ephesus
• (98 - 138 AD)
• Claudia Galena
• (131-211 AD).

• Dutch artists of the 15th-16th centuries.

• A clinical and pathological description of rickets was given by the English orthopedist F. Glisson in 1650. The English name rickets comes from the Old English wrickken, which means “to bend,” and Glisson changed it to the Greek rhachitis (spine), since rickets primarily affects the skeletal system.

• Francis Glisson -
• "De Rachitide" 1650

• 19th century - rickets is rampant among poor children living in polluted industrial cities
• “Disappearance of rickets” in the first half of the 20th century:
• Uses of fish oil
• Improving children's nutrition
• Control over polluting industries
• Recent "revival of rickets"
• In the last 2–3 years, there has been an almost 2-fold increase in the admission to hospitals of children with manifestations of severe rickets in developed countries (USA, Japan, Europe).

• Rickets. Historical reference

• children's disease
• first year of life
• which occurs with hypovitaminosis D, is characterized by a violation of all types
• metabolism (mineral),
• damage to the musculoskeletal system , internal organs,
• decreased body reactivity

• growth and development of the skeletal system (rickets, osteoporosis, osteomalacia)

• metabolism of calcium, magnesium and phosphorus

• Anti-spill
• ferrative effects

• Endocrine system
• (diabetes)

• Skin system
• (psoriasis, atopic dermatitis)

• renin-angiotensin-aldosterone system (RAS)

• Digestive system

• Cardiovascular system (atherosclerosis, ischemic heart disease, hypertension)

• The immune system

• Vitamin

• Helps the body control calcium and phosphorus levels
• stimulates calcium absorption in the intestines
• promotes increased serum calcium and phosphorus levels and bone mineral deposition
• stimulates bone mineral deposits
• affects bone resorption
• increases the reabsorption of phosphates by the kidneys and reduces their excretion in the urine

• Intestines
• absorption of Ca,P
• ↓Mg absorption
• Parathyroid glands
• ↓ PTH synthesis and secretion
• Bones
• bone mineralization
• Kidneys
• autoregulation of calcitriol secretion by the kidneys
• reabsorption of P in the kidneys

• The effects of calcitriol increase the concentration of calcium and phosphorus in the extracellular fluid, leading to osteoid calcification

• Effects of calcitriol

• With vitamin D deficiency, the regulation of Ca and P levels is disrupted

• When Ca and P levels in the blood become low, bone matrix destruction occurs

• Vitamin D deficiency
• Absorption of Ca, P
• Hypocalcemia
• Operation
• parathyroid glands

• Increased secretion of parathyroid hormone
• Urinary P excretion Bone decalcification
• P, Ca in blood
• Rickets

• In the initial period of rickets, the level of calcium and phosphorus in the blood decreases
• Under the influence of parathyroid hormone, calcium levels usually return to normal values, but phosphorus levels remain low
• Alkaline phosphatase, which is synthesized by hyperactive osteoblasts, enters the extracellular fluid, and its concentration also increases in the blood

• hypovitaminosis D
• exogenous or endogenous origin

• Lack of vitamin D intake from food (yolk, butter, liver);
• Lack of phosphate and calcium intake;
• Insufficient sun exposure;

• Endogenous causes:
• * Violation of absorption processes in the intestines (diarrhea, malabsorption);
• Violation of Vit D conversion processes
• into an active form (liver disease, kidney disease,
• genetic pathology);
• Impaired functional activity of vitamin D receptors (genetic pathology);
• Fast growth, increased needs
• Use of medications (antacids, anticonvulsants, loop diuretics, glucocorticoids)

• Can vitamin D deficiency occur in breastfed children???

• What are the main causes of vitamin D deficiency in children?

• Where does vitamin D transformation occur in the body?

• What are the effects of 1.25 dihydroxycalciferol on the child’s body:
• A. Increased bone mineralization
• B. Decreased secretion of parathyroid hormone
• C. Increased intestinal Ca absorption
• D. Increased P reabsorption in the kidneys
• E. All answers are correct

• Which vitamin D metabolite is formed during the first stage of hydroxylation?
• A. cholecalciferol
• B. ergocalciferol
• C. calcidiol
• D. calcitriol

• Classic vitamin D deficiency is rickets.
• Vitamin D-dependent rickets is associated with a genetic defect in the synthesis of 1,25(OH)₂D₃ in the kidneys or with resistance of target organs to it.
• Vitamin D-resistant rickets (tubulopathies, hypophosphatasia).
• Secondary rickets in liver diseases, malabsorption syndrome, etc.

• The medical history of a patient with manifestations of rickets should include the following information::
• Gestational age, dietary features (detailed nutritional history, including a survey of foods for vitamin D and Ca content), duration of sun exposure
• Family history (short stature, bone abnormalities, alopecia, dental problems, consanguineous marriages do not exclude hereditary rickets).

• Patient examination

• Head:
• craniotabes (softening of areas of the parietal bones, less often areas of the occipital bone);
• deformations of the skull bones;
• frontal and parietal tubercles “caput quadratum”; "Olympic" forehead

• Head: late closure of the large fontanel

• Head:
• eruption disorder
• teeth (untimely, incorrect),
• defects in tooth enamel.

• Head:
• Violation of the ratio
• upper and lower jaw
• Recessed nose bridge (“saddle nose”)

• Rib cage
• deformation of the clavicle (increased curvature);
• expansion of the lower aperture and narrowing of the upper one, compression of the chest from the sides;
• Scaphoid depressions on the lateral surfaces of the chest;

• pectus excavatum

• Chest deformities

• pectus carinatum

• Chest deformities

• Pelvic bones:
• Flat pelvis

• Spine:
• Kyphosis in the lower thoracic vertebrae, kyphosis or lordosis in the lumbar spine, scoliosis in the thoracic spine
• Rachitic hump (kyphoscoliosis)

• Limbs:
• upper limbs:
• curvature of the humerus and forearm bones;
• Deformation in the joint area: “bracelets” (thickening in the area of ​​the wrist joints), “strings of pearls” (thickening in the area of ​​the diaphysis of the phalanges of the fingers).

• Limbs:
• b) lower limbs:

• Marfan's sign

• Limbs:
• b) lower limbs:
• curvature of the hips forward and outward;
• various curvatures of the lower extremities (O- or X-shaped deformities);
• deformities in the joint area.

• X and O-shaped
• limbs

• Clinical
• manifestations

• Harrison's groove -
• (E. Harrison, 1766-1838, English doctor)
• deformation of the chest during rickets in the form of a transverse depression located corresponding to the line of attachment of the diaphragm

• Harrison groove

• frequent respiratory infections
• iron deficiency anemia of varying severity, latent anemia
• changes in other organs and systems (deafness of heart sounds, tachycardia, systolic murmur, atelectatic areas in the lungs and the development of prolonged pneumonia, enlargement of the liver, spleen)
• the development of conditioned reflexes slows down, and acquired reflexes weaken or completely disappear

• Laboratory signs of rickets
• Laboratory examination should include determination of levels of:
• Alkaline phosphatase
• Parathyroid hormone
• 25-hydroxyvitamin D
• 1,25-dihydroxyvitamin D

• Level Reduction:
• Blood Ca
• Blood P
• Calcidiol
• Calcitriol
• Sa urine

• The most typical laboratory signs of rickets

• Level Up:
• P urine

• Visible in almost every part of the skeleton, which manifests itself in the form of osteoporosis, but the changes of greatest practical interest are primarily in the epiphyses (heads of tubular bones).

• Reduced calcification leads to thickening of growth zones:
• "Fringed" ends of metaphyses
• “Goblet/saucer-shaped” distal parts of the radius, ulna, fibula
• Expansion of the distal parts and metaphyses

• Direct and lateral views of the wrist demonstrate the saucer shape and fringed frequency of the metaphyses

• Classic radiographic signs of rickets

• X-ray of the knee joint shows “fringe frequency” (discharge) of the metaphyses

• Decalcification of bone ends - porosity, fringe, saucer-shaped

• (A) Rickets in a 3-month-old child

• (B) After 28 days of treatment

• (C) After 41 days of treatment

• In the bones of the limbs:
• radiologically visible darkening of the marginal line of the bone;
• delayed development of bone growth points;
• decreased density, delamination of the periosteum or curvature of the diaphyses of long bones.

• X-ray signs

• Fractures of the ulna and radius

• Rachitic changes in the distal radius and ulna

• X-ray signs of rickets

• Initial period
• The first symptoms of rickets are autonomic disorders (age 3-4 months):
• sleep disorders;
• irritability;
• tearfulness;
• increased sweating: most of the face, scalp;
• “sour” sweat → rubbing the head on the pillow → baldness of the back of the head;
• Red dermographism.
• Bone compliance - edges of the greater fontanelle → lesser fontanelle → sagittal suture (minor osteoporosis).

• Alopecia of the back of the head

• Laboratory signs:
• Ca, P - N or ↓ insignificant
• ALP - N or slightly
• 25-OH-D3 ↓
• X-ray signs:
• absent or minimally expressed

• Initial period

• Changes in the nervous system, skin Changes in the bone system:
• 3 months – skull bones;
• 3-5 months – chest,
• 6-8 months – limbs;
• Scull: craniotabes, flattening of the occiput, softening of the bones of the skull, the edges of the fontanelle, enlargement of the frontal and parietal tubercles;
• Rib cage: rachitic “rosary”, deformation of the HA, spine, Harrison’s groove, loose joints;

• Changes in the bone system: 6-8 months – limbs ( O-or X-shaped curvature), pelvic bones;
• Muscle c-ma: hypotonia of the abdominal muscles, “frog belly”, diastasis

• lungs– reduced excursion, tachypnea,
• violation of the towing function;
• cardiovascular system– tachycardia, expansion of the heart’s boundaries, weakened sounds;
• digestive organs-  appetite,  enzyme activity, flatulence, changes in bowel movements;

• Hypophosphatemia - P in the blood  (up to 0.48 mmol/l);
•  P in urine – hyperphosphaturia;
• Hypocalcemia - Ca in the blood  (up to 2.00-2.20);
• Increased level of alkaline phosphatase - ;
• Acidosis;
• Anemia,  immunological reactivity;
• X-ray: osteoporosis, goblet expansion of the metaphyses;

• High period

• Reverse development:
• Decrease in neurological
• vegetative changes.
• Saved: muscle hypotonia, bone deformities
• Laboratory: P, alkaline phosphatase – normal
• Sa – reduced;

• After suffering from rickets II, III century. bone deformities remain
• Diagnosis after 2-3 years of age

• All clinical symptoms disappear.
• Biochemical and radiological abnormalities are restored.

• I - mild: changes in the nervous system, bone changes in one part of the skeleton ;
• II – moderate severity: changes in all organs and systems , changes in two parts of the skeleton
• III - severe: dysfunction of all organs and systems , changes in three parts of the skeleton

• Severity of rickets

• The processes of osteomalacia predominate ( craniotabes, increase in size of BR, open MR, deformation of the bones of the skull, collarbones, pelvis, chest);
• Often in children of the first half of the year;
• Carbohydrate nutrition (cookies, porridge)

• Predominance
• osteoid hyperplasia
• (enlargement of the frontal, parietal tubercles; rachitic “rosary”, thickening of the epiphyses of the bones of the forearm (rachitic bracelets, strings of pearls);
• Gradual onset;
• Often in children with malnutrition;

• Alternating periods of exacerbation and improvement;
• Ro-logically – the presence of several zones of calcification in the metaphyses;
• Relapses in intercurrent diseases;

• Rickets II degree,
• subacute course,
• peak period

• Type 1
• Autosomal recessive
• Mutation in the gene encoding the kidney enzyme 1-hydroxylase, which converts 25-hydroxyvitamin D3 to the active metabolite 1,25-dihydroxyvitamin D3
• Observed in the first 2 years of life
• Clinical signs are the same as for classic rickets

• Vitamin D-dependent rickets

• Type 2
• Autosomal recessive
• Mutation in the gene encoding the vitamin D receptor, which mediates the physiological response to the active metabolite 1,25-dihydroxyvitamin D3
• Alopecia – 50-70%

• A defective gene on the X chromosome, but female carriers of this gene are affected (X-linked dominant type)
• Clinical signs: limb deformities, growth retardation - leading symptoms, delayed teething, dental abscesses, hypophosphatemia
• Laboratory signs - hyperphosphaturia, hypophosphatemia, alkaline phosphatase, PTH and Ca - are normal.
• Treatment – ​​P, calcitriol

• Vitamin D-resistant rickets
• (X-linked hypophosphatemic rickets)

• A 6-year-old boy with vitamin D-resistant rickets

• A 6-year-old boy with renal tubular acidosis

• Prevention
• Rickets
• Antenatal

• Prevention
• rickets
• Antenatal

• Prevention
• rickets
• Postnatal

• Prevention
• rickets
• Postnatal

• Prevention
• rickets
• Postnatal

• Prevention
• rickets
• Postnatal

• Vitamin D3
• 2000-5000 IU/day
• within 30-45 days
• with transition to a prophylactic dose

• Lightweight
• degree – 2000 IU
• Average degree
• severity - 4000 IU
• Severe – 5000 IU/day

• Vitamin D3
• (Cholecalciferol)
• Water solution
• 1 drop –
• 500 IU Vit D3
• Videin-3,
• 1 tablet – 2000 IU

• Microcephaly;
• Small sizes of BR;
• Birth injury;
• Intracranial hemorrhage;
• Pathological jaundice;

• Calcium preparations –
• Daily dose
• 100-200 mg/day
• calcium glycerophosphate,
• calcemin
• 0.1 x 2 times / day,
• 3 weeks;
• Products,
• enriched with Ca:

• To normalize the function of the parathyroid glands - magnesium preparations (panangin, asparkam) - 10 mg/kg/day, 3 weeks;
• To stimulate metabolic processes -
• Potassium orotate – 10-20 mg/kg/day
• 20% carnitine hydrochloride 4-12 k. 3 times/day;
• 1% ATP – 0.5 ml IM No. 15

• Vitamins: A, B, C, E
• Massage, exercise therapy;
• Pine baths
• (1 tsp extract
• for 10 liters of water);
• Salt baths (2 tablespoons per 10 liters of water);
• Aromatic baths (plantain, string, calamus root, chamomile, oak bark);

• is a disease characterized by the tendency of a child during the first 6-18 months. life to convulsions and spastic conditions, which are pathogenetically associated with rickets. It is observed mainly in boys, most often in early spring, with increased insolation.

• hypocalcemia due to electrolyte imbalance and alkalosis, caused by a rapid, almost sudden increase in the amount of the active metabolite of vitamin D in the blood.
• when taking a large dose of vitamin D2 or D3 simultaneously (“impact” method of treatment),
• with prolonged exposure of large areas of bare skin to the spring sun, the radiation of which is especially rich in ultraviolet rays.
• Dysfunction of the parathyroid glands,
• decreased absorption of calcium in the intestine or increased excretion in the urine.
• decrease in blood levels of magnesium, sodium, chlorides, vitamins B, B6.

• Latent form

• Trousseau's sign -
• compression of the neurovascular bundle in the area of ​​the biceps groove with the help of a cuff causes convulsive contraction of the fingers (obstetrician’s hand)

• Maslov's symptom - respiratory arrest with a slight skin prick
• Erb's symptom (increased excitability to galvanic current) - when a cathode is applied to the area of ​​the perineal or median nerve, muscle contraction appears at a current strength below 5 mA.
• Lust's sign - pressure on the perineal nerve below the head of the fibula causes flexion and abduction of the foot.

• 1. Laryngospasm

• 2. Tetany or carpopedal spasm
• 3. Eclampsia

• Tetany is one of the most common forms of spasmophilia. It is characterized by carpopedal spasms: the hand is bent, the thumb is brought to the palm, the rest are extended and tense (obstetrician's hand). Feet in equinovarus position. These cramps last for several hours, and sometimes days, and are painful. Swelling often appears on the extremities. Carpopedal spasms can be combined with general tonic convulsions, convergent strabismus, tension in the facial muscles (tetanic face) and neck muscles.

• Laryngospasm is manifested by convulsive tension of the vocal cords and closure of the larynx, which leads to respiratory failure (expiratory apnea). The child throws his head back, turns pale, and cyanosis of the mucous membranes appears. Then the spasm weakens, a noisy inhalation occurs and the child’s condition improves. If the spasm continues for a long time, there may be loss of consciousness and general tonic-clonic convulsions.

• At elevated temperatures or in complete health, tonic-clonic or clonic convulsions occur with loss of consciousness.

• First aid
• For laryngospasm, pat the child’s cheeks and wash the child with cold water;
• For convulsions - Seduxen (0.5% solution, 0.1 mg / kg), simultaneously with calcium preparations - 20 mg / kg intravenously for 10-20 minutes
• or 2 ml/kg 10% calcium gluconate, 0.7 ml/kg 10% calcium chloride
• II. Nutrition correction
• III. Calcium preparations (10% calcium gluconate 50 mg/kg/day).
• After normalizing the level of calcium in the blood, treatment of rickets with vitamin D3 (2000-5000 IU for 30-45 days, depending on the severity of rickets).

• Hypervitaminosis D
• is caused by hypercalcemia and manifests:
• Nausea and vomiting
• Thirst and polyuria
• Pain in joints and muscles
• Confusion and coma

• Calcification of soft tissues
• Lungs, heart, blood vessels
• Hypercalcemia
• Elevated calcium levels in the blood lead to the formation of kidney stones formation in kidneys
• Loss of appetite
• Thirst and polyuria

• Thank you for your attention!

Rickets (Greek rhahis - spinal ridge) is a disease of infants and young children with a disorder of bone formation and insufficiency of bone mineralization, the leading pathogenetic link of which is a deficiency of vitamin D and its active metabolites during the period of the most intensive growth of the body.

Vitamin D resistant rickets (phosphate diabetes). The classic type of vitamin D-resistant rickets has a dominant, X-linked type of inheritance. The genesis of the disease is associated with the shutdown of the regulatory gene of the X chromosome (HYP gene) for the synthesis of phosphate transport protein. This defect is associated with a disruption of the synthesis of 1, 25 dihydroxyvitamin in the kidneys, although it is secondary. Disturbances in the active transport of phosphates in the renal tubules create their constant deficiency, which leads to the formation of rickets-like changes in the skeleton. Pathogenetic mechanisms for the development of the disease include: 1) a primary defect in phosphate reabsorption in the renal tubules; 2) secondary disruption of activation processes by vitamins D; 3) a combined defect in the reabsorption of calcium and phosphorus in the intestines and kidneys.

Most often, the first signs of the disease appear in the second year of life and are progressive. Less commonly, manifestation is at the end of the first year of life or even at 6-10 years of age. Clinical manifestations. The leading signs of the disease are rickets-like changes in the skeleton, mainly in the lower extremities, such as varus deformities and general osteoporosis. There is a delay in physical development and a disturbance in the child’s gait (“duck walk”). Skeletal lesions are progressive in nature and contribute to a delay in the development of static motor functions of a sick child. In 50% of patients, Arnold Chiari anomaly is detected - ectopia of the cerebellar tonsils, their displacement into the spinal canal, but in most children it is not clinically manifested. The intellectual development of children is not impaired.

X-ray changes in bones are detected 3-4 months after the manifestation of the disease: generalized osteoporosis, enlargement of the metaphyses, metaphyseal surfaces have uneven contours, and as the disease progresses, deeper changes appear.

Vitamin D-resistant rickets is characterized by clinical polymorphism. There are 4 clinical and biochemical variants of the disease: Option 1 – characterized by early manifestation (in the first year of life) of the disease, a slight degree of bone deformation, good response to treatment with vitamin D. Option 2 – characterized by later manifestation (in the second year of life), pronounced bone changes, resistance to high doses of vitamin D. Pathogenesis is due to a predominant defect of the renal tubules (decreased phosphorus reabsorption) and losses of phosphates mainly in the urine. Option 3 is characterized by late manifestation of the disease (after 6 years of age), severity of skeletal abnormalities, and pronounced resistance to vitamin D. The pathogenesis of this option is associated with the predominant involvement of the intestine in the pathological process, impaired intestinal absorption of calcium and osphorus. f 4th variant – characterized by increased sensitivity to vitamin D and a tendency to develop hypervitaminosis D. The first clinical signs of the disease are detected in the second year of life and are characterized by a moderate degree of bone deformation.

Characteristic biochemical signs of phosphate diabetes: hypophosphatemia - 0.5 0.7 mmol/l (with a norm of 1.0-1.6 mmol/l); Hyperphosphaturia – more than 20 mmol/day; high renal phosphate clearance; normal serum calcium levels; blood alkaline phosphatase activity increased by 1.5-2 times; normal level of parathyroid hormone in the blood; reduced level of 1.25 dihydroxyvitamin D 3.

Treatment should be early, comprehensive, aimed at correcting metabolic disorders, preventing complications and disability of the child. The basic drugs are vitamin D and its synthetic analogues. Initial doses of vitamin D are 10,000 to 15,000 IU per day. Increasing doses is carried out under the control of the level of calcium and inorganic phosphates in the blood serum and urine, the activity of blood alkaline phosphatase, which should be examined every 10-14 days. An increase in the level of phosphates in the blood serum, a decrease in the clearance of urine phosphates and indicators of blood alkaline phosphatase activity, as well as the restoration of bone tissue structure according to X-ray data, gives grounds not to increase the dose of vitamin D. Maximum daily doses of vitamin D depending on the clinical and biochemical variants of vitamin D-resistant rickets , linked to chromosome X, are: with the 1st variant of pathology - 85,000 100,000 ME, with 2 m, 150,000 200,000 ME, with 3 m - 200,000 300,000 ME. With option 4, the administration of vitamin D is contraindicated. In the autosomal dominant form of the disease, the daily dosage of vitamin D is 15,000–45,000 IU.

Vitamin D metabolites include oxidevit, alfacalcidiol (alpha D 3 Teva), calcitriol (osteotriol) in a daily dose of 0.25 3 mcg. When prescribing them, strict control of blood calcium levels is necessary (determination once every 7-10 days). Contraindications for therapy with vitamin D and its metabolites: individual intolerance to vitamin D; severe hyperkaliuria (more than 3.5-4 mmol/day); absence of active rachitic process according to laboratory and x-ray studies of bones. To improve the absorption of phosphorus and calcium in the intestine, long-term use of citrate mixtures (citric acid 24.0, sodium citrate 48.0 and distilled water 500.0) is recommended, 20-50 ml per day.

Indicators of the effectiveness of conservative therapy are: improvement in the general condition of the child; accelerating the growth rate of patients; normalization or significant improvement in phosphorus-calcium metabolism; decreased alkaline phosphatase activity in blood plasma; positive dynamics of structural changes in the skeletal system according to X-ray examination of bones.

Vitamin D dependent rickets is a disease with an autosomal recessive type of inheritance. There are 2 types of vitamin D dependent rickets, the genes of both types of the disease are mapped on chromosome 12: type 1 - associated with a deficiency of 25 oxycholecalciferol 1 hydroxylase in the kidneys and insufficient formation of 1, 25 dioxycholecalciferol in the body; Type 2 - due to the insensitivity of target organ receptors to 1.25 dioxycholecalciferol, while the synthesis of this metabolite is not impaired.

The pathogenetic mechanisms of the first type of disease are associated with a violation of the conversion of 25 oxyvitamin D 3 into 1, 25 dioxyvitamin D 3 in the kidneys. Schematically, the pathogenesis of type 1 vitamin D dependent rickets can be represented as follows: deficiency of 1 alpha hydroxylase of the kidneys Þ insufficient synthesis of 1, 25(OH) D 3 Þ impaired absorption of calcium in the intestine Þ hypocalcemia Þ secondary hyperparathyroidism Þ disturbance of phosphorus metabolism Þ rickets-like skeletal changes. The genesis of vitamin D dependent rickets of the second type is associated with a mutation of the receptor gene for 1, 25 dihydroxyvitamin D 3 in target organs - the intestines, kidneys, bone tissue, skin, hair follicles. Unlike vitamin D dependent rickets type 1, in this type of disease the formation of vitamin D metabolites is not impaired. Therefore, the plasma level of 1.25 dihydroxyvitamin D 3 remains either normal or even elevated.

Clinical manifestations. Vitamin D dependent rickets manifests itself in the first 3–5 months of a child’s life and is progressive in nature, despite previous prevention of rickets or antirachitic treatment. Less commonly, the disease may begin at 5–6 years of age or later. The first signs of vitamin D-dependent rickets are characterized by functional changes in the nervous system (sweating, sleep disturbances, trembling, etc.), which are later joined by bone changes (deformities of the lower extremities, often saber-shaped or varus types, chest, skull, rachitic " rosary beads, bracelets), as well as muscle hypotonia. Sometimes short-term convulsions are observed, often provoked by hyperthermia. Clinical signs of the disease progress, and by the end of the first year of life the full symptom complex of vitamin D dependent rickets becomes pronounced. With vitamin D dependent rickets of the second type, the above clinical picture of the disease is often accompanied by total baldness, which occurs at the age of 14-16 months of life.

Biochemical disorders: hypocalcemia (1.7 2.0 mmol/l); normal or slightly reduced level of inorganic phosphates in blood serum (0.8 0.9 mmol/l); increased activity of blood alkaline phosphatase; a significant decrease in calcium excretion in the urine (up to 0.3 mmol/day at a rate of 1.5 mmol/day or 0.15 mmol/kg body weight); generalized hyperaminoaciduria (daily excretion of amino acids in urine can reach 1-1.5 g).

Differential diagnosis. The greatest difficulties arise in distinguishing between vitamin D-dependent rickets and ordinary vitamin D-deficient rickets. The main arguments in favor of vitamin D dependent rickets are: the progressive nature of bone deformations, despite traditional antirachitic treatment; low serum calcium levels; normal content of 25 hydroxyvitamin D 3 in the blood; normal level is 1.25 dihydroxyvitamin D 3 for type 2 disease.

Features of therapy. Oxidevit, alphacalcidiol (alpha D 3 Teva), which are 1 α hydroxyvitamin D 3, are used. The daily dose is 0.5 3 mcg. Once in the body, this drug is hydroxylated in the liver to form 1.25 dihydroxyvitamin D 3. The use of calcitriol (osteotriol), which is an analogue of the active metabolite of vitamin D - 1.25 dihydroxycholecalciferol, increases the effectiveness of treatment. In vitamin D dependent rickets of the second type, the therapeutic effect from the use of vitamin D metabolites is observed only with high doses - 2-10 mcg per day and the use of calcium supplements. In the absence of active vitamin D metabolites, vitamin D can be used, but with less clinical effect. Initial doses are 10,000-15,000 IU, maximum - 40,000-60,000 IU per day. The treatment complex includes calcium and phosphorus preparations, vitamins A, C, E, citrate mixtures, in courses of 3-5 months.

When using vitamin D preparations and its active compounds, it is necessary (once every 10-14 days) to monitor the levels of total calcium and inorganic phosphates in the blood serum and their excretion in the urine. An increase in the level of calcium in the blood more than 2.8 mmol/l or its excretion in the urine above 6 mg/kg (0.15 mmol/kg) indicates the development of hypervitaminosis D and requires discontinuation of the drug. Re-prescription of vitamin D or oxidevit is possible only after 7-10 days at half (the original) dose with clinical and laboratory monitoring.

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