Phosphorus-calcium metabolism and its regulation. The main functions of calcium in the body
The formation of the bone skeleton, which, like a strong frame, holds the entire body, is a very long process. Its effectiveness depends on factors such as the functioning of internal organs, the content of certain chemical substances in the blood and the general condition of the child's body. And yet the most important condition for the normal and full development of bones is the proper functioning of phosphorus-calcium metabolism. Vitamin D is equally important for the formation of the skeleton.
Bones begin to form in fetal development in the first weeks of pregnancy, and by the end of the 15th week, the body of the unborn child and its bone apparatus are already fully formed. But this process continues long time until puberty in adolescence. Therefore, very important attention must be paid to sufficient intake of calcium, phosphorus and vitamin D already during pregnancy.
On the role of calcium in the body:
Calcium is an element that is present in sufficient quantities in the human body. Bones are 99% calcium. In addition, it is responsible for the normal functioning of nerves, muscles and is involved in the regulation of blood clotting. Calcium is also extremely important for the proper formation and growth of teeth in a child.
Calcium enters the body mainly with food - milk and dairy products.
Important! The daily requirement for calcium is:
In children from 0 to 6 months, 400 mg per day;
- In infants from 6 months to 1 year - 50 mg per 1 kg of body weight. So, a baby in the second half of life should receive about 600 mg of calcium per day. Please note that 100 ml of breast milk contains 30 mg of calcium, and 100 ml cow's milk- 120 mg of calcium;
- From 1 year to 10 years - 800 mg of calcium per day;
- Children aged 11 to 25 years - 1200 mg per day.
About the role of phosphorus:
Phosphorus makes up no more than 1% of the human body weight. About 85% of it is concentrated in the bones, and the rest in the muscles and tissues in the form of compounds. Foods rich in phosphorus are meat and milk. An extremely important element for the formation of musculoskeletal tissue and teeth.
Important! The daily requirement of children for phosphorus is:
From 0 to 1 month - 120 mg;
- From 1 to 6 months - 400 mg;
- From 7 to 12 months - 500 mg;
- From 1 to 3 years - 800 mg;
- From 4 to 7 years - 1450 mg.
It is important to understand that when breastfeeding, the baby's need for phosphorus is fully satisfied with mother's milk.
Features of bone formation:
The absorption of phosphorus and calcium occurs in the intestine. From normal functioning The mucous membrane of the digestive system depends on the success and completeness of absorption. Phosphorus and calcium are transported through the intestinal wall with the help of certain chemical compounds-vitamin D3 or parathyroid hormone produced by the parathyroid glands.
Important! First of all, diet is important to maintain normal levels of calcium and phosphorus in the body. The optimal ratio of calcium and phosphorus in the food consumed should be 2:1, respectively. That is, calcium should be supplied 2 times more than phosphorus.
It must be borne in mind that with a large amount of calcium, hypercalcemia may develop. This condition is dangerous because, against the background of an increase in the amount of calcium, an acute shortage of phosphorus develops, and calcification of internal organs occurs.
With an excess of phosphorus, hypocalcemia develops. In the early stages of such a disease, the body can cope on its own, but with a protracted course, there is a violation of bone mineralization and their curvature.
It greatly affects the formation of the bone skeleton and the process of assimilation of fats. As a result of diseases of the liver, pancreas, the likelihood of violations in the formation of the bone skeleton increases.
An important factor that interferes with the normal absorption of calcium is the so-called alkalization of the digestive tract. This phenomenon occurs when taking enveloping drugs, an excessive increase in the amount coli. Such disorders most often affect children who are artificially fed with mixtures based on cow's milk. This is easily explained by the fact that when feeding with a mixture, calcium enters the body in the form of insoluble salts and is excreted very quickly.
Phosphorus is absorbed much worse with increased acidity of the intestine, as well as with an excess of calcium and magnesium in the body.
Depot calcium and phosphorus:
After absorption, calcium and phosphorus are distributed throughout the body, including to the bones. There, calcium is deposited in two forms: easily removed and difficult to remove deposits. Of the easily soluble compounds, calcium easily returns back to the blood in the event of hypocalcemia or increased acidity of fluids inside the body.
Important! Increased acidity of the blood develops with prolonged ailments of the child, for example, with diarrhea. This leads to a significant decrease in the content of calcium and phosphorus in bone tissue baby. Thanks to this process in the body, it is possible to short time normalize the pH level. Stocks of spent trace elements must be restored with baby food.
In children suffering chronic diseases, in which the pH level in the blood is significantly disturbed (diseases gastrointestinal tract, kidneys) develop very dangerous violations of this regulatory mechanism. As a result, there are serious violations phosphorus-calcium metabolism, which leads to a significant slowdown in the growth of the child due to excessive leaching of calcium and phosphorus from bone tissue.
The mechanism of excretion of phosphorus and calcium:
The final link of phosphorus-calcium metabolism in the body of a child is the kidneys. They filter vital blood important elements including calcium and phosphorus. They, depending on the needs of the body, either return to the blood or are excreted in the urine from the body.
Important! The factors that ensure the smooth operation of this system are a sufficient amount of vitamin D3 and parathyroid hormone, as well as the proper functioning of the kidneys. If one of these three factors is disturbed, a rather strong violation of the metabolism of phosphorus and calcium develops.
In young children, the main manifestations of such disorders are softening of the occipital bones and excessive sweating.
About Vitamin D:
Under the influence of ultraviolet rays, 7-dehydrocholesterol contained in human skin is converted into its active form - cholecalciferol (in this case, a slight burn appears on the skin, which we refer to as sunburn). This is the best form of vitamin D3 for the body.
Important! It is impossible to artificially reproduce cholecalciferol. Taken as part of multivitamins or in monocomponent products, it is inactive and is mostly deposited in adipose and muscle tissues.
One part of vitamin D3 is metabolized in the liver and the excess is excreted in the bile or kidneys from the body. The other part is metabolized in the kidneys. It is this form that is active and has a direct effect on the organs that are involved in phosphorus-calcium metabolism. The renal metabolite of vitamin D3 is responsible for the proper absorption of calcium and phosphorus and other substances in the intestines and their fixation in bone tissue.
With an excess of vitamin D3, part of it is deposited in the muscles in the active form.
Important! With a significant increase in the content of vitamin D3 in the body, poisoning of the child develops. There are babies who experience signs of poisoning even with normal amounts of vitamin D3. This is due to their characteristics and predisposition. These children require less cholecalciferol.
Symptoms of a violation of phosphorus-calcium metabolism:
Regardless of the causes of such disorders in the initial stage, they are almost asymptomatic.
Symptoms of a violation of the metabolism of phosphorus and calcium in the body are as follows:
Increased perspiration in the occiput or other parts of the head. This is the very first sign that may indicate disorders in the metabolism of phosphorus and calcium. Thus, the body begins to more intensively remove chloride ions from the body both with urine and sweat, in order to compensate for the imbalance;
The back of the baby's head becomes flat and soft to the touch. If such symptoms are observed, then it is already safe to talk about the presence of a malfunction in the exchange of calcium and phosphorus in the baby's body;
Bone deformity. It develops, as a rule, if no measures have been taken to eliminate metabolic disorders;
Bone fractures. This is a very serious and dangerous complication of the disease, which requires a fairly long or lifelong treatment.
signs high content vitamin D3 in the body:
Strong thirst. Accordingly, the child very often asks for a potty or urinates on a diaper;
- Increased separation of urine;
- Lack of appetite;
- Increased anxiety of the baby;
- Sleep disorders;
- Regurgitation;
- Vomit;
- Decreased muscle tone;
- No increase in body weight;
- Hidden symptoms: calcification of the kidneys, kidney stones, high blood pressure.
Diagnostics:
It is very important that the doctor establishes as soon as possible exact reason violations of phosphorus-calcium metabolism in a child. This will make it possible to prescribe timely and correct treatment.
When collecting an anamnesis, the doctor must ask the parents what the baby eats. If the child is breastfed, then the mother's diet is specified.
Next, it turns out if the baby has problems with the digestive tract, as this can lead to malabsorption of vital important trace elements. As a result, the formation of bones in the baby will be disrupted.
In addition to the survey, the doctor prescribes a number of tests, among which the following are considered very informative:
fecal studies;
smears for bacteriological examination;
Urinalysis to detect excreted calcium from the body. For this analysis, urine is collected in the morning on an empty stomach. Based on the results of this analysis, the doctor concludes that there is hypercalciuria, which is associated with a very high content of vitamin D3 in the body;
Blood test, which consists in determining the level of calcium, phosphorus and alkaline phosphatase- an enzyme that indicates the growth of new cells in the baby's bone tissue). Thanks to this analysis, it is also possible to establish the correct functioning of the liver and kidneys;
Blood and urine tests to determine the correct functioning of the steam thyroid gland;
Determination of the level of vitamin D3 and its metabolites. This analysis is optional. But it may be necessary if it is not possible to establish the cause of violations of phosphorus-calcium metabolism in the child's body. This analysis is very complex and requires state-of-the-art equipment.
Treatment:
Important! Never give your baby own will drops containing vitamin D3, since its excess in the body is very dangerous. Any treatment should be prescribed only by a doctor after a preliminary examination.
The main directions of treatment of any disorder of calcium and phosphorus metabolism are as follows:
Proper diet. Depending on the problem, the doctor will recommend products that should be given preference, and which ones should be abandoned or limited;
- Calcium is found in large quantities in such foods: fresh vegetables (beets, celery, carrots, cucumbers), fruits and berries (currants, grapes, strawberries, strawberries, apricots, cherries, pineapples, oranges, peaches), nuts, meat, liver, seafood, dairy products.
Phosphorus is rich in foods such as cheese, cottage cheese, liver, meat, legumes, cauliflower, cucumbers, nuts, eggs, seafood
- Additional intake of vitamin D3 in the composition medicines(monocomponent or complex multivitamin) with an established deficiency;
- Additional intake of drugs containing daily or increased doses of calcium and phosphorus;
- Means for the treatment of pathologies that are the causes of violations of phosphorus-calcium metabolism in the baby's body.
Vitamin D3 Requirements:
Very important for a small child is the amount of vitamin D that the mother received during pregnancy, especially in the third trimester.
Important! Full-term, healthy babies whose mothers take adequate amounts of vitamin D usually do not require additional amounts from food.
Babies who are breastfed most often do not experience problems with calcium deficiency. After all, the calcium that is contained in breast milk is best absorbed in the body of a newborn baby.
Children who are fully or partially formula-fed receive additional vitamin D from formula milk. Its concentration in them, as a rule, is about 400 IU. That is, one liter of the mixture contains daily rate vitamin D.
Vitamin D3, which is present in the skin of a child, covers the daily requirement by 30%. In those areas where there is a very large number of sunny days, such coverage is possible up to 100%.
Important! Be sure to monitor the amount of vitamin D3 that the baby receives from food. If there is a deficiency, be sure to compensate for it.
Important! The oral drops contain 300 IU of vitamin D3.
Take care of the health of your kids! They are your best!
When we talk about rickets, we first of all mean vitamin D deficiency (vitamin D-deficient rickets). Children of the first months of life fall ill with such classic rickets as a result of feeding defects and violations of the general daily regimen.
Rickets used to be more common in children living in poor living conditions, without enough fresh air and natural ultraviolet radiation. Undoubtedly, these factors play a leading role in the development of the disease. However, now rickets is much more common, in almost every second child, since predisposing factors have become more common: prenatal development, intrauterine fetal hypoxia and other perinatal diseases.
Rickets is a disease of the whole organism and is accompanied by significant changes in all types of metabolism. Even mild forms of rickets with subtle manifestations change the reactivity of the child's body, lowering its resistance. The ego creates the preconditions for the emergence of a number of other diseases, often occurring with various complications. Therefore, rickets is the so-called "unfavorable background." Vitamin D-deficient rickets contributes to the severe course of concomitant diseases, slowing down the pace of physical and neuropsychic development, and can be the cause of irreversible bone changes, for example, pelvic bones, which is of no small importance in girls.
The main cause of rickets is a deficiency, or hypovitaminosis D, which occurs in a child as a result of a violation of the natural synthesis of vitamin D in the skin and insufficient intake of it with food. For full-term breastfed infants, the daily requirement for vitamin D is 150-400 IU/day, for premature infants who are bottle-fed - 800 IU/day or more. The immediate causes of vitamin D deficiency is insufficient formation of it in the skin from provitamin under the influence of ultraviolet rays. The formation of vitamin D is hampered by exposure to diffused light, dusty air, excessive wrapping of children. The second important factor is not balanced diet, not balanced in the amount of protein, calcium and phosphorus, with an excess of fat or predominantly vegetable. Vitamin D is found in egg yolk, butter, liver of fish and birds. There is little of it in women's and cow's milk. But in women's milk, it is in an active form and is completely absorbed by the child's body. In addition, breast milk has the most optimal ratio of calcium and phosphorus.
Rickets is promoted by the rapid growth characteristic of children in the first months of life, but especially premature ones, as well as prolonged infectious and gastrointestinal diseases, lack of physical and emotional activity of children.
In the development of the disease, the leading role is played by a violation of phosphorus-calcium metabolism, a violation of bone formation and their calcification caused by vitamin D deficiency. Bone changes occur in areas of the most intensive growth.
Rickets may be secondary to diseases of the digestive system that contribute to malabsorption of vitamin D.
The first manifestations usually occur at the 2-3rd month, in premature babies - earlier. Early manifestations are associated with dysfunction nervous system against the background of a reduced level of phosphorus (anxiety, sweating, mild excitability in response to weak stimuli, softening of the seams and edges of the fontanelle, muscular dystonia). After 2-6 weeks, the peak period of rickets begins, which is characterized by more pronounced disorders, the child becomes lethargic, inactive, there is a decrease in muscle tone, skeletal changes develop (flattening of the occiput, change in configuration chest, frontal and parietal tubercles appear, thickenings in the wrist area). When examining a child, one can see thickenings on the ribs resembling beads - “rachitic rosaries”, on the child’s arms in the wrist area thickenings of bones are determined - “rachitic bracelets”, as a result of relaxation of the muscles of the abdominal wall, the stomach increases - “frog belly”. On x-rays, you can see rarefaction of bone tissue - osteoporosis. In the blood, the content of calcium (hypocalcemia) and phosphorus (hypophosphatemia) is reduced.
Treatment is carried out with vitamin D for 30-45 days against the background of a diet and regimen adequate for age, vitamin therapy (C, B). Courses of massage, exercise therapy, ultraviolet irradiation, salt and coniferous baths are held.
Under the influence of treatment, the general condition improves, neurological signs are eliminated, and the violation of muscle tone (dystonia) and skeletal deformity persist much longer.
With mixed and artificial feeding, appropriate nutrition correction is necessary. In addition, with rickets, it is recommended to introduce complementary foods 1-1.5 months earlier than healthy children. The first complementary foods are introduced from 3.5-4 months and always in the form of vegetable puree with yolk; the second complementary food - porridge on vegetable broth - from 4.5-5 months; at 5 months - the liver; at 6-6.5 months - meat in the form of mashed potatoes.
Prevention. From the first days of life, children need a rational diet and nutrition, preventive courses of vitamin D 500 IU once a day, excluding the summer months.
Hereditary rickets-like diseases
Rickets-like diseases have similar symptoms with rickets - a group of diseases whose symptoms are similar to rickets, but are not associated with a deficiency of vitamin D entering the body. Skeletal anomalies are their leading manifestation.
Such diseases include phosphate diabetes, hypophosphatasia, achondroplasia.
Phosphate diabetes
(hypophosphatemic vitamin D-resistant rickets)
Phosphate-diabetes is a hereditary disease transmitted in a dominant type linked to the X chromosome, manifested by severe disorders of phosphorus-calcium metabolism, which cannot be restored with normal doses of vitamin D. There is an assumption that the disease is associated with the pathology of enzymes that ensure the absorption of phosphates in the renal tubules .
The characteristic laboratory signs of this disease are a decrease in phosphates in the blood with their simultaneous increase in the urine (4-5 times) and no change in the calcium content in the blood.
Phosphate diabetes has similar features to vitamin D-deficient rickets, but differs from it in that the general condition of the child remains satisfactory. The disease affects mainly the lower extremities - the bones are bent and the knee and ankle joints are deformed.
Signs of the disease begin to appear towards the end of the first year of life, when the baby begins to stand and walk, and are clearly detected after the second year of life.
With a timely diagnosis and no treatment, the child becomes disabled - he cannot move.
When a child is diagnosed, they are treated large doses vitamin D, several times higher than those in classic rickets. With the improvement of the child's condition, the doses are gradually reduced. Great importance has an additional intake of phosphorus with food and as part of medicines.
The risk of re-birth of a child with this pathology is 50%.
Debre de Toni-Fanconi syndrome
Debre de Toni-Fanconi syndrome is a hereditary disease, also characterized by rickets-like changes, but, unlike phosphate diabetes, it manifests itself with more severe symptoms - malnutrition, a decrease in resistance to infections. Signs of the disease are growth retardation (nanism) and changes in the composition of the urine. Increase in urine of phosphates, glucose, amino acids, calcium is characteristic.
The disease begins to manifest towards the end of the first year of life, when the child begins to stand and walk. There is a delay in the increase in height and body weight, signs of rickets and muscular hypotension, frequent infectious diseases.
Treatment consists in prescribing high doses of vitamin D, increasing the protein content in the baby's diet. The child must be under the supervision of a pediatrician.
The prognosis may be unfavorable - mortality is high due to acute renal failure.
Achondroplasia
Achondroplasia (chondrodystrophy, Parro-Marie's disease) is a congenital genetically determined disease that manifests itself in damage to cartilage tissue and leads to various kinds deformities and shortening of the bones. The cause of the disease is still unclear.
The disease manifests itself as dwarfism. Along with the lag in growth, O-shaped deformities of the femoral and tibia(type "riding breeches"). The bones are flattened in diameter and twisted. The appearance of the skull is characteristic: a large head with prominent frontal and parietal tubercles.
Surgical treatment to correct deformities.
The prognosis for functions is usually favorable.
Prevention of the disease is medical genetic counseling.
Hypophosphatasia
Hypophosphatasia is a rare autosomal recessive hereditary disease caused by the absence or decrease in the activity of the phosphatase enzyme.
An early malignant form can be detected already in the neonatal period and in children under one year old. It is similar to the manifestations of classical rickets in bone changes, anxiety of the child, increased sensitivity to external stimuli, mouse hypotension, and a decrease in blood phosphates, but it differs in a more malignant course. The bones of the skull become soft, the limbs are short, deformed. There may be fever, convulsions.
Signs of the disease sometimes disappear spontaneously as the child matures. In severe cases, death from kidney failure can occur early.
Prevention of the disease is medical genetic counseling.
Hypervitaminosis D (D-vitamin intoxication, vitamin D poisoning)
This disease is caused by an increase in the content of calcium in the blood and changes in organs and tissues due to an overdose of vitamin D or individual hypersensitivity to it.
An overdose of vitamin D may result from the use of uncontrolled repeated courses of vitamin therapy, the use of vitamin D in the summer in combination with ultraviolet irradiation, calcium preparations, the use of a large amount of cow's milk and cottage cheese. The development of the disease is facilitated by increased sensitivity to this drug as a result of the prevention of rickets in the prenatal period, especially in conditions of fetal hypoxia, unbalanced nutrition of a pregnant woman with an excess of calcium or phosphorus in food, deficiency of complete protein, vitamins A, C and group B.
Calcium is deposited in the vessels, causing irreversible changes in the kidneys and heart. There are shifts in metabolism, lack of immunity, a tendency to various kinds of infections.
Acute D-vitamin intoxication is manifested by the syndrome of intestinal toxicosis or neurotoxicosis after 2-10 weeks of vitamin D intake. Refusal of food, vomiting, weight loss, dehydration, high temperature appear. Convulsions, development of renal failure, urination disorders are possible. In the blood, calcium is sharply increased (hypercalcemia), the Sulkovich test is positive (determines calcium in the urine). Chronic vitamin D intoxication manifests itself against the background of 6-8 or more months of taking vitamin D in moderate doses, but exceeding the physiological need. There are irritability, premature closure of the large fontanelle and fusion of the sutures of the skull, signs chronic pyelonephritis the child is not gaining weight.
Treatment consists in reducing intoxication, replenishing the deficiency of fluid, protein and salts. Calcium-rich foods are excluded from the diet - cottage cheese, cow's milk. It is recommended to take vegetable dishes, fruit juices, drink plenty of water, glucose-salt solutions, 3% ammonium chloride solution, which promotes the excretion of calcium in the urine, alkaline mineral waters, vitamin therapy (C, A and group B).
With timely treatment, the prognosis is relatively favorable.
99% of calcium and more than 80% of phosphorus is found in the body as crystalline hydroxyapatite in the bones. Bones consist of matrices composed of collagen fibrils and a ground substance (containing mucoproteins and chondroitin sulfate, in which apatite crystals are placed in the direction of the fibrils. Some of the calcium and phosphorus ions are weakly bound and relatively easily exchanged with the corresponding ions of the extracellular fluid.
Despite the fact that the extracellular fluid contains only a small part of all calcium, it physiological significance large: calcium plays a role in membrane permeability, in conduction nerve impulse, in the excitability of muscles, in the processes of blood coagulation. Phosphates that are organically bound to proteins are building blocks cells, take part in transport mechanisms, in the activity of enzymes, in the processes of energy exchange, in the transfer of genetic information. Inorganic phosphates are important for the processes of ossification, as well as in the renal excretion of H + ions, that is, in the regulation of the acid-base balance of body fluids.
homeostasis of calcium and phosphorus. Plasma calcium concentration is one of the most closely monitored organism constants: deviations from the average value - 10 mg% - do not exceed 1 mg%. More than half of the calcium in the blood is in the form of ions, about 1/3 is associated with protein, and a small amount is in the composition of complex salts. The content of inorganic phosphorus in the body of a growing child is somewhat higher than in the body of an adult; in a child, the concentration of phosphorus fluctuates around 5 mg%.
In the exchange of calcium and phosphates, a decisive role is played by parathyroid hormone, vitamin D, synthesized in thyroid gland calcitonin and bones. Ca and HPO4 ions enter the bones and, as necessary, can be mobilized from there at any age.
The level of calcium in plasma is significantly influenced by the amount of intestinal absorption corresponding to endogenous demand, and not by the amount of renal excretion, which in healthy person almost constant. It has been established that vitamin D3 (cholecal-ciferol) supplied with food undergoes successive transformations in the body. The first step is the hydroxylation of vitamin D at the 25th carbon atom, resulting in the formation of 25-hydroxycholecalciferol, which is hydroxylated again at the 1st carbon atom in the kidneys. It has been established that 1,25-dihydroxyvitamin D formed as a result of these transformations has the properties of a hormone, since this compound directly affects the genetic apparatus of intestinal and kidney cells, stimulating the synthesis of a specific protein that provides active calcium transport.
In a rapidly growing body, in accordance with the enormous needs of bone growth, a much larger part of the calcium that has entered the body is absorbed and retained than in an adult body. With a deficiency of vitamin D and with a high content of phosphorus in the diet, calcium absorption is reduced. Parathyroid hormone has a relatively slow action, calcitonin is mobilized very quickly: due to its influence, the concentration of Ca decreases, thus compensating for the action of parathyroid hormone, which increases the level of Ca.
The amount of renal excretion has a more significant effect on the level of phosphorus in the blood than the amount of enteral absorption. The latter largely depends on the amount of absorption of Ca. With a significant intake of calcium or with its reduced absorption due to a lack of vitamin D, poorly soluble calcium phosphates are formed in the intestine, which reduces the absorption of phosphorus.
If glomerular filtration is normal, then renal excretion of phosphorus depends on the amount of tubular reabsorption.
Tubular reabsorption, in other words, the amount of phosphorus excretion, is determined by the maximum reabsorption capacity of the tubules (Ttr) and the amount of parathyroid hormone secretion. With an increased intake of phosphorus, TTR is reached quickly, most of the accepted phosphorus is released. This process regulates the upper limit of the phosphorus content. However, with a sharp decrease in glomerular filtration, the concentration of phosphorus in the blood increases. Parathyroid hormone enhances the renal excretion of phosphorus, and its absence weakens it. Although, under the influence of the parathyroid hormone, phosphorus can also be mobilized from the bones along with calcium, the renal effect of this hormone is more pronounced - increased excretion of phosphorus. Therefore, in hyperparathyroidism, along with hypercalcemia, hypophosphatemia is also detected, and in hypoparathyroidism, along with hyperphosphatemia, hypocalcemia develops. At pathological conditions changes in the concentration of calcium and phosphorus usually have the opposite character.
Most important role Vitamin D in these processes is to increase the intestinal resorption of calcium and phosphorus, thereby providing the substances necessary for bone growth. Parathyroid hormone and vitamin D have opposite effects on the calcium content in the bones.
An estimate of the amount of renal calcium excretion can be made on the basis of a convenient clinical practice semi-quantitative Sulkovich test: the reagent is obtained by dissolving 2.5 g of oxalic acid and ammonium oxalate and 5 ml of acetic acid in 150 ml of water. One part of the reagent is mixed with 2 parts of urine. With hypercalciuria, severe turbidity immediately occurs or a precipitate precipitates. With normal excretion of calcium, slight turbidity occurs after 1-2 minutes. With hypocalciuria, the Sulkovich test is negative.
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Chapter V. Rickets, violation of phosphorus-calcium metabolism
rickets (R). Currently, P is understood as a violation of the mineralization of the growing bone, caused by a temporary mismatch between the needs of a growing organ ism in phosphates and calcium and the insufficiency of systems that ensure their delivery to the child's body. R is the most common illness associated with a violation of phosphorus-calcium homeostasis in children of the 1st year of life. P and hypovitaminosis D are ambiguous concepts!
AT International classification diseases of the 10th revision (ICD-10) P is included in the diseases section endocrine system and metabolism (code E55.0). At the same time, the importance of hypovitaminosis D in its development is not denied.
The development of bone signs of P in young children is due to rapid growth rates, high speed of skeletal modeling and deficiency in the growing body of phosphates and calcium with imperfection of their transport, metabolism and utilization pathways (maturing heterochrony). Therefore, at present, P is referred to as borderline states.
Epidemiology. The frequency of P in children remains unexplored due to changes in ideas about the nature of this pathology. In the study of the level of calcitriol in children with clinic P, a decrease in the level of vitamin D in the blood was detected only in 7.5% of the examined children. According to modern authors, R occurs in young children with a frequency of 1.6 to 35%.
Factors contributing to the development of R:
1. High rates of growth and development of children, increased need for mineral components (especially in premature babies);
2. Deficiency of calcium and phosphates in food;
3. Malabsorption of calcium and phosphates in the intestine, increased secretion them in the urine or impaired utilization of them in the bones;
4. Decrease in the level of calcium and blood phosphates with prolonged alkalosis, imbalance of zinc, magnesium, strontium, aluminum, due to various reasons;
5. Exogenous and endogenous vitamin D deficiency;
6. Reduced motor and support load;
7. Violation of the physiological ratio of osteotropic hormones - parathyroid hormone and calcitonin.
Etiology
Phosphorus-calcium metabolism in the body is due to:
1. absorption of phosphorus and calcium in the intestine;
2. their interchange between blood and bone tissue;
3. release of calcium and phosphorus from the body - reabsorption in the renal tubules.
All factors leading to impaired calcium metabolism are partially compensated by the leaching of calcium from the bones into the blood, which leads to the development of osteomalacia or osteoporosis.
The daily requirement for calcium in infants is 50 mg per 1 kg of weight. Dairy products are the most important source of calcium. Calcium absorption in the intestine depends not only on its amount in food, but also on its solubility, ratio with phosphorus (optimal 2: 1), the presence of bile salts, the pH level (the more pronounced alkaline reaction the worse the absorption). Vitamin D is the main regulator of calcium absorption.
The bulk (more than 90%) of calcium and 70% of phosphorus is in the bones in the form of inorganic salts. Throughout life, bone tissue is in a constant process of creation and destruction, due to the interaction of three types of cells: osteoblasts, osteocytes and osteoclasts. Bones are actively involved in the regulation of calcium and phosphorus metabolism, maintaining their stable level in the blood. With a decrease in the level of calcium and phosphorus in the blood (the product of Ca × P is a constant value and equal to 4.5-5.0), bone resorption develops due to the activation of the action of osteoclasts, which increases the flow of these ions into the blood; with an increase in this coefficient, excessive deposition of salts in the bone occurs.
The excretion of calcium and phosphorus by the kidneys is parallel to their content in the blood. With a normal calcium content, its excretion in the urine is insignificant, with hypocalcemia this amount decreases sharply, hypercalcemia increases the calcium content in the urine.
The main regulators of phosphorus-calcium metabolism, along with vitamin D are parathyroid hormone (PG) and calcitonin (CT)- thyroid hormone.
The name "vitamin D" means a group of substances (about 10) contained in products of plant and animal origin, which have an effect on calcium-phosphorus metabolism. The most active of them are ergocalciferol (vitamin D 2) and cholecalciferol (vitamin D 3). Ergocalciferol is found in small amounts in vegetable oil, wheat germ; cholecalciferol - in fish oil, milk, butter, eggs. The physiological daily requirement for vitamin D is quite stable and amounts to 400-500 IU. During pregnancy and lactation breast milk it increases by 1.5, maximum 2 times.
Rice. 1.19.The scheme of regulation of phosphorus-calcium metabolism in the body
Normal supply Vitamin D in the body is associated not only with its intake with food, but also with the formation in the skin under the influence of UV rays. At the same time, ergocalciferol is formed from ergosterol (the precursor of vitamin D 2), and cholecalciferol is formed from 7-dehydrocholesterol (the precursor of vitamin D 3).
Rice. 1.20.Biotransformation of vitamin D
With sufficient insolation (a 10-minute irradiation of the hands is enough), the skin is synthesized necessary for the body the amount of vitamin D. With insufficient natural insolation: climatic and geographical features, living conditions ( countryside or an industrial city), household factors, season, etc. the missing amount of vitamin D must come from food or in the form of drugs. In pregnant women, vitamin D is deposited in the placenta, which provides the newborn with anti-rachitic substances for some time after birth.
Vitamins D 2 and D 3 have very little biological activity. Physiological action on target organs (intestines, bones, kidneys) is carried out by their metabolites formed in the liver and kidneys as a result of enzymatic hydroxylation. In the liver, under the influence of hydroxylase, 25-hydroxycholecalciferol 25(OH)D 3 -calcidierol is formed. In the kidneys, as a result of another hydroxylation, dihydroxycholecalciferol is synthesized - 1,25- (OH) 2 D 3 -calcitrierol, which is the most active metabolite of vitamin D. In addition to these two main metabolites, other vitamin D 3 compounds are synthesized in the body - 24.25 (OH) 2 D 3 , 25.26 (OH) 2 D 3 , 21.25 (OH) 2 D 3 , the effect of which has not been studied enough.
The main physiological function of vitamin D (i.e., its active metabolites) in the body is the regulation and maintenance of the body's phosphorus-calcium homeostasis at the required level. This is ensured by its effect on the absorption of calcium in the intestines, on the deposition of its salts in the bones (bone mineralization) and on the reabsorption of calcium and phosphorus in the renal tubules.
The mechanism of calcium absorption in the intestine is associated with the synthesis of calcium-binding protein (BCP) by enterocytes. CSC synthesis is induced by calcitriol through the genetic apparatus of cells, i.e. according to the mechanism of action, 1,25 (OH) 2 D 3 is similar to hormones.
Under conditions of hypocalcemia, vitamin D temporarily increases bone resorption, enhances calcium absorption in the intestines and its reabsorption in the kidneys, thereby increasing the level of calcium in the blood. With normocalcemia, it activates the activity of osteoblasts, reduces bone resorption and its cortical porosity.
AT last years it has been shown that the cells of many organs have receptors for calcitriol, which thereby participates in the universal regulation of intracellular enzyme systems. Activation of the corresponding receptors through adenylate cyclase and cAMP mobilizes calcium and its association with the calmodulin protein, which promotes signal transmission and enhances the function of the cell, and, accordingly, of the entire organ.
Vitamin D stimulates the pyruvate-citrate reaction in the Krebs cycle, has an immunomodulatory effect, regulates the level of secretion thyroid-stimulating hormone pituitary, directly or indirectly (through calcium) affects the production of insulin by the pancreas.
The second most important regulator of phosphorus-calcium metabolism is parathyroid hormone (PG). The production of this hormone by the parathyroid glands increases in the presence of hypocalcemia, and, especially, with a decrease in the concentration of ionized calcium in plasma and extracellular fluid. The main target organs for parathyroid hormone are the kidneys, bones and, to a lesser extent, the gastrointestinal tract.
The action of parathyroid hormone on the kidneys is manifested by an increase in the reabsorption of calcium and magnesium. At the same time, phosphorus reabsorption decreases, which leads to hyperphosphaturia and hypophosphatemia. It is also believed that parathyroid hormone increases the ability of the kidneys to form calcitriol, thereby enhancing the absorption of calcium in the intestine.
In the bone tissue, under the influence of parathyroid hormone, calcium of bone apatites passes into a soluble form, due to which it is mobilized and released into the blood, which is accompanied by the development of osteomalacia and even osteoporosis. Thus, parathyroid hormone is the main calcium-sparing hormone. It carries out rapid regulation of calcium homeostasis, constant regulation of calcium metabolism is a function of vitamin D and its metabolites. The formation of PG is stimulated by hypocalcemia, with high level calcium in the blood, its production decreases.
The third regulator of calcium metabolism is calcitonin (CT)- a hormone produced by C-cells of the parafollicular apparatus of the thyroid gland. By its action on calcium homeostasis, it is a parathyroid hormone antagonist. Its secretion increases with an increase in the level of calcium in the blood and decreases with a decrease. Diet with large quantity calcium in food also stimulates the secretion of calcitonin. This effect is mediated by glucagon, which is thus a biochemical activator of CT production. Calcitonin protects the body from hypercalcemic conditions, reduces the number and activity of osteoclasts, reducing bone resorption, enhances calcium deposition in bones, preventing the development of osteomalacia and osteoporosis, and activates its excretion in the urine. The possibility of an inhibitory effect of CT on the formation of calcitriol in the kidneys is assumed.
Phosphorus-calcium homeostasis, in addition to the three above described (vitamin D, parathyroid hormone, calcitonin), is influenced by many other factors. Trace elements Mg, Al are calcium competitors in the process of absorption; Ba, Pb, Sr and Si can replace it in salts found in bone tissue; thyroid hormones, growth hormone, androgens activate the deposition of calcium in the bones, reduce its content in the blood, glucocorticoids contribute to the development of osteoporosis and leaching of calcium into the blood; vitamin A is an antagonist of vitamin D in the process of absorption in the intestine. However Negative influence These and many other factors on phosphorus-calcium homeostasis is manifested, as a rule, with significant deviations in the content of these substances in the body. The regulation of phosphorus-calcium metabolism in the body is shown in Figure 1.19.
Pathogenesis
The main mechanisms of P pathogenesis are:
1. Malabsorption of calcium and phosphates in the intestines, increased excretion of them in the urine or impaired utilization of them in the bones.
2. Decrease in the level of calcium and phosphates in the blood and impaired bone mineralization. This is facilitated by: prolonged alkalosis, deficiency of zinc, magnesium, strontium, aluminum.
3. Violation of the physiological ratio of osteotropic hormones - parathyroid hormone and calcitonin.
4. Exo- and endogenous vitamin D deficiency, as well as more low level vitamin D metabolite. This is facilitated by: diseases of the kidneys, liver, intestines, nutritional deficiencies.
Violations of phosphorus-calcium metabolism in young children are most often manifested by hypocalcemia various origins with clinical manifestations of the musculoskeletal system. The most common disease is R. The cause of hypocalcemia may be a deficiency of vitamin D and disorders of its metabolism, due to the temporary immaturity of the enzyme systems of organs (kidneys, liver) that regulate this process. Less common are primary genetically determined diseases of the kidneys, gastrointestinal tract, parathyroid glands, skeletal system accompanied by disturbances of phosphorus-calcium homeostasis with a similar clinical picture.
Classification(see table 1.40).
Tab. 1.40.Rickets classification
Research: general analysis blood and urine, blood alkaline phosphatase, blood calcium and phosphorus, bone radiography.
Clinic. It is currently believed that children with Р I degree only the presence of bone changes is mandatory. THEN. the neurological changes previously described for this severity of rickets do not apply to P.
For R II degree pronounced changes in the bones are characteristic: frontal and parietal tubercles, rosaries, deformity of the chest, often varus deformity of the extremities. Radiologically, there is an expansion of the metaphyses of the tubular bones, their cup-shaped deformation.
For R III degree characterized by gross deformities of the skull, chest, lower extremities, delayed development of static functions. In addition, are determined: shortness of breath, tachycardia, liver enlargement.
Initial signs P- softening of the edges of a large fontanel, craniotabes. The question of the so-called initial signs R in the form of sweating, restlessness, startle, etc. has not been completely resolved.
peak period- signs of bone osteomalacia or osteoid hyperplasia, osteoporosis. The most pronounced clinical and radiological changes coincide with severe hypophosphatemia.
convalescence period – reverse development clinics R. Pri x-ray examination a clear line of calcification appears in the metaphyseal zone, the level of phosphates normalizes, slight hypocalcemia persists, and a moderate increase in the level of alkaline phosphatase.
Current R– sharp and subacute At acute course manifestations of osteomalacia predominate, and in subacute course - osteoid hyperplasia. Manifestations of osteomalacia are: softening of the edges of the large fontanel, craniotabes, rachitic kyphosis, curvature of the limbs, rachitic deformity of the chest.
Signs of osteoid hyperplasia include: rachitic rosary, frontal and occipital protuberances, "strings of pearls", etc.
Diagnosis. AT outpatient settings Clinical manifestations are sufficient to make a diagnosis of R.
Laboratory confirmation of P I degree- slight hypophosphatemia and increased activity of alkaline phosphatase.
Laboratory confirmation of P II degree– decrease in the level of phosphates, calcium, increased activity of alkaline phosphatase.
Laboratory confirmation of P III degree- X-ray examination shows a rough restructuring of the pattern and development of bones, expansion and blurring of the metaphyseal zone, fractures or displacements are possible. In the blood, a pronounced decrease in the levels of phosphates and calcium, an increase in the level of alkaline phosphatase are determined.
The only reliable sign of the diagnosis of P is a decrease in the level of vitamin D in the blood (determination of the level of 25-OH-D 3).
Differential Diagnosis R is carried out with: D-resistant forms of rickets, D-dependent forms of rickets I and II types, phosphate diabetes, de Toni-Debre-Fanconi syndrome, renal tubular acidosis, osteoporosis.
Tab. 1.41.Differential diagnosis of rickets
| signs | Vitamin D-deficient rickets | Phosphate diabetes | Renal tubular acidosis | De Toni-Debre-Fanconi disease |
| Inheritance type | Not | Dominant. X-linked | Possibly autosomal recessive or autosomal dominant | autosomal recessive or autosomal dominant |
| Dates of manifestation | 1.5-3 months | Over 1 year old | 6 months-2 years | Older than 1-2 years |
| First clinical manifestations | Damage to the skeletal system | Severe deformity of the lower extremities, bracelets, hypotension, | Polyuria, polydipsia, tearfulness, muscle pain, hypotension | Unexplained fever, polyuria, polydipsia, muscle pain |
| Specific features | Craniotabes, frontal and occipital protuberances, bracelets, limb deformity | Progressive varus deformity of the extremities | Polyuria, polydipsia, hypotension to atony, adynamia, liver enlargement, constipation, valgus deformity of the legs | Fever, progressive multiple bone deformities, liver enlargement, decreased blood pressure, constipation |
| Physical development | Without features | Growth deficiency at normal weight | Decreased height and weight | Decreased height and weight |
| blood calcium | lowered | Norm | Norm | More often the norm |
| Phosphorus | lowered | Dramatically reduced | lowered | Dramatically reduced |
| Potassium | norm | norm | lowered | lowered |
| Sodium | Norm | norm | lowered | lowered |
| KOS | More often acidosis | metabolic acidosis | Severe metabolic acidosis | |
| Aminoaciduria | there is | norm | norm | expressed |
| Phosphaturia | there is | pronounced | moderate | pronounced |
| Calciuria | lowered | norm | significant | significant |
| X-ray of the bones of the skeleton | Goblet expansions of the metaphyses | Rough goblet expansions of the metaphyses, thickening of the cortical layer of the periosteum | Spicy systemic osteoporosis. Blurred contours of the metaphyses, concentric bone atrophy | Osteoporosis, trabecular striation in the distal and proximal diaphyses |
| The effect of vitamin D treatment | good effect | Minor | Satisfactory effect at high doses |
Osteoporosis- a decrease in bone mass and a violation of the structure of bone tissue - can be associated not only with P, but also with other factors. The causes of osteoporosis are: endocrine - metabolic disorders; malnutrition and digestion; the use of a number of drugs (hormones, anticonvulsants, antacids, heparin); genetic factors(imperfect osteogenesis, Marfan's syndrome, homocystinuria); prolonged immobilization; malignant tumors; chronic renal failure. In these cases, the diagnosis of P is invalid, despite the clinical similarity.
Treatment. Treatment goals: restoration of vitamin D deficiency in the body, correction of phosphorus-calcium metabolism disorders, relief of manifestations of P (bone deformity, muscle hypotension, dysfunction of internal organs).
The scheme of treatment.Mandatory activities: vitamin D preparations, regimen, solar and air procedures.
Auxiliary treatment: diet, vitamin therapy, water procedures, massage calcium preparations.
the need for an in-depth examination (conducting a differential diagnosis), the lack of effect from the appointment of vitamin D preparations.
Mode, appropriate for the age of the child, prolonged exposure to the air with sufficient insolation (at least 2-3 hours daily).
Diet - natural feeding, with artificial feeding, the use of adapted mixtures corresponding to the age of the child. The timely introduction of complementary foods is important.
Tab.1. 42. Vitamin D medicines
| Name of the drug | Vitamin D content |
| Aquadetrim Vitamin D 3, Water solution | 1 ml - 30 drops; 1 drop - 500 IU |
| Videhol, oil solution D 3 , 0.125% | 1 drop 500 IU |
| Videhol, oily solution, 0.25% | 1 drop -1000 IU |
| Ergocalciferol solution (vitamin D 2) oil solution, 0.0625% | 1 drop - 625 IU |
| Solution of ergocalciferol (vitamin D 2) in oil in capsules | 1 capsule - 500 IU |
| Dragee ergocalciferol (vitamin D 2) | 1 dragee - 500 IU |
| Ergocalciferol solution (vitamin D 2 in oil, 0.125% | 1 drop - 1250 IU |
| Ergocalciferol solution (vitamin D 2 in oil, 0.5% | 1 drop - 5000 IU |
| Oxidevit (calcitriol, 1,25(OH)2D 2 | 1 capsule - 1 mcg 0.00025 mg |
| Fish fat in capsules (Norway), Meller | 1 capsule - 52 IU |
Nearly all pediatricians now agree that specific treatment It is advisable to carry out R with small therapeutic doses of vitamin D. The daily dose of vitamin D at I-II degree P while it is 1500-2000 IU, the course is 100,000-150,000 IU; at II-III degree - 3000-4000 IU, course 200000-400000 IU. This treatment is carried out during the peak period, confirmed by biochemical data (decrease in blood calcium and phosphorus, increase in alkaline phosphatase). At the end of the course, if necessary, it is advisable to switch to a prophylactic (physiological) dose of vitamin D. Recommended in the past shock, semi-shock methods, repeated treatment courses currently not in use. When carrying out specific therapy, it is necessary to monitor the level of calcium in the blood by regular (1 time in 10-14 days) setting the Sulkovich reaction (degree of calciuria).
Tab. 1.43. Modern calcium-containing preparations
| Name | Ca content | Producing country |
| Preparations containing calcium carbonate | ||
| UPSAVIT calcium | France | |
| Additive calcium | Poland | |
| Calcium-D 3 -Nycomed | 1250+D 3 200 units | Norway |
| Vitrum calcium | 1250+D 3 200 units | USA |
| Ideos | 1250+D 3,400 units | France |
| Vitacalcin | Slovakia | |
| Osteokea | Great Britain | |
| Ca-sandos forte | Switzerland | |
| Complex preparations | ||
| Osteogenon | Ca 178, P 82, growth factors | France |
| Vitrum osteomag | Ca, Mg, Zn, Cu, D 3 | USA |
| Berocca Ca and Mg | Ca, Mg and vitamins | Switzerland |
| Calcium SEDICO | Ca, D 3 , vit. FROM | Egypt |
| Kaltsinova | Ca, P, vit. D, A, C, B 6 | Slovenia |
Calcium preparations are indicated for premature babies, breastfed children, in courses of 2-3 weeks. The dose is selected depending on the age, severity of R and the degree of metabolic disorders.
It is advisable to combine vitamin D preparations with vitamins of group B (B 1, B 2, B 6), C, A, E.
To reduce the severity of vegetative disorders, the use of potassium and magnesium preparations (panangin, asparkam) at the rate of 10 mg / kg / day for 3-4 weeks is indicated.
Prevention. At present, non-specific antenatal prophylaxis of R is to create optimal conditions for the growth and development of the fetus for a pregnant woman: rational nutrition with sufficient intake of not only proteins, fats, carbohydrates, but also micro- and macroelements (including calcium and phosphorus), vitamins ( including vitamin D) the prohibition of a pregnant woman to take toxic (especially for the fetus) substances - tobacco, alcohol, drugs; exclusion of the possibility of contact of a pregnant woman with other toxic substances - chemicals, drugs, pesticides, etc. A pregnant woman must physically active image life, as much as possible (at least 4-5 hours a day) to be fresh air, observe the regime of the day with sufficient rest day and night. In this case, there is no need to additionally prescribe vitamin D to the pregnant woman.
Antenatal specific prophylaxis R by prescribing 200-400 IU of vitamin D per day from 32 weeks of gestation for 8 weeks (only in winter or spring). For pregnant women at risk, specific P prophylaxis is carried out regardless of the season of the year.
Postnatal non-specific prevention of P includes: breastfeeding; timely introduction of complementary foods (it is better to start with vegetable puree), juices; daily stay in the fresh air, free swaddling, massage, gymnastics, light-air and hygienic baths.
The physiological need of a child for vitamin D is 200 IU per day.
Postnatal specific prophylaxis of R is carried out for children only in the period of late autumn - early spring at a dose of 400 IU per day, starting from 4 week old. Additional administration of vitamin D in the 2nd year of life is not advisable. The mixtures used for artificial feeding contain all the necessary vitamins and minerals in physiological doses, and therefore there is no need for additional introduction vitamin D. For children with small fontanels, it is preferable to use non-specific methods for the prevention of R.
For preterm infants, the issue of prophylactic administration of vitamin D should only be considered after optimizing dietary intake of calcium and phosphorus. It has been established that hypovitaminosis D is practically not detected in premature infants. In the development of osteopenia in them crucial is deficient in calcium and phosphate. It is traditionally considered that the prophylactic dose of vitamin D for premature babies is 400-1000 IU per day.
SPASMOPHILIA (C)- a peculiar condition of young children with signs of rickets, due to a violation mineral metabolism, hypofunction of the parathyroid glands, manifested by signs of increased neuromuscular excitability and a tendency to convulsions.
Epidemiology. C occurs almost exclusively in children in the first 2 years of age, in about 3.5-4% of all children.
Pathogenesis. Violations of mineral metabolism in C are more pronounced than in rickets and are characterized by some features. Indicators of metabolic changes are hypocalcemia, severe hypophosphatemia, hypomagnesemia, hyponatremia, hypochloremia, hyperkalemia and alkalosis. Calcium deficiency develops due to a decrease in the content of free and bound calcium. Main metabolic disorders at C are hypocalcemia and alkalosis, which are explained by a decrease in the function of the parathyroid glands. The main clinical manifestations of C (spasms and convulsions) are explained by a sharp lack of calcium and the resulting increased excitability of the nerves. Additional factors, contributing to the occurrence of seizures, consider the lack of sodium and chlorine, as well as a pronounced lack of magnesium and an increased concentration of potassium (since sodium reduces the excitability of the neuromuscular system). The occurrence of seizures can also be explained by a lack of vitamin B 1, which is present in C. With its pronounced deficiency, sharp disturbances occur in the glycolytic chain with the formation pyruvic acid, which plays a large role in the occurrence of seizures.
C occurs in all seasons of the year, but more often develops in the spring.
The development of any disease with high temperature, frequent vomiting in gastrointestinal diseases, as well as strong crying, excitement, fear, etc. In these conditions, a shift in acid-base balance towards alkalosis, with the creation of conditions for the manifestations of S.
Classification(E.M. Lepsky, 1945):
1. hidden form;
2. Explicit form (laryngospasm, carpo-pedal spasm, eclampsia).
Research. Determination of the content of calcium and phosphorus in blood plasma; determination of the activity of alkaline phosphatase in blood plasma, the study of CBS, ECG.
Anamnesis, clinic. In the anamnesis it is possible to identify early improper artificial feeding, abuse of cow's milk, flour products, lack of prevention of rickets. Seizure C is provoked feverish conditions, frequent vomiting in gastrointestinal diseases, fear, agitation, strong crying, increased ultraviolet radiation.
In a child with C, the examination should show signs of rickets.
Signs of hidden C(symptoms of increased excitability of the neuromuscular apparatus):
a) Chvostek's symptom- slight tapping at the exit facial nerve(between zygomatic arch and corner of mouth) causes contraction or twitching muscular musculature the corresponding side of the face;
b) peroneal Lust sign - percussion behind and slightly below the head of the fibula causes dorsiflexion and abduction of the foot outward;
in) Trousseau's sign - compression of the neurovascular bundle on the shoulder causes convulsive contraction of the muscles of the hand - "obstetrician's hand";
G) Maslov's symptom - an injection in the heel causes cessation of breathing instead of its increase (carried out under the control of a pneumogram);
e) Erb's symptom - opening of the cathode applied to median nerve, causes muscle contraction at a current strength of less than 5 mA.
Signs of explicit C:
a) laryngospasm - sudden difficulty in inhaling with the appearance of a peculiar noisy breathing. With a more pronounced narrowing of the glottis - a frightened facial expression, a child open mouth"catching air", cyanosis of the skin, cold sweat on the face and body. After a few seconds, a noisy breath appears and normal breathing is restored. Attacks of laryngospasm can be repeated during the day;
b) carpo-pedal spasm - tonic contraction of the muscles of the limbs, especially in the hands and feet, from several minutes to several days, which may recur. With prolonged spasm, elastic swelling appears on the back of the hands and feet.
The spastic state can also spread to other muscle groups: eye, masticatory (temporary strabismus or trismus), spasms of the respiratory muscles are unfavorable prognostically (inspiratory or expiratory apnea), less often - a spastic state of the heart muscle (cardiac arrest and sudden death). Spasms occur smooth muscle internal organs, which leads to a disorder of urination, defecation;
in) eclampsia - clonic-tonic convulsions with involvement in the process of striated and smooth muscles of the whole body; the attack begins with twitching of facial muscles, then convulsive contractions of the limbs, respiratory muscles join, cyanosis occurs. Consciousness is usually lost at the onset of an attack. The duration of the attack is from several minutes to several hours. Tonic and clonic seizures can be isolated, combined or sequential. Clonic convulsions more often observed in children in the first year of life, tonic - in children older than a year.
Diagnosis C is based on the identification of signs of overt or latent S. in a child with rickets.
Laboratory data: a) biochemical research blood - hypocalcemia (up to 1.2-1.5 mmol / l) against the background of a relatively elevated level of inorganic phosphorus.
b) an increase in the numbers of the numerator or a decrease in the denominator in the Gyorgy formula: P0 4 - HC0 3 -K +
Ca++ Mg++ H+
Differential Diagnosis C is carried out with diseases manifested by hypocalcemia: chronic kidney failure, hypoparathyroidism, malabsorption syndrome, taking drugs that reduce calcium levels
Tab. 1.44. Differential diagnosis of spasmophilia
| sign | Spasmophilia | Hypoparathyroidism | CRF | Malabsorption syndrome |
| convulsions | Yes | Yes | +/- | Possible |
| Rachitic bone changes | Characteristically | Not | Osteoporosis | Osteoporosis |
| chronic diarrhea | No | No | +/- | characteristically |
| SW. urea, creatinine | Not | Not | Yes | Not |
| Symptoms of increased neuromuscular excitability | Yes | Yes | Yes | Yes |
| PTH↓ level, phosphorus | Not | Not | Not | Yes |
| Blood calcium ↓ | Yes | Yes | Yes | Yes |
Treatment. Treatment goals: normalization of neuromuscular excitability, indicators of mineral metabolism; relief of convulsions and other manifestations of C, treatment of rickets.
Therapy regimen
Mandatory activities: relief of hypocalcemia, syndromic therapy of manifestations of C, treatment of rickets.
Helper Methods treatment: regimen, diet, vitamin therapy.
Indications for hospitalization: convulsions, eclampsia, laryngospasm.
Mode: limit as much as possible or extremely carefully perform procedures that are unpleasant for the child.
Diet: exclusion of cow's milk for 3-5 days, carbohydrate nutrition, gradual transition to a balanced, age-appropriate diet.
For eclampsia: calcium chloride or calcium gluconate 10% solution, 2-3 ml, intravenously microstream. Sodium hydroxybutyrate 50–100 mg/kg IV slowly or droperidol 0.25% solution 0.1 mg/kg IV slowly or Seduxen 0.5% solution 0.15 mg/kg IM or IV, or magnesium sulfate 25% solution, 0.8 ml/kg, intramuscularly, but not more than 8.0 ml.
With carpo-pedal spasm: inside calcium chloride or gluconate, phenobarbital, bromides.
For laryngospasm: splash the patient with cold water, press your finger on the root of the tongue, according to indications - artificial respiration, drug therapy like in eclampsia.
After rendering emergency care : calcium preparations inside, ammonium chloride 10% solution, 1 tsp. 3 times a day, vitamin D 4000 ME daily from 4-5 days; vitamin therapy.
Prevention C primarily associated with the detection and treatment of rickets. The rational feeding of the child is important. Special attention draw on the early introduction of cow's milk products into the diet. It is necessary to prevent strong crying, fear.
VITAMIN D HYPERVITAMINOSIS (HD) occurs with an overdose of vitamin D or with individual hypersensitivity to it.
Epidemiology. Currently, due to the revision of approaches to the prevention and treatment of rickets, HD in children is rare.
PhysiologyMineral metabolism disorders are changes in the level of calcium, phosphorus or magnesium. Calcium is essential for cell function. In the process of regulating the homeostasis of these main mineral macronutrients, three organs are mainly involved - the kidneys, bones and intestines, and two hormones - calcitriol and parathyroid hormone.
The role of calcium in the body
About 1 kg of calcium is contained in the skeleton. Only 1% general content calcium in the body circulates between intracellular and extracellular fluid. Ionized calcium is about 50% total calcium circulating in the blood, about 40% of which is associated with proteins (albumin, globulin).
When assessing the level of calcium in the blood, it is necessary to measure the ionized fraction or both total calcium and blood albumin, on the basis of which the level of ionized calcium can be calculated using the formula (Ca, mmol / l + 0.02x (40 - albumin, g / l).
The normal level of total calcium in the blood serum is 2.1-2.6 mmol/L (8.5-10.5 mg/dL).
The role of calcium in the body is diverse. We list the main processes in which calcium takes part:
provides bone density, being the most important mineral component in the form of hydroxyapatite and carbonate apatite;
participates in neuromuscular transmission;
regulates cell signaling systems through work calcium channels,
regulates the activity of calmodulin, which affects the functioning of enzyme systems, ion pumps and cytoskeletal components;
participates in the regulation of the coagulation system.
homeostasis of calcium and phosphorus
The following are the main mechanisms involved in the regulation of calcium levels.
The active metabolite of vitamin D - the hormone calcitriol (1,25 (OH) 2calciferol) is formed during the hydroxylation of cholecalciferol under the action of sunlight and with the participation of two main hydroxylation enzymes - 25-hydroxylase in the liver and 1-a-hydroxylase in the kidneys. Calcitriol is the main hormone that stimulates the absorption of calcium and phosphorus in the intestine. In addition, it enhances the reabsorption of calcium and excretion of phosphorus in the kidneys, as well as the resorption of calcium and phosphorus from the bones, like parathyroid hormone. The level of calcitriol is regulated directly by blood calcium, as well as by the level of parathyroid hormone, which affects the activity of 1-a-hydroxylase.
The calcium-sensitive receptor is located on the surface of the cells of the parathyroid glands and in the kidneys. Its activity normally depends on the level of ionized calcium in the blood. An increase in the level of calcium in the blood leads to a decrease in its activity and, as a result, a decrease in the level of parathyroid hormone secretion in the parathyroid gland and an increase in calcium excretion in the urine. On the contrary, with a decrease in the level of calcium in the blood, the receptor is activated, the level of secretion of parathyroid hormone increases and the excretion of calcium in the urine decreases. Defects in the calcium-sensitive receptor lead to impaired calcium homeostasis (hypercalciuric hypocalcemia, familial hypocalciuric hypercalcemia).
Parathyroid hormone is synthesized by the cells of the parathyroid glands. It exerts its effect through a G-protein-coupled receptor on the surface of cells of target organs - bones, kidneys, intestines. In the kidneys, parathyroid hormone stimulates the hydroxylation of 25 (OH) D with the formation of the hormone calcitriol, which plays one of the main roles in the regulation of calcium homeostasis. In addition, parathyroid hormone increases calcium reabsorption in the distal nephron, increases calcium absorption in the intestine. The effect of parathyroid hormone on bone metabolism is twofold: it enhances both bone resorption and bone formation. Depending on the level of parathyroid hormone, the duration of exposure to its high concentration, the state of the bone tissue changes in different ways. different departments(cortical and trabecular). In calcium homeostasis, the dominant effect of parathyroid hormone is to increase bone resorption.
Parathormone-like peptide is structurally identical to parathyroid hormone only in the first eight amino acids. However, it can bind to the parathyroid hormone receptor and have the same effects. The clinical significance of parathyroid hormone is only in malignant tumors that can synthesize it. In normal practice, the level of parathormone-like peptide is not determined.
Calcitonin is synthesized in the C-cells of the thyroid gland, stimulates the excretion of calcium in the urine, and inhibits the function of osteoclasts. A significant role of calcitonin in calcium homeostasis in fish and rats is known. In humans, calcitonin does not have a pronounced effect on blood calcium levels. This is confirmed by the absence of disturbances in calcium homeostasis after thyroidectomy, when C-cells are removed. The level of calcitonin is clinical significance only for the diagnosis of malignant tumors - C-cell thyroid cancer and neuroendocrine tumors, which can also synthesize calcitonin (insulinoma, gastrinoma, VIPoma, etc.).
Glucocorticoids normally do not significantly affect the level of calcium in the blood. AT pharmacological doses Glucocorticoids significantly reduce calcium absorption in the intestine and reabsorption in the kidneys, thereby lowering the level of calcium in the blood. High doses Glucocorticoids also affect bone metabolism by increasing bone resorption and reducing bone formation. These effects are of importance in patients receiving glucocorticoid therapy.
