Phosphorus-calcium metabolism and its regulation. The main functions of calcium in the body
The formation of a bone skeleton, which holds the entire body like a strong frame, 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 normal and complete bone development is the proper functioning of phosphorus-calcium metabolism. Vitamin D is no less important for the formation of the skeleton.
Bones begin to form during intrauterine development in the first weeks of pregnancy and by the end of the 15th week the body of the unborn child and its skeletal apparatus are already fully formed. But this process continues quite long time, up to puberty in adolescence. Therefore, very important attention must be paid to sufficient intake of calcium, phosphorus and vitamin D already during pregnancy.
About 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 a child’s teeth.
Calcium enters the body mainly through 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. It must be taken into account that 100 ml of breast milk contains 30 mg of calcium, and 100 ml cow's milk– 120 mg calcium;
- From 1 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 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. Phosphorus-rich foods - 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 intestines. From normal functioning the success and completeness of absorption depends on the mucous membrane of the digestive system. Phosphorus and calcium are transported through the intestinal walls using 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 food consumed should be 2:1, respectively. That is, calcium should be supplied 2 times more than phosphorus.
It must be taken into account 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 lack of phosphorus develops, and calcification of internal organs also 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 prolonged course, a violation of bone mineralization and their curvature occurs.
It has a very strong effect on the formation of the bone skeleton and the process of fat absorption. As a result of diseases of the liver and pancreas, the likelihood of disturbances 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 bottle-fed with formulas 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 less well with increased intestinal acidity, as well as with an excess of calcium and magnesium in the body.
Calcium and phosphorus depot:
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. From easily soluble compounds, calcium easily returns back into the blood when hypocalcemia occurs or when fluids inside the body are highly acidic.
Important! Increased blood acidity develops with prolonged illnesses of the child, for example, with diarrhea. This leads to a significant decrease in the calcium and phosphorus content in bone tissue baby. Thanks to this process in the body, it is possible to short time normalize the pH level. The reserves of spent microelements must be restored with the baby’s food.
In children suffering chronic diseases, in which the pH level in the blood is significantly disturbed (diseases gastrointestinal tract, kidneys) very dangerous violations of this regulatory mechanism develop. As a result, there are serious violations phosphorus-calcium metabolism, which leads to a significant slowdown in the child’s growth 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 a child’s body is the kidneys. They filter blood from vital important elements, including calcium and phosphorus. They, depending on the needs of the body, either return to the blood or are excreted from the body through urine.
Important! Factors that ensure the smooth functioning 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 disrupted, a fairly strong disturbance in 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 (and a slight burn appears on the skin, which we call a tan). This is the best form of vitamin D3 for the body.
Important! It is impossible to reproduce cholecalciferol artificially. Taken as part of multivitamins or in monocomponent products, it is inactive and is mostly deposited in fat and muscle tissue.
One part of vitamin D3 is metabolized in the liver and its excess is excreted through 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 organs that participate 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 intestine and their fixation in bone tissue.
When there is an excess of vitamin D3, part of it is deposited in the muscles active form.
Important! With a significant increase in the content of vitamin D3 in the body, child poisoning develops. There are babies who experience signs of poisoning even with a normal amount of vitamin D3. This is due to their characteristics and predisposition. Such children require less cholecalciferol.
Symptoms of phosphorus-calcium metabolism disorders:
Regardless of the causes of such disorders, in the initial stage they are practically asymptomatic.
Symptoms of disturbances in the metabolism of phosphorus and calcium in the body are as follows:
Increased sweating in the back of the head or other parts of the head. This is the very first sign that may indicate disturbances in the metabolism of phosphorus and calcium. Thus, the body begins to more intensively remove chlorine ions from the body both in 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 we can speak with confidence about the presence of a malfunction in the metabolism of calcium and phosphorus in the baby’s body;
Bone deformation. As a rule, it develops 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 quite long or lifelong treatment.
Signs high content vitamin D3 in the body:
Intense thirst. Accordingly, the child very often asks to use the potty or urinate on the diaper;
- Increased urine output;
- Lack of appetite;
- Increased anxiety in the baby;
- Sleep disorders;
- Regurgitation;
- Vomit;
- Decreased muscle tone;
- No weight gain;
- Hidden symptoms: kidney calcification, kidney stones, high blood pressure.
Diagnostics:
It is very important that the doctor determines as early as possible exact reason disturbances of phosphorus-calcium metabolism in a child. This will make it possible to prescribe timely and correct treatment.
When collecting 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 becomes clear whether the baby has problems with the digestive tract, since this can lead to impaired absorption of vital nutrients. important microelements. As a result, bone formation 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:
Stool examinations;
Smears for bacteriological examination;
Urine analysis to detect calcium excreted from the body. For this test, urine is collected in the morning on an empty stomach. Based on the results of this analysis, the doctor makes a conclusion about the presence of hypercalciuria, which is associated with a very high content of vitamin D3 in the body;
A blood test, which consists of determining the levels 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 if steam is functioning properly 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 disturbances in 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 at 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 for any disorder of calcium and phosphorus metabolism are as follows:
The right diet. Depending on the problem, the doctor will recommend products that should be given preference and which ones should be abandoned or limited in their use;
- Calcium is found in large quantities in the following 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-rich 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 multivitamins) with established deficiency;
- Additional intake of medications containing daily or increased doses of calcium and phosphorus;
- Means for the treatment of pathologies that cause disturbances in phosphorus-calcium metabolism in the baby’s body.
Vitamin D3 Requirements:
The amount of vitamin D that the mother received during pregnancy, especially in the third trimester, is very important for a small child.
Important! Full-term healthy babies whose mothers took sufficient amounts of vitamin D, as a rule, do not require additional amounts from food.
Babies who are breastfed most often do not experience problems with calcium deficiency. After all, the calcium contained in breast milk is absorbed best by the body of a newborn baby.
Children who are fully or partially bottle-fed receive additional vitamin D from formula milk. Its concentration in them is usually about 400IU. That is, one liter of the mixture contains daily norm vitamin D
Vitamin D3, which is present in the child’s skin, covers the daily requirement by 30%. In areas where there are a very large number of sunny days, coverage of up to 100% is possible.
Important! It is imperative to monitor the amount of vitamin D3 that your baby receives from food. If there is a deficiency, be sure to compensate for it.
Important! Oral drops contain 300 IU of vitamin D3.
Take care of the health of your kids! They are the best!
When we talk about rickets, we first of all mean vitamin D deficiency (vitamin D-deficiency rickets). This classic rickets affects children in the first months of life as a result of defects in feeding and violations of the general daily routine.
Rickets used to be more common in children living in poor living conditions, without sufficient fresh air and natural ultraviolet radiation. Of course, these factors play a leading role in the development of the disease. However, now rickets occurs much more often, in almost every second child, since predisposing factors have become more common: delay intrauterine 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, reducing its resistance. Ego creates the preconditions for the emergence of a number of other diseases, often occurring with various complications. Therefore, rickets is a so-called “unfavorable background.” Vitamin D deficiency rickets contributes to the severe course of concomitant diseases, a slowdown in the rate of physical and neuropsychic development, and can cause irreversible bone changes, for example, the pelvic bones, which is of no small importance in girls.
The main cause of rickets is deficiency, or hypovitaminosis D, which occurs in a child as a result of disruption of the natural synthesis of vitamin D in the skin and insufficient intake of it with food. For full-term infants who are breast-fed, 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 are its insufficient formation in the skin from provitamin under the influence of ultraviolet rays. The formation of vitamin D is hampered by exposure to diffuse light, dusty air, and excessive wrapping of children. The second important factor is not balanced diet, unbalanced in the amount of protein, calcium and phosphorus, with excess fat or predominantly vegetable. Vitamin D is found in egg yolk, butter, fish and bird liver. There is little of it in human and cow's milk. But in human milk it is in active form and is completely absorbed by the child’s body. In addition, breast milk contains the most optimal ratio of calcium and phosphorus.
Rickets is promoted by rapid growth, characteristic of children in the first months of life, but especially premature ones, as well as long-term infectious and gastrointestinal diseases, and a lack of motor and emotional activity in children.
In the development of the disease, the leading role is played by disturbances in phosphorus-calcium metabolism, disturbances in bone formation and 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 impair the absorption of vitamin D.
The first manifestations usually appear at the 2-3rd month, in premature infants - earlier. Early manifestations are associated with dysfunction nervous system against the background of a reduced level of phosphorus (restlessness, sweating, mild excitability in response to mild stimuli, softening of the sutures and edges of the fontanel, muscular dystonia). After 2-6 weeks, the height of rickets begins, which is characterized by more pronounced disorders, the child becomes lethargic, inactive, a decrease in muscle tone is observed, skeletal changes develop (flattening of the occiput, changes in configuration chest, frontal and parietal tubercles appear, thickenings in the wrist area). When examining a child, you can see thickenings on the ribs that resemble beads - “rachitic rosaries”; on the child’s arms in the area of the wrists thickenings of the bones are visible - “rachitic bracelets”; as a result of relaxation of the muscles of the abdominal wall, the abdomen increases - “frog belly”. X-rays show loss of bone tissue - osteoporosis. The blood levels of calcium (hypocalcemia) and phosphorus (hypophosphatemia) are reduced.
Treatment is carried out with vitamin D for 30-45 days against the background of an age-appropriate diet and regimen, vitamin therapy (C, B). Courses of massage, exercise therapy, ultraviolet irradiation, salt and pine baths are provided.
Under the influence of treatment, the general condition improves, neurological signs are eliminated, impaired muscle tone (dystonia) and skeletal deformation persist much longer.
With mixed and artificial feeding, appropriate nutritional correction is necessary. In addition, for rickets, it is recommended to introduce complementary foods 1-1.5 months earlier than for healthy children. The first complementary foods are introduced from 3.5-4 months and always in the form of vegetable puree with yolk; second complementary food - porridge with vegetable broth - from 4.5-5 months; at 5 months - liver; at 6-6.5 months - meat in the form of puree.
Prevention. From the first days of life, children need a rational diet and nutrition, preventive courses of vitamin D of 500 IU once a day, excluding the summer months.
Hereditary rickets-like diseases
Rickets-like diseases have similar symptoms to rickets - a group of diseases whose symptoms are similar to rickets, but are not associated with a deficiency of vitamin D entering the body. Their leading manifestation is skeletal abnormalities.
These diseases include phosphate diabetes, hypophosphatasia, and achondroplasia.
Phosphate diabetes
(hypophosphatemic vitamin D-resistant rickets)
Phosphate-diabetes is a hereditary disease, transmitted in a dominant manner linked to the X chromosome, manifested by severe disturbances in phosphorus-calcium metabolism, which cannot be restored with regular doses of vitamin D. There is an assumption that the disease is associated with pathology of enzymes that ensure the absorption of phosphates in the renal tubules .
Characteristic laboratory signs of this disease are a decrease in phosphates in the blood with a simultaneous increase in urine (4-5 times) and no change in calcium levels in the blood.
Phosphate diabetes has similar features to vitamin D-deficient rickets, but differs from it in that the child’s general condition remains satisfactory. The disease mainly affects 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 visible after the second year of life.
If the diagnosis is not made in time and there is no treatment, the child becomes disabled - he cannot move.
Once a diagnosis is made, the child is treated large doses vitamin D, several times higher than those in classic rickets. As the child's condition improves, the dose is gradually reduced. Great importance has additional phosphorus intake from food and in medications.
The risk of having a child with this pathology again 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, decreased resistance to infections. Signs of the disease include growth retardation (nanism) and changes in urine composition. An increase in urine phosphates, glucose, amino acids, and calcium is typical.
The disease begins to manifest itself 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 muscle hypotonia, frequent infectious diseases.
Treatment consists of prescribing high doses of vitamin D and increasing the protein content in the baby’s diet. The child should be under the supervision of a pediatrician.
The prognosis may be unfavorable - mortality is high due to acute renal failure.
Achondroplasia
Achondroplasia (chondrodystrophy, Parrot-Marie disease) is a congenital genetically determined disease manifested by damage to cartilage tissue and leading to various kinds deformations and shortening of bones. The cause of the disease is still unclear.
The disease manifests itself as dwarfism. Along with growth retardation, O-shaped deformities of the femoral and tibia(type "breeches"). The bones are flattened across 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 function is usually favorable.
Prevention of the disease is through medical genetic counseling.
Hypophosphatasia
Hypophosphatasia is a rare hereditary disease, transmitted in an autosomal recessive manner, caused by the absence or decreased activity of the phosphatase enzyme.
An early malignant form can be detected already in the neonatal period and in children under one year of age. It is similar to the manifestations of classic rickets in bone changes, child anxiety, increased sensitivity to external irritants, hypotonicity of the mouse, decreased phosphates in the blood, but differs in a more malignant course. The bones of the skull become soft, the limbs become short and deformed. There may be fever and convulsions.
Signs of the disease sometimes disappear spontaneously as the child matures. In severe cases, death may occur early from renal failure.
Prevention of the disease is through medical genetic counseling.
Hypervitaminosis D (D-vitamin intoxication, vitamin D poisoning)
This is a disease caused by an increase in 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 can 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 supplements, consuming large amounts 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 the pregnant woman with excess calcium or phosphorus in food, deficiency of complete protein, vitamins A, C and group B.
Calcium is deposited in blood vessels, causing irreversible changes in the kidneys and heart. Shifts in metabolism, immunity deficiency, and a tendency to various types of infections appear.
Acute D-vitamin intoxication is manifested by the syndrome of intestinal toxicosis or neurotoxicosis after 2-10 weeks of taking vitamin D. Refusal of food, vomiting, weight loss, dehydration, and high fever appear. Convulsions, development of renal failure, and urinary disorders are possible. There is a sharp increase in calcium in the blood (hypercalcemia), the Sulkovich test is positive (determines calcium in the urine). Chronic D-vitamin intoxication manifests itself against the background of 6-8 or more months of taking vitamin D in moderate doses, but exceeding the physiological need. Irritability, premature closure of the large fontanelle and fusion of the sutures of the skull appear, signs chronic pyelonephritis, the child is not gaining weight.
Treatment consists of reducing intoxication, replenishing the deficiency of fluid, protein and salts. Foods rich in calcium, such as cottage cheese and cow's milk, are excluded from the diet. It is recommended to take vegetable dishes, fruit juices, drink plenty of fluids, glucose-saline 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 are found in the body as crystalline hydroxyapatite in the bones. Bones consist of matrices composed of collagen fibrils and ground substance (containing mucoproteins and chondroitin sulfate, in which apatite crystals are located in the direction of the fibrils. Some of the calcium and phosphorus ions are weakly bound and are relatively easily exchanged with the corresponding ions of the extracellular fluid.
Despite the fact that extracellular fluid contains only a small portion of total calcium, it physiological significance great: calcium plays a role in membrane permeability, conduction nerve impulse, in muscle excitability, in blood clotting processes. Phosphates that are in organic connection with proteins are structural elements cells, take part in transport mechanisms, in the activity of enzymes, in energy exchange processes, 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 concentrations are among the most carefully maintained body 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 bound to protein, and a small amount is found in complex salts. The content of inorganic phosphorus in the body of a growing child is slightly higher than in the body of an adult; In a child, the phosphorus concentration fluctuates around 5 mg%.
Parathyroid hormone and vitamin D, synthesized in thyroid gland calcitonin and bones. Ca and HPO4 ions enter the bones and can be mobilized from there as needed 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 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 carbon 25, resulting in the formation of 25-hydroxycholecalciferol, which is rehydroxylated at carbon 1 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 ensures active calcium transport.
In a rapidly growing body, in accordance with the colossal needs of bone growth, a much larger part of the calcium entering the body is absorbed and retained than in the body of an adult. With vitamin D deficiency and high phosphorus content in food, calcium absorption decreases. Parathyroid hormone has a relatively slow effect, calcitonin is mobilized very quickly: due to its influence, the concentration of Ca decreases, thus compensating for the effect of parathyroid hormone, which increases the level of Ca.
The level of phosphorus in the blood is influenced more significantly by the amount of renal excretion than by the amount of enteral absorption. The latter largely depends on the magnitude of Ca absorption. With a significant intake of calcium or with 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 tubular reabsorption capacity (TtR) and the amount of parathyroid hormone secretion. With an increased intake of phosphorus, TTP is achieved quickly, and most of the ingested phosphorus is released. This process regulates the upper limit of phosphorus content. However, with a sharp decrease in glomerular filtration, the concentration of phosphorus in the blood increases. Parathyroid hormone increases the renal excretion of phosphorus, and its absence weakens it. Although phosphorus can also be mobilized from the bones along with calcium under the influence of parathyroid hormone, the renal effect of this hormone is more pronounced - increasing the excretion of phosphorus. Therefore, with hyperparathyroidism, along with hypercalcemia, hypophosphatemia is also detected, and with hypoparathyroidism, along with hyperphosphatemia, hypocalcemia develops. At pathological conditions changes in the concentrations of calcium and phosphorus are usually of the opposite nature.
Most important role vitamin D in these processes is to enhance the intestinal resorption of calcium and phosphorus, thereby providing the substances necessary for bone growth. Parathyroid hormone and vitamin D have opposite effects on bone calcium levels.
An estimate of the amount of renal calcium excretion can be made on the basis of a convenient clinical practice Sulkovich's semi-quantitative test: the reagent is prepared 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 or sediment immediately occurs. With normal calcium excretion, slight turbidity occurs after 1-2 minutes. With hypocalciuria, the Sulkovich test is negative.
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Chapter V. Rickets, disturbance of phosphorus-calcium metabolism
RICKHS (R). Currently, P is understood as a violation of the mineralization of growing bone, caused by a temporary discrepancy between the needs of a growing organ isma in phosphates and calcium and insufficiency of systems that ensure their delivery to the child’s body. P is the most frequent illness associated with disturbances of phosphorus-calcium homeostasis in children 1 year of life. P and hypovitaminosis D are ambiguous concepts!
IN 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 rates of skeletal modeling and a deficiency of phosphates and calcium in the growing body with imperfect ways of their transport, metabolism and utilization (heterochrony of maturation). Therefore, at present P is classified as a borderline state.
Epidemiology. The frequency of R in children remains unstudied due to changes in ideas about the nature of this pathology. When studying 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, P occurs in young children with a frequency of 1.6 to 35%.
Factors contributing to the development of P:
1. High rates of growth and development of children, increased need for mineral components (especially in premature infants);
2. Deficiency of calcium and phosphates in food;
3. Impaired absorption of calcium and phosphates in the intestines, increased secretion them in the urine or a violation of their utilization in the bones;
4. Decrease in the level of calcium and phosphates in the blood during 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 determined by:
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 bones into the blood, which leads to the development of osteomalacia or osteoporosis.
The daily calcium requirement for infants is 50 mg per 1 kg of body weight. The most important source of calcium is dairy products. The absorption of calcium in the intestine depends not only on its amount in food, but also on its solubility, the ratio with phosphorus (optimal 2:1), the presence of bile salts, the pH level (the more pronounced alkaline reaction, the worse the absorption). The main regulator of calcium absorption is vitamin D.
The bulk (more than 90%) of calcium and 70% of phosphorus is found in the bones in the form of inorganic salts. Throughout life, bone tissue is in a constant process of creation and destruction, caused by 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 levels in the blood. With a decrease in the level of calcium and phosphorus in the blood (the product 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; When this coefficient increases, excessive deposition of salts in the bone occurs.
The excretion of calcium and phosphorus by the kidneys parallels 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” refers to a group of substances (about 10) contained in foods of plant and animal origin that have an effect on phosphorus-calcium metabolism. The most active of them are ergocalciferol (vitamin D 2) and cholecalciferol (vitamin D 3). Ergocalciferol is found in small quantities in vegetable oil, wheat sprouts; 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.Scheme of regulation of phosphorus-calcium metabolism in the body
Normal support The body's supply of vitamin D is associated not only with its intake from food, but also with its formation in the skin under the influence of UV rays. In this case, ergocalciferol is formed from ergosterol (precursor of vitamin D 2), and cholecalciferol is formed from 7-dehydrocholesterol (precursor of vitamin D 3).
Rice. 1.20.Biotransformation of vitamin D
With sufficient insolation (10-minute irradiation of the hands is sufficient), the skin synthesizes necessary for the body amount of vitamin D. In case of insufficient natural insolation: climatic and geographical features, living conditions ( countryside or industrial city), household factors, time of year, etc. the missing amount of vitamin D must come from food or in the form of medications. In pregnant women, vitamin D is deposited in the placenta, which provides the newborn with antirachitic 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 sufficiently studied.
The main physiological function of vitamin D (i.e., its active metabolites) in the body is the regulation and maintenance of phosphorus-calcium homeostasis in the body at the required level. This is achieved through its influence on the absorption of calcium in the intestine, the deposition of its salts in the bones (bone mineralization) and 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 (CBP) by enterocytes. The synthesis of BSC is induced by calcitriol through the genetic apparatus of cells, i.e. The mechanism of action of 1,25(OH) 2 D 3 is similar to hormones.
In conditions of hypocalcemia, vitamin D temporarily increases bone resorption, enhances the absorption of calcium in the intestine and its reabsorption in the kidneys, thereby increasing the level of calcium in the blood. In normocalcemia, it activates the activity of osteoblasts, reduces bone resorption and its cortical porosity.
IN 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 c-AMP mobilizes calcium and its connection with the calmodulin protein, which promotes signal transmission and enhances the function of the cell, and accordingly, 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 gland, directly or indirectly (through calcemia) 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 when the concentration of ionized calcium in the plasma and extracellular fluid decreases. The main target organs for parathyroid hormone are the kidneys, bones and, to a lesser extent, the gastrointestinal tract.
The effect 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 intestines.
In bone tissue, under the influence of parathyroid hormone, calcium from bone apatites turns 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 - a function of vitamin D and its metabolites. PG formation is stimulated by hypocalcemia, when high level calcium in the blood, its production decreases.
The third regulator of calcium metabolism is calcitonin (CT)– a hormone produced by the C-cells of the parafollicular apparatus of the thyroid gland. In terms of its effect on calcium homeostasis, it is a parathyroid hormone antagonist. Its secretion increases when the level of calcium in the blood increases and decreases when it decreases. Diet with big amount 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 described above (vitamin D, parathyroid hormone, calcitonin), is influenced by many other factors. Microelements Mg, Al are competitors of calcium in the absorption process; 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 the leaching of calcium into the blood; Vitamin A is an antagonist of vitamin D during absorption in the intestine. However Negative influence These and many other factors on phosphorus-calcium homeostasis manifest themselves, 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 presented in Fig. 1.19.
Pathogenesis
The main mechanisms of P pathogenesis are:
1. Impaired absorption of calcium and phosphates in the intestine, increased excretion in the urine or impaired utilization of them in the bones.
2. Reduced levels of calcium and phosphate 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 metabolite of vitamin D. This is facilitated by: diseases of the kidneys, liver, intestines, and nutritional defects.
Phosphorus-calcium metabolism disorders in young children most often manifest as hypocalcemia of various origins with clinical manifestations from the musculoskeletal system. The most common disease is R. The cause of hypocalcemia may be a deficiency of vitamin D and disturbances in its metabolism, caused by the temporary immaturity of the enzyme systems of the 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).
Table 1.40.Classification of rickets
Research: general analysis blood and urine, blood alkaline phosphatase, blood calcium and phosphorus, bone radiography.
Clinic. It is currently believed that children with P I degree Only the presence of bone changes is mandatory. THAT. the neurological changes previously described for this severity of rickets do not apply to P.
For P II degree Characterized by pronounced changes in the bones: frontal and parietal tubercles, rosary, deformation of the chest, often varus deformity of the limbs. Radiologically, expansion of the metaphyses of the tubular bones and their cup-shaped deformation are noted.
For P III degree Characterized by gross deformations of the skull, chest, lower extremities, and delayed development of static functions. In addition, the following are determined: shortness of breath, tachycardia, liver enlargement.
Initial signs of P– softening of the edges of the large fontanelle, craniotabes. Question about the so-called initial signs R in the form of sweating, anxiety, trembling, etc. has not been completely resolved.
High period– signs of osteomalacia of bones or osteoid hyperplasia, osteoporosis. The most pronounced clinical and radiological changes coincide with severe hypophosphatemia.
Convalescence period – reverse development clinic R. Pri x-ray examination A clear line of calcification appears in the metaphyseal zone, phosphate levels are normalized, slight hypocalcemia remains, and a moderate increase in alkaline phosphatase levels.
Current P– acute and subacute, At acute course manifestations of osteomalacia predominate, and in the subacute course - osteoid hyperplasia. Manifestations of osteomalacia are: softening of the edges of the large fontanel, craniotabes, rachitic kyphosis, curvature of the limbs, rachitic deformation of the chest.
Signs of osteoid hyperplasia include: rachitic rosary, frontal and occipital protuberances, “strings of pearls”, etc.
Diagnosis. IN outpatient setting Clinical manifestations are sufficient to make a diagnosis of P.
Laboratory confirmation of P I degree– slight hypophosphatemia and increased alkaline phosphatase activity.
Laboratory confirmation of P II degree– decrease in the level of phosphates, calcium, increase in alkaline phosphatase activity.
Laboratory confirmation of P III degree– X-ray examination reveals a gross restructuring of the pattern and development of bones, expansion and blurring of the metaphyses, possible fractures or displacements. In the blood, a pronounced decrease in the levels of phosphates and calcium and an increase in the level of alkaline phosphatase are determined.
The only reliable sign for diagnosing P is a decrease in the level of vitamin D in the blood (determining the level of 25-OH-D 3).
Differential diagnosis R is carried out with: D-resistant forms of rickets, D-dependent forms of rickets types I and II, phosphate diabetes, de Toni-Debreu-Fanconi syndrome, renal tubular acidosis, osteoporosis.
Table 1.41.Differential diagnosis of rickets
| Signs | Vitamin D deficiency rickets | Phosphate diabetes | Renal tubular acidosis | De Toni-Debreu-Fanconi disease |
| Inheritance type | No | Dominant. X-linked | Possibly autosomal recessive or autosomal dominant | autosomal recessive or autosomal dominant |
| Timing of manifestation | 1.5-3 months | Over 1 year old | 6 months-2 years | Over 1-2 years old |
| First clinical manifestations | Damage to the skeletal system | Severe deformation of the lower extremities, bracelets, hypotension, | Polyuria, polydipsia, tearfulness, muscle pain, hypotension | Unreasonable fever, polyuria, polydipsia, muscle pain |
| Specific signs | Craniotabes, frontal and occipital protuberances, bracelets, limb deformity | Progressive varus deformity of the limbs | Polyuria, polydipsia, hypotension to atony, adynamia, liver enlargement, constipation, valgus deformity of the legs | Fever, progressive multiple bone deformities, enlarged liver, decreased blood pressure, constipation |
| Physical development | Without features | Growth deficiency in normal weight | Decrease in height and weight | Decrease in height and weight |
| Blood calcium | reduced | Norm | Norm | More often the norm |
| Phosphorus | reduced | Sharply reduced | reduced | Sharply reduced |
| Potassium | norm | norm | reduced | reduced |
| Sodium | Norm | norm | reduced | reduced |
| CBS | More often acidosis | Metabolic acidosis | Severe metabolic acidosis | |
| Aminoaciduria | There is | norm | norm | expressed |
| Phosphaturia | There is | Sharply expressed | moderate | pronounced |
| Calciuria | reduced | norm | significant | significant |
| X-ray of skeletal bones | Goblet-shaped extensions of the metaphyses | Rough goblet-shaped expansion of the metaphyses, thickening of the cortical layer of the periosteum | Spicy systemic osteoporosis. Blurred contours of the metaphyses, concentric bone atrophy | Osteoporosis, trabecular striations in the distal and proximal diaphysis |
| Effect of vitamin D treatment | Good effect | Minor | Satisfactory effect at high doses |
Osteoporosis– decreased bone mass and disruption of bone tissue structure – may be associated not only with P, but also with other factors. The causes of osteoporosis are: endocrine -metabolic disorders; eating and digestive disorders; the use of a number of medications (hormones, anticonvulsants, antacids, heparin); genetic factors(osteogenesis imperfecta, Marfan syndrome, homocystinuria); long-term immobilization; malignant tumors; chronic renal failure. In these cases, the diagnosis of P is incorrect, despite the clinical similarity.
Treatment. Treatment objectives: restoration of vitamin D deficiency in the body, correction of phosphorus-calcium metabolism disorders, relief of manifestations of vitamin D (bone deformation, muscle hypotension, dysfunction of internal organs).
Treatment scheme.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 (differential diagnosis), lack of effect from prescribing vitamin D medications.
Mode, appropriate for the child’s age, prolonged exposure to air with sufficient insolation (at least 2-3 hours daily).
Diet - natural feeding; when artificial feeding, use adapted formulas appropriate to the child’s age. Timely introduction of complementary foods is important.
Table1. 42. Vitamin D medications
| 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, oil 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 |
| Ergocalciferol (vitamin D 2) tablets | 1 tablet – 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 |
| Oksidevit (calcitriol, 1,25(OH)2D 2 | 1 capsule – 1 mcg 0.00025 mg |
| Fish fat in capsules (Norway), Meller | 1 capsule – 52 IU |
Currently, almost all pediatricians agree that specific treatment It is advisable to carry out small therapeutic doses of vitamin D. Daily dose of vitamin D for I-II degree P at the same time it is 1500-2000 IU, the course is 100,000–150,000 IU; at II-III degrees – 3000-4000 IU, course 200000-400000 IU. This treatment is carried out during the peak period, confirmed by biochemical data (decreased calcium and phosphorus in the blood, increased alkaline phosphatase). At the end of the course, if necessary, it is advisable to switch to a preventive (physiological) dose of vitamin D. Impact, semi-impact methods recommended in the past, repeated treatment courses currently not in use. When carrying out specific therapy, the level of calcium in the blood should be monitored by regularly (once every 10-14 days) the Sulkovich reaction (degree of calciuria).
Table 1.43. Modern calcium-containing preparations
| Name | Ca content | Manufacturer 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 | |
| Osteocea | Great Britain | |
| Ca-Sandoz forte | Switzerland | |
| Complex drugs | ||
| 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. WITH | Egypt |
| Kaltsinova | Ca, P, vit. D, A, C, B 6 | Slovenia |
Calcium preparations are indicated for premature babies and breastfed children in courses of 2-3 weeks. The dose is selected depending on age, severity of P 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 autonomic disorders, the use of potassium and magnesium preparations (panangin, asparkam) at a rate of 10 mg/kg/day for 3-4 weeks is indicated.
Prevention. Currently, nonspecific antenatal prevention of R consists of creating optimal conditions for the pregnant woman for the growth and development of the fetus: balanced nutrition with a sufficient supply of not only proteins, fats, carbohydrates, but also micro- and macroelements (including calcium and phosphorus), vitamins ( including vitamin D); prohibition for a pregnant woman to take toxic (especially for the fetus) substances - tobacco, alcohol, drugs; eliminating the possibility of contact of a pregnant woman with other toxic substances - chemicals, drugs, pesticides, etc. A pregnant woman should be physically active image life, as much as possible (at least 4-5 hours a day) to be on fresh air, maintain a daily routine with sufficient rest day and night. In this case, there is no need for additional vitamin D administration to the pregnant woman.
Antenatal specific prevention R by prescribing 200-400 IU of vitamin D per day from the 32nd week of pregnancy for 8 weeks (carry out only in the winter or spring). For pregnant women at risk, specific prophylaxis P is carried out regardless of the season of the year.
Postnatal nonspecific 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.
A child’s physiological need for vitamin D is 200 IU per day.
Postnatal specific prevention of P is carried out for children only in the period late autumn - early spring at a dose of 400 IU per day, starting from 4 one 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 microelements in physiological doses, and therefore there is no need for additional introduction vitamin D. For children with small fontanelles, it is preferable to use nonspecific methods of preventing R.
For premature infants, the issue of prophylactic administration of vitamin D should be decided only after optimizing dietary intake of calcium and phosphorus. It has been established that hypovitaminosis D is practically undetectable in premature infants. In the development of osteopenia in them crucial has calcium and phosphate deficiency. It is traditionally believed that the prophylactic dose of vitamin D for premature infants is 400-1000 IU per day.
SPASMOPHILIA (C)- a peculiar condition of young children with signs of rickets, caused by a violation mineral metabolism, hypofunction of the parathyroid glands, manifested by signs of increased neuromuscular excitability and a tendency to seizures.
Epidemiology. C occurs almost exclusively in children in the first 2 years of age, in approximately 3.5-4% of all children.
Pathogenesis. Disorders of mineral metabolism in C are more pronounced than in rickets and are characterized by certain 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 with 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 are considered to be a 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 B1, which is present in C. With its severe deficiency, sharp disturbances occur in the glycolytic chain with the formation pyruvic acid, which plays a big role in the occurrence of seizures.
C occurs in any season of the year, but develops more often in the spring.
Attack C can be provoked by the development of any disease with high temperature, frequent vomiting due to gastrointestinal diseases, as well as severe crying, agitation, 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 calcium and phosphorus content in blood plasma; determination of alkaline phosphatase activity in blood plasma, CBS study, ECG.
History, 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. Attack C is provoked febrile conditions, frequent vomiting due to gastrointestinal diseases, fear, agitation, severe crying, increased ultraviolet radiation.
When examining a child with C, signs of rickets should be revealed.
Signs of hidden C(symptoms of increased excitability of the neuromuscular system):
A) Chvostek's sign- light tapping at the exit site facial nerve(between the zygomatic arch and the corner of the mouth) causes contraction or twitching muscle musculature the relevant side of the person;
b) Lusta's peroneal sign - tapping behind and slightly below the head of the fibula causes dorsiflexion and abduction of the foot outward;
V) 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 breathing to stop instead of increasing speed (carried out under the control of a pneumogram);
d) Erb's sign - opening of the cathode attached to median nerve, causes muscle contraction at a current intensity of less than 5 mA.
Signs of obvious 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 expression on the face, child open mouth“catching air”, cyanosis of the skin, cold sweat on the face and torso. After a few seconds, a noisy inhalation appears and normal breathing is restored. Attacks of laryngospasm may be repeated throughout 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: ocular, masticatory (temporary strabismus or trismus), spasms of the respiratory muscles (inspiratory or expiratory apnea) are prognostically unfavorable, less often - a spastic state of the heart muscle (cardiac arrest and sudden death). Spasms occur smooth muscle internal organs, which leads to urination and defecation disorders;
V) eclampsia - clonic-tonic convulsions involving striated and smooth muscles of the whole body; the attack begins with twitching of the facial muscles, then convulsive contractions of the limbs and respiratory muscles join, and cyanosis occurs. Consciousness is usually lost at the beginning of the attack. The duration of the attack is from several minutes to several hours. Tonic and clonic seizures can be isolated, combined or sequential. Clonic seizures are more often observed in children in the first year of life, tonic - in children older than one year.
Diagnosis C is based on identifying signs of obvious 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 increased level of inorganic phosphorus.
b) increasing the numerator digits or decreasing the denominator in György’s formula: P0 4 -- HC0 3 –K +
Ca++Mg++H+
Differential diagnosis C is carried out with diseases manifested by hypocalcemia: chronic renal failure, hypoparathyroidism, malabsorption syndrome, taking drugs that reduce calcium levels
Table 1.44. Differential diagnosis of spasmophilia
| Sign | Spasmophilia | Hypoparathyroidism | chronic renal failure | Malabsorption syndrome |
| Convulsions | Yes | Yes | +/- | Possible |
| Rachitic bone changes | Characteristic | No | Osteoporosis | Osteoporosis |
| Chronic diarrhea | No | No | +/- | typical |
| Uv. urea, creatinine | No | No | Yes | No |
| Symptoms of increased neuromuscular excitability | Yes | Yes | Yes | Yes |
| PTH↓ level, phosphorus | No | No | No | Yes |
| Blood calcium ↓ | Yes | Yes | Yes | Yes |
Treatment. Treatment objectives: normalization of neuromuscular excitability, mineral metabolism indicators; relief of seizures and other manifestations of C, treatment of rickets.
Treatment regimen
Mandatory activities: relief of hypocalcemia, syndromic therapy for manifestations of C, treatment of rickets.
Helper Methods treatment: regime, diet, vitamin therapy.
Indications for hospitalization: convulsions, eclampsia, laryngospasm.
Mode: limit as much as possible or perform extremely carefully procedures that are unpleasant for the child.
Diet: exclusion of cow's milk for 3-5 days, carbohydrate diet, gradual transition to balanced, age-appropriate food.
For eclampsia: calcium chloride or gluconate 10% solution, 2-3 ml, intravenous micro-jet. Sodium hydroxybutyrate 50-100 mg/kg slow intravenous or droperidol 0.25% solution 0.1 mg/kg, slow intravenous or Seduxen 0.5% solution, 0.15 mg/kg, intramuscular or intravenous, or magnesium sulfate 25% solution, 0.8 ml/kg, intramuscularly, but not more than 8.0 ml.
For carpo-pedal spasm: inside calcium chloride or gluconate, phenobarbital, bromides.
For laryngospasm: Sprinkle cold water on the patient, press your finger on the root of the tongue, according to indications - artificial respiration, drug therapy, as in eclampsia.
After rendering emergency care : calcium preparations orally, ammonium chloride 10% solution, 1 tsp. 3 times a day, vitamin D 4000 IU daily from 4-5 days; vitamin therapy.
Prevention C primarily associated with the identification and treatment of rickets. Rational feeding of the child is important. Special attention pay attention to the early introduction of cow's milk products into the diet. It is necessary to prevent strong crying and fear.
VITAMIN D HYPERVITAMINOSIS (HD) occurs with an overdose of vitamin D or with individual hypersensitivity to it.
Epidemiology. Currently, thanks to the revision of approaches to the prevention and treatment of rickets, HD in children is rare.
PhysiologyMineral metabolism disorders are changes in the levels of calcium, phosphorus or magnesium. Calcium is of primary importance in cell function. In the process of regulating the homeostasis of these basic mineral macroelements, mainly three organs - kidneys, bones and intestines - and two hormones - calcitriol and parathyroid hormone - take part.
The role of calcium in the body
About 1 kg of calcium is contained in the skeleton. Only 1% general content Calcium circulates in the body 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 simultaneously 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 operation 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
Below 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 influence 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-sensing 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 consequence, 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, when the level of calcium in the blood decreases, the receptor is activated, the level of parathyroid hormone secretion increases and the excretion of calcium in the urine decreases. Defects in the calcium-sensing receptor lead to disruption of 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 to form the hormone calcitriol, which plays a major role in the regulation of calcium homeostasis. In addition, parathyroid hormone increases calcium reabsorption in the distal nephron and 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 and the duration of exposure to its high concentration, the condition of bone tissue changes differently in different departments(cortical and trabecular). In calcium homeostasis, the dominant effect of parathyroid hormone is to enhance bone resorption.
Parathyroid hormone-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. Parathyroid hormone has clinical significance only for malignant tumors that can synthesize it. In routine practice, the level of parathyroid hormone-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 suppresses the function of osteoclasts. The essential role of calcitonin in calcium homeostasis in fish and rats is known. In humans, calcitonin does not have a significant effect on blood calcium levels. This is confirmed by the absence of disturbances in calcium homeostasis after thyroidectomy, when C-cells are removed. Calcitonin levels have 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. IN pharmacological doses glucocorticoids significantly reduce calcium absorption in the intestine and reabsorption in the kidneys, thereby reducing blood calcium levels. High doses glucocorticoids also influence bone metabolism, increasing bone resorption and decreasing bone formation. These effects are important in patients receiving glucocorticoid therapy.
