FOSFATEMYYa (phosphate[s] - f Greek haima blood) — the content in blood of the inorganic phosphorus presented by preferential free anions of phosphoric acid (NR (At, H2P04) and its salts — phosphate sodium, potassium, calcium and magnesium. Normal their concentration in blood averages 4 — 5 mg / 100 ml. Concentration phosphate ions, forming phosphatic buffer system, is connected with concentration of hydrogen ions.
Level F. also its moving to fabrics, the hl depends on intake of phosphorus with food. obr. in bone, containing 80 — 87% of all phosphorus which is a part of a human body and also of release of phosphates from an organism. Daily the person receives 0,8 — 1,5 g of phosphorus with food, 70 — 90% to-rogo are soaked up in a small bowel with the participation of D3 vitamin. Phosphates generally with urine (see Fosfaturiya), to a lesser extent with a stake are excreted.
Constancy of level F. it is supported first of all by hormonal regulation reabsorbtsin phosphates in renal tubules, edges raises under the influence of somatotropic hormone, thyroxine, insulin and the tirokaltsitonina, a hydrocortisone, and also vitamin D decreases under the influence of parathormone (see Kidneys, physiology). Methods of quantitative definition of inorganic phosphorus (see) in blood and urine are based on education from phosphates and molybdenic to - you a phosphatomolybdic complex, to-ry under the influence of reducers (hydrochinone, ascorbic to - that, tin chloride, etc.) turns into molybdenic blue, painting solution. The intensity of coloring estimated colorimetric is proportional to amount of the phosphates which are contained in solution. There are also ultramicromethods of assessment of a fosfatemiya.
At various diseases and patol. states it is possible as increase in content of inorganic phosphorus in blood (hyperphosphatemia), and its decrease (hypophosphatemia). The hypophosphatemia has the greatest value, edges are given by iv to decrease in oxidizing phosphorylation and cellular energy resources (see biological oxidation), to reduction of synthesis 2,3-difosfoglsh Herat in erythrocytes, to shift to the left of curve dissociation of an oksigemoglobpn (see Hemoglobin) and to development of a fabric hypoxia (see).
Hypophosphatemia — a nonspecific symptom of disturbances of exchange and acid-base equilibrium at many diseases. The reasons of a hypophosphatemia can be insufficient receipt in an organism of phosphates at plentiful repeated vomiting (see), starvation (see), a syndrome of malabsorption (see Maljabsorbtion a syndrome), diseases of intestines and pancreas, a hypovitaminosis of D (see Calciferols) or the strengthened removal their kidneys at primary hyperparathyreosis (see), a myeloma (see. Multiple myeloma), a nephrotic syndrome (see) various genesis, gepato-tserebraljny dystrophy (see), primary euzymatic tubulopatiya — phosphate diabetes (see), de Tony's syndrome — Debra — Fankoni (see De Tony — Debra — Fankoni a syndrome), a cystinosis (see), renal canalicular acidosis (see). The hypophosphatemia develops also at alcoholism (especially in the period of abstinence), a respiratory alkalosis, extensive burns. The hypophosphatemia at treatment is possible the nek-ry adsorbents connecting phosphorus in intestines (magnesium oxide, aluminum hydroxide, etc.), at reception of diuretics, a hemodialysis (see), therapy of diabetic ketoacidosis, administration of glucose and insulin (the increased consumption of phosphorus on phosphorylation of hexoses).
Clinically the hypophosphatemia is shown by weakness, irritability, anorexia, dispeptic frustration, paresthesias, development of a myopathy and ataxy, an abnormal liver function and hearts. Hemolysis, leucio-and thrombocytopenia, decrease in aggregation of thrombocytes, tendency to infections (is observed up to a colisepsis), osteomalacy. Confusion of consciousness, and then coma appears in hard cases. In the presence of a hypophosphatemia recommend intravenous administration of phosphates.
The hyperphosphatemia is observed at children and newborns (especially in the first two days after the birth), at a heavy exercise stress, a hypoparathyrosis (see) and a pseudohypoparathyroidism (see), a thyrotoxicosis (see), toxicosis of pregnant women (see), against the background of healing of bone changes, at hemolysis (see), leukoses (see), primary and metastatic tumors of bones (see the Bone), at a renal failure (see), sometimes at congestive heart failure (see). The hyperphosphatemia can be caused also by overdose of vitamin D, excess UF-radiation, a hemotransfusion, the use in a large amount of milk at diseases of a stomach, administration of heparin, tetracycline. Correction of a hyperphosphatemia is carried out by elimination of the reason which caused it including treatment of a basic disease.
See also Mineral metabolism, Phosphoric exchange.
Bibliography: Natochin Yu. V. Ionoreguliruyushchaya function of a kidney, L., 1976; Irving J. T. Calcium and phosphorus metabolism, N. Y. — L., 1973;
Stoff J. S. Phosphate homeostasis and hypophosphatemia, Amer. J. Med., v. 72, p. 489, 1982, bibliogr. V. K. Velikov.