Clinic of hypervitaminosis D extensively discussed in the works of E. E. Malinau (1941), E. M. Lepskaya (1953), G. M. Hass a. oth. (1958), K. A. Svyatkina (1964, 1971), L. M. Pleskovo and others (1962), A. F. Round (1965, 1966). However, timely diagnosis of the disease is often very difficult. Thus, according to centuries Checkoway et al. (1971), 98 observed children with Dr. vitamin a intoxication only 7 patients were hospitalized with the diagnosis.
The expansion of pre-calcification, increased deposition of salts of calcium in the periarterial areas.
Thus, the diagnosis of hypervitaminosis D is based on the set of a number of historical, clinical, and laboratory biochemical and radiological indicators. In typical cases, the diagnosis of hypervitaminosis D straightforward. However, polymorphism clinic of hypervitaminosis D with a varied combination of symptoms is the reason for the difficulty in diagnosis. Gipervitaminoz D in children has the features characteristic of other diseases. In this connection there is a need to differentiate gipervitaminoz D with a number of diseases associated with hypercalcemia, hypophosphatemia, hypercalciuria, hyperphosphatemia, kidney function, and some other signs D-vitamin intoxication.
First of all it is necessary to differentiate D-vitamin a intoxication from hypercalcemia other etiology. Earlier one of the main causes of hypercalcemia was considered widespread use of calcium during the treatment of edema syndrome in children. Currently, the most common cause of hypercalcemia in children are hypervitaminosis D, gipofosfatemia, giperparatireoidizm, hypofunction of thyroid gland, idiopathic hypercalcemia, bone tumor, leukemia. Mostly these diseases must differential diagnosis of hypervitaminosis D.
Giperparatireoidizm is a common disease of the body, characterized by increased secretion of parathyroid hormone. To this pathology O. C. Mykolayiv and B. N. Tarceva (1974) include primary hyperparathyroidism arising on the basis of one or more giperfunktsionalnaya adenomas or diffuse parathyroid hyperplasia, and secondary parathyroid hyperplasia caused by hypovitaminosis D, rickets, chronic kidney disease, disorder or impaired calcium absorption in the intestine.
Primary hyperparathyroidism is most similar to the clinic with Dr. vitamin a intoxication. Due to excess production of parathormone increases resorption of bone tissue, leading to the development of hypercalcemia and hypercalciuria. At the same time the surplus of parathormone increases glomerular filtration and reduces tubular reabsorption of phosphorus. All this leads to the development of giperfosfatemii and gipofosfatemia. Thus, there are violations of calcium and phosphorus metabolism, such hypervitaminosis D.
The clinical picture of the disease characterized by a gradual onset: bone pain, General weakness, poor appetite, constipation, and sometimes nausea, vomiting. Due to softening of the bones are formed multiple fractures, leading to deformation of the skeleton. Often develop heart failure due to myocardial degeneration, kidney (pyelonephritis, calcification of the kidneys and bladder). In the result of hypercalcemia occurs metastatic calcification of various organs and systems. In patients with giperparatireoidizm on x-rays of the bones expressed osteoporosis, thinning of the cortical layer, skull "moth-eaten", vertebrae flattened. For biochemical analysis of blood of children are marked hypercalcemia, a positive test of Sulkowice, hypophosphatemia, hyperphosphaturia. Hyperparathyroidism disease (Recklinghausen) from hypervitaminosis D differs progressive course of the disease, the lack of communication of the disease with the use of vitamin D. in Addition, the disease is observed in older age.