Hypercalcemia
Hypercalcemia is almost always the result of increased calcium intake into the blood from resorbed bone tissue or from food in conditions of a decrease in its kidney clearance. More than 90% of cases of hypercalcemia are due to primary hyperparathyroidism and malignant neoplasms.
Primary hyperparathyroidism is the main cause of hypercalcemia in outpatients. This is a very common pathology, especially in older women. Approximately 85% of cases of hypercalcemia are caused by an adenoma of one of the parathyroid glands, 15% by hyperplasia of all four glands and 1% by parathyroid carcinoma. Usually, hypercalcemia is asymptomatic and is found by chance during dispensary examinations. Elevated blood pressure accompanies 30-70% of cases of primary hyperparathyroidism. In these cases, treatment with thiazide diuretics can mask hypercalcemia.
Malignant neoplasms are the cause of most cases of hyperkalcemia in hospitalized patients and in the elderly. In this case, there are two main mechanisms.
■ Local osteolytic hypercalcemia, in which the products of the vital activity of tumor cells stimulate local bone resorption with osteoclasts. This form of hypercalcemia occurs only with extensive damage to the bones by the tumor;most often with metastases of breast cancer, myeloma and lymphoma.
■ Humoral paraneoplastic hypercalcemia, in which tumor metabolites have a common effect, stimulating bone resorption and decreasing calcium excretion. Humoral paraneoplastic hypercalcemia is most often caused by squamous cell carcinoma of the lungs, head and neck, esophagus, kidney, bladder and ovarian carcinoma.
Other causes of hypercalcemia are rarely observed. Sarcoidosis, tuberculosis, and histoplasmosis may be accompanied by hypercalcemia. The cause of hypercalcemia in these diseases is an increased absorption of calcium in the small intestine when the formation of the active form of vitamin D is enhanced. Hypercalcemia is possible in pediatric practice, especially in conditions of insufficient intake of vitamin D. In these situations, vitamin therapy helps normalize the calcium and phosphorus levels in the blood. Hypercalcemia may result from intoxication with vitamin D.
A comparison of laboratory signs of primary hyperparathyroidism, humoral paraneoplastic hypercalcemia and familial benign hypercalcemia is given in Table 1.
Table Laboratory features of primary hyperparathyroidism, humoral paraneoplastic hypercalcemia and familial benign hypercalcemia [Lavin N., 1999]
TableLaboratory features of primary hyperparathyroidism, humoral paraneoplastic hypercalcemiaand familial benign hypercalcemia [Lavin N., 1999]
Note: T is a slight increase;TT - a significant increase;I - decrease;H is the norm.
Note: T is a slight increase;TT - a significant increase;I - decrease;H is the norm.
The frequency of hypercalcemia in peptic ulcer is higher than in other types of pathology. Long-term immobilization with Paget's disease or complex fractures is accompanied by mild osteoporosis and an increase in the calcium content in the blood. Steroid-induced gipercalcemia can be observed with androgens, estrogens and HA.Long stay of the patient in bed is accompanied by hypercalcemia. Clinical manifestations of pancreatitis are also associated with a violation of calcium metabolism. In the first week of acute pancreatitis, hypocalcemia may develop, which can later be replaced by hypercalcemia.
Clinical manifestations of hypercalcemia are observed with a calcium concentration in the blood above 3 mmol / l, and they are more pronounced with the rapid development of hypercalcemia. The renal manifestations include polyuria and urolithiasis. Gastrointestinal disorders include anorexia, nausea, vomiting and constipation. Among the neurological symptoms are weakness, fatigue, confusion, stupor and coma. On ECG - shortening of the QT interval. If the concentration of calcium in the blood serum exceeds 3.75 mmol / l, renal failure and ectopic soft tissue calcification are possible. The content of
serum calcium below 3 mmol / l corresponds to mild, and above 3.38 mmol / l - severe hypercalcemia.
The basis for the study of calcium in blood serum is considered to be urolithiasis, bone pathology, hypertension, gout, myopathy, peptic ulcers of the stomach, pronounced weight loss, pancreatitis. Calcium studies are performed in patients with acute renal failure and chronic renal failure, hemodialysis and extracorporeal treatment. Monitoring of calcium content is performed during large surgical interventions, especially in conditions of artificial circulation. The study of calcium in the blood serum is also shown in renal colic, hematuria, pyelonephritis.