3.4 - Non-tumor-induced hypercalcemia

Abstract

All hypercalcemias that cause diseases other than malignant bone disease fall within the category of non-tumor-induced hypercalcemia. An increase in blood calcium can be due to increased flux of calcium from bone or the intestine, to an increase in tubular reabsorption of calcium in the kidney, or both. An increase in calcium flux from bone, following accelerated bone destruction, is by far the most common mechanism. Examples are hyperparathyroidism, which is the most frequent cause, thyrotoxicosis, and certain cases of acute osteoporosis, as during immobilization. Often, more than one mechanism is involved, such as in primary hyperparathyroidism, where the increase in blood calcium originates from both bone and kidney. The clinical picture is that of the hypercalcemic syndrome. Disturbances involve the central and peripheral nervous system, the digestive system, cardiovascular and renal systems, and the muscles. Dangerous complications are acute hypercalcemic crisis, which can be fatal, and ectopic calcification. The latter occurs especially in the kidney, where renal failure can result, and in the urinary tract in the form of urolithiasis. Most hypercalcemias are relatively resistant to treatment other than that which is directed to the underlying disease. Drugs used include corticosteroids, prostaglandin inhibitors, calcitonin, and furosemide, but the results are most often disappointing, except for corticosteroids in granulomatous diseases and in vitamin D toxicity. The animal experiments which give the basis for the use of bisphosphonates in hypercalcemia in humans have been discussed extensively.