The effect of an intravenous chelating agent, edathamil disodium (Na 2-EDTA), in 3 cases of sarcoidosis.

The cause or causes of hypercalcemia and hypercalcuria in sarcoidosis are obscure. Harrell and Fisher (1) were the first to emphasize that hypercalcemia, hyperproteinemia and elevated serum alkaline phosphatase could occur in this disease. Dent etat (2) believed that bone destruction represented the cause of hypercalcemia. Anderson et at (3) concluded from their studies that increased calcium absorption was the cause of hypercalcemia in sarcoidosis. Recently, Henneman et at (4) further explored the possible mechanisms in the causation of sarcoid hypercalcemia and, based on four complete calcium balance studies on three patients with sarcoidosis they were able to demonstrate that the hypercalcuria in this disease appeared to be due to endogenous hypervitaminosis D. The abnormalities of calcium metabolism in these subjects appeared to embrace three actions of Vitamin D: (1) increased calcium absorption from the intestine (decreased fecal calcium excretion), (2) parathyroid hormone-like action and (3) increased absorption of nitrogen, sodium, potassium, magnesium and iron. These workers also studied the effects of cortisone and sodium phytate, a calcium immobilizing agent, upon their subjects and noted that both of these substances decreased urinary calcium excretion and increased fecal calcium excretion. Terepka et at (5), using controlled technics for the determination of ultraffiterable calcium in human serum, noted that in Boeck's sarcoid the concentration of ultrafilterable calcium was distinctly elevated while the percentage of the total serum calcium which was ultrafilterable (ratio of ultrafilterable to total serum calcium) was normal or only slightly elevated. They postulated that the alteration in the concentration of ultrafilterable