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Increased 1,25-Dihydroxycholecalciferol as a Cause of Abnormal Calcium Metabolism in Sarcoidosis

YOSHINOBU KOIDE^*, NOBUO KUGAI, SATOSHI KIMURA, TOSHIRO FUJITA, NOBUKI YAMASHITA, TSUTOMU HIRAMOTO, JUN SUKEGAWA, ETSURO OGATA and KAMEJIRO YAMASHITA

Institute of Clinical Medicine, University of Tsukuba, Niihari-gun Ibaraki-ken 305, Japan

The mechanism of abnormal calcium metabolism in sarcoidosis was studied in two patients with hypercalcemia and two patients with normocalcemia. Serum immunoreactive parathyroid hormone levels and urinary cAMP excretion were suppressed in two patients with hypercalcemia. Plasma 25-hydroxycholecalciferol was within the normal range in all patients and showed no significant correlation to serum calcium levels or urinary calcium excretion. However, plasma 1,25-dihydroxycholecalciferol [1,25-(OH)₂D₃] in the patients with hypercalcemia was inappropriately elevated in spite of the coexistent functional hypoparathyroidism and normophosphatemia. In addition, 1,25-(OH)₂D₃ showed significant positive correlations with serum calcium concentrations and urinary calcium excretion in patients with hypercalcemia. Prednisolone normalized plasma 1,25-(OH)₂D₃ levels as well as urinary cAMP excretion and corrected hypercalcemia and hypercalciuria.

It is concluded that the increased 1,25-(OH)₂D₃ of unknown etiology is the most probable cause of the abnormal calcium metabolism in sarcoidosis.

^* To whom requests for reprints should be addressed.

Present address: Endocrine Division, National Cancer Center Research Institute, Chuo-ku, Tokyo 104, Japan.

Present address: The Fourth Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 112, Japan.

Received August 4, 1980.

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