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Accelerated Bone Formation Causing Profound Hypocalcemia in Acute Leukemia

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▸Requests for reprints should be addressed to Kenneth Miller, M.D.; Tufts-New England Medical Center, 171 Harrison Avenue; Boston, MA 02111.

Boston, Massachusetts; and Atlanta, Georgia

© 1986 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1986;105(3):375-378. doi:10.7326/0003-4819-105-3-375
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A patient with acute monocytic leukemia and fibrosis presented with severe hypocalcemia producing tetany, myocardial failure, and ventricular tachycardia with torsades de pointes configuration. Hypophosphatemia, hypomagnesemia, an elevated alkaline phosphatase level, and osteosclerosis were also present. Bone marrow biopsy samples showed fibrosis and thickened bony trabeculae lined with large osteoblasts. Tetracycline labeling showed an increased rate of calcification. Complete remission of the leukemia and fibrosis was achieved with a single 3-week course of low-dose cytarabine and hydroxyurea, with resolution of the hypocalcemia and hypophosphatemia. Calcitriol and etidronate disodium were also administered. The calculated left ventricular ejection fraction increased from 15% to 55% with correction of the hypocalcemia. The hypocalcemia and hypophosphatemia in this patient probably resulted from accelerated bone formation stimulated by the leukemic cells. The high dose of calcitriol that this patient received may have contributed to the remission of the leukemia.





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