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Calcitriol in Prolonged Hypocalcemia due to the Tumor Lysis Syndrome

Robert W. Dunlay, MD; Mark A. Camp, MD; Michael Allon, MD; Paolo Fanti, MD; Hartmut H. Malluche, MD; and Francisco Llach, MD
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Requests for Reprints: Michael Allon, MD, Nephrology Section (111G), Veterans Administration Medical Center, 921 N.E. 13th Street, Oklahoma City, OK 73104.

Current Author Addresses: Drs. Dunlay, Camp, Allon, and Llach: Nephrology Section (111G), Veterans Administration Medical Center, 921 N.E. 13th Street, Oklahoma City, OK 73104.

Drs. Fanti and Malluche: Division of Nephrology, Bone and Mineral Metabolism, Room MN 572, University of Kentucky Medical School, 800 Rose Street, Lexington, KY 40536.

Ann Intern Med. 1989;110(2):162-164. doi:10.7326/0003-4819-110-2-162
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This excerpt has been provided in the absence of an abstract.

The tumor lysis syndrome is recognized by the development of hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia shortly after the administration of therapy for neoplastic disorders (1, 2). The syndrome has most often been associated with rapidly dividing hematopoetic malignancies, such as acute leukemias and high-grade lymphomas. Hypocalcemia in the tumor lysis syndrome has been attributed to precipitation of calcium phosphate salts (2), but the reasons it persists after the hyperphosphatemia is corrected have not been elucidated.

We report a case of acute tumor lysis syndrome with prolonged hypocalcemia in a patient with Burkitt lymphoma. Serial biochemical measurements during the course of


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