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Lymphoma, Hypercalcemia, and the Sunshine Vitamin

Malcolm Cox, MD; and John G. Haddad, MD
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Veterans Affairs Medical Center; Philadelphia, PA 19104 Hospital of the University of Pennsylvania; Philadelphia, PA 19104 Requests for Reprints: Malcolm Cox, MD, Medical Service RF 111, Veterans Affairs Medical Center, University and Woodland Avenues, Philadelphia, PA 19104.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1994;121(9):709-712. doi:10.7326/0003-4819-121-9-199411010-00012
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Under normal circumstances, parathyroid hormone and 1 α,25-dihydroxycholecalciferol (calcitriol) jointly defend the plasma calcium concentration. Parathyroid hormone increases renal distal tubular calcium reabsorption and mobilizes calcium from bone. Calcitriol, the active product of vitamin D metabolism, enhances gastrointestinal calcium absorption and also mobilizes calcium from bone. The roles of parathyroid hormone and calcitriol in calcium homeostasis are intimately interrelated. Parathyroid hormone is the primary trophic stimulator of renal 1 α-hydroxylase, the enzyme that converts 25-hydroxycholecalciferol into calcitriol. Calcitriol, in turn, inhibits parathyroid hormone secretion by at least two different mechanisms: direct repression of the preproparathyroid hormone gene and inhibition of the synthesis and release of the hormone as an indirect consequence of the increase in the plasma calcium concentration. Thus, parathyroid hormone is a primary regulator of vitamin D metabolism, and calcitriol is a primary feedback inhibitor of parathyroid hormone secretion.

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