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Inability of Short-Term, Low-Dose Hydroxychloroquine to Resolve Vitamin D-Mediated Hypercalcemia in Patients with B-Cell Lymphoma¹

The Burns and Allen Research Institute and Division of Endocrinology and Metabolism, Cedars-Sinai Medical Center, University of California Los Angeles, Los Angeles, California 90048

Address correspondence and requests for reprints to: John S. Adams, M.D., B131, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048.

The 4-aminoquinolines, including chloroquine and hydroxychloroquine, have been successfully employed to treat patients with granuloma-forming disease-associated, vitamin D metabolite-mediated hypercalcemia. The calcium-lowering efficacy of these drugs has not been prospectively evaluated in patients with lymphoma and elevated 1,25-(OH)₂D levels. Four such hypercalcemic patients with stage IV B-cell lymphoma were treated, two each, with either 400 mg daily oral hydroxychloroquine or a single course of prednisone-containing antitumor chemotherapy (CHOP). Antitumor therapy normalized the serum calcium and 1,25-(OH)₂D concentration within 5 days. Over a 15-day period, hydroxychloroquine failed to reduce either the serum calcium or 1,25-(OH)₂D level in lymphoma patients. In contrast, within 5 days 400 mg of hydroxychloroquine daily lowered elevated levels of calcium and 1,25-(OH)₂D by 37% and 72%, respectively, in a hypercalcemic patient with sarcoidosis. These data suggest that regulation of the vitamin D-1-hydroxylase in lymphoma cells, the putative source of hormone in lymphoma patients, is refractory to the inhibitory actions of the aminoquinolines and that glucocorticoid-containing antitumor regimens are the antihypercalcemic therapies of choice in lymphoma patients with high 1,25-(OH)₂D levels.

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