Hypocalcemia in multiple myeloma secondary to unrecognised vitamin D deficiency: A case report

Abstract

Vitamin D deficiency is now recognized as one of the most common nutritional deficiency world wide. The primary function of the vitamin is to maintain calcium homeostasis by enhancing intestinal calcium absorption and mobilising calcium from the skeleton. Vitamin D also has important nonskeletal actions. It has been suggested that the production of 1,25 (OH)2D by macrophages locally regulates both activated T and B lymphocyte activities. The consequences of vitamin D deficiency on the skeleton are two fold. The secondary hyperparathyroidism induced by vitamin D deficiency will increase the number of osteoclasts, causing the removal of the mineral and matrix from the skeleton, which can result in osteopenia and osteoporosis. The secondary hyperparathyroidism also causes phosphaturia which can result in osteomalacia. Recent studies have reported a high prevalence of vitamin D deficiency in multiple myeloma (MM) patients (Badros et al. 2008). We present a case to illustrate how unrecognised vitamin D deficiency can lead to refractory hypocalcemia during periods of acute illness, in patients with MM.