Hiroshi Noto *,1,2

Abstract: We describe the clinical and laboratory findings in 2 cases of hypocalcemia secondary to vitamin D deficiency in intensive care unit and the response of calcium to treatment. We also discuss the mechanism and review pertinent lit-erature. The first patient was admitted due to stroke. Laboratory data included serum calcium 7.6 mg/dl, intact parathyroid hormone (PTH) 891.6 pg/ml, 25-hydroxyvitamin D (25-OH-D) 7 ng/ml (17.5 nmol/l), 1,25-dihydroxyvitamin D (1,25-OH-D) 43 pg/ml (103.2 nmol/l), and corrected QT (QTc) interval 494 msec. After two weeks of treatment with oral cal-cium and ergocalciferol, serum calcium and intact PTH levels and QTc interval normalized. The second patient was trans-ferred for the management of disseminated cytomegalovirus infection. Laboratory work-up revealed serum calcium 7.7 mg/dl, creatinine 4.3 mg/dl, intact PTH 207.5 pg/ml, 25-OH-D <5 ng/ml (<12.5 nmol/l), 1,25-OH-D <10 pg/ml (<24 nmol/l), and QTc interval 505 msec. After treatment for vitamin D deficiency and infection, we observed normalization of creatinine, corrected calcium, intact PTH and QTc interval. The clinical courses were uneventful in both cases. In conclu-sion, we would like to emphasize that vitamin D status should be evaluated in patients with hypocalcemia in acute settings because vitamin D deficiency is common and readily treatable, and there may be clear life-threatening consequences if it is not treated