The Open Endocrinology Journal

2009, 3 : 1-4
Published online 2009 February 18. DOI: 10.2174/1874216500903010001
Publisher ID: TOEJ-3-1

Vitamin D Deficiency as an Ignored Cause of Hypocalcemia in Acute Illness: Report of 2 Cases and Review of Literature

Hiroshi Noto and Howard J. Heller
Division of Endocrinology and Metabolism, Department of Medicine, Toshiba Hospital, 6-3-22 Higashi Oi, Shinagawa, Tokyo, 140-8522, Japan.

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 literature. 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 calcium and ergocalciferol, serum calcium and intact PTH levels and QTc interval normalized. The second patient was transferred 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 conclusion, 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.

Keywords:

Vitamin D, hypocalcemia, hyperparathyroidism.