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The Multifactorial Basis for Hypocalcemia During Sepsis: Studies of the Parathyroid Hormone-Vitamin D Axis

GARY P. ZALOGA, M.D.; and BART CHERNOW, M.D.
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The opinions expressed herein are those of the authors and are not to be construed as reflecting the views of the Department of the Navy, the Naval Service at large, or the Department of Defense.

Presented in part at the annual meeting of the Society of Critical Care Medicine, Washington, D.C., May 1986.

▸Requests for reprints should be addressed to Bart Chernow, M.D.; Department of Anaesthesiology, Massachusetts General Hospital; Boston, MA 02114.


Bethesda, Maryland


Ann Intern Med. 1987;107(1):36-41. doi:10.7326/0003-4819-107-1-36
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To learn about the pathogenesis of sepsis-associated hypocalcemia, we measured serum ionized calcium concentrations in 60 critically ill patients with bacterial sepsis; 12 (20%) had hypocalcemia. The mortality rate in the hypocalcemic patients with sepsis (50%) was higher than that in the normocalcemic patients with sepsis (29%). Only patients with gram-negative sepsis became hypocalcemic, and hypocalcemia contributed to hypotension in 7 of the 12 hypocalcemic patients. Serum calcium concentrations returned to normal in each of those patients with sepsis who survived. Hypocalcemia during sepsis occurred in previously normocalcemic patients and was multifactorial in origin, resulting from acquired parathyroid gland insufficiency, renal 1α-hydroxylase insufficiency, vitamin D deficiency, and acquired calcitriol resistance. We conclude that the hypocalcemia of sepsis is associated with a high mortality rate and usually occurs in previously normocalcemic patients who acquire a defect in the parathyroid-vitamin D axis.

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