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The Hypocalcemia of Acute Pancreatitis
- GORDON C. WEIR, M.D.;
- PAUL B. LESSER, M.D.;
- LAMBERTUS J. DROP, Ph.D., M.D.;
- JOSEF E. FISCHER, M.D.; and
- ANDREW L. WARSHAW, M.D.
Abstract
Variables of calcium metabolism were measured in 11 patients with clearly documented acute pancreatitis. Total and ionized calcium levels were either low or in the low-normal range as were phosphorus and total magnesium levels. Parathyroid hormone levels were high, and there was a significant inverse correlation with ionized calcium. Gastrin levels were normal, calcitonin values were uniformly below the detection limit of the assay, and pancreatic glucagon levels were elevated. The hypocalcemia of acute pancreatitis was probably not caused by abnormalities of glucagon, calcitonin, or gastrin secretion. Furthermore, parathyroid hormone secretion was apparently not impaired. Hypomagnesemia possibly played a minor role. This study suggests that the hypocalcemia of acute pancreatitis is secondary to extraskeletal calcium sequestration or an as yet unidentified defect of bone metabolism, or both.
Article and Author Information
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▸From the Diabetes and Gastrointestinal Units, Department of Medicine; the Department of Anesthesiology; and the Department of Surgery; the Massachusetts General Hospital and Harvard Medical School; Boston, Massachusetts.
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Grant support: grants from the William F. Milton Fund and the John A. Hartford Foundation, Inc., and USPHS grant GM 15904-05. Dr. Weir is a Daland Fellow of the American Philosophical Society.
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▸Requests for reprints should be addressed to Gordon C. Weir, M.D., Diabetes Unit, Massachusetts General Hospital, Boston, MA 02114.
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- Received January 24, 1975.
- Accepted April 25, 1975.
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