Document Type
Article
Original Publication Date
1976
Journal/Book/Conference Title
The New England Journal of Medicine
Volume
294
Issue
10
First Page
512
Last Page
516
DOI of Original Publication
10.1056/NEJM197603042941002
Date of Submission
January 2015
Abstract
Abstract
We studied nine consecutive hypocalcemic patients with acute pancreatitis to elucidate the mechanism of hypocalcemia. Mean serum ionized calcium, 0.97 mM, was below the normal mean of 1.16 mM (P < 0.001). Seven of eight patients tested had normal parathyroid hormone levels. All responded to parenteral parathyroid extract by increasing serum ionized calcium and urinary cyclic AMP, indicating parathyroid-hormone-responsive target organs. Calcitonin and glucagon concentrations were increased above normal in some patients, but there was no relation with serum ionized calcium. Parenteral glucagon had no significant effect on serum ionized calcium or calcitonin concentrations. These findings suggest that neither glucagon nor calcitonin was primarily responsible for the hypocalcemia, which did not produce expected increases in serum parathyroid hormone concentrations. Relative parathyroid insufficiency may account for the persistent hypocalcemia frequently observed in patients with acute pancreatitis. (N Engl J Med 294:512–516, 1976)
Rights
From The New England Journal of Medicine, Robertson, G.M., Moore, E.W., Switz, D.M., et al. Inadequate Parathyroid Response in Acute Pancreatitis, Vol. 294, Page 512, Copyright © 1976 Massachusetts Medical Society. Reprinted with permission.
Is Part Of
VCU Internal Medicine Publications
Comments
Originally published at http://dx.doi.org/10.1056/NEJM197603042941002