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Hypocalcemia in Critical Illness
Gary Paul Zaloga, MD;
Bart Chernow, MD
JAMA. 1986;256(14):1924-1929.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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CALCIUM is an essential ion required for many biologic processes, including neuronal conduction, synaptic transmission, hormone secretion, mitotic division, cardiac automaticity, and excitation-contraction coupling in muscle. Calcium is also a major intracellular messenger, is needed for cellular processes that require movement, and is required by many enzymes for full activity. Deficiency of circulating concentrations of this important ion are common in patients with critical illness.
Physiologic Regulation of the Serum Calcium Concentration
The serum calcium concentration is maintained within normal limits by the combined effects of parathyroid hormone (PTH) and vitamin D. Dietary calcium is not required, since these hormones can maintain the serum calcium level via their skeletal effects. A deficiency in either hormone, however, may lead to hypocalcemia. Deficiency in PTH may result from parathyroid gland damage, as may occur after neck surgery, or from parathyroid gland suppression. The parathyroid glands may be suppressed by hypercalcemia, hypomagnesemia, or
. . . [Full Text PDF of this Article]
Author Affiliations
From the Department of Critical Care Medicine, Naval Hospital, and the Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Md (Dr Zaloga); and the Departments of Anesthesiology, Massachusetts General Hospital and Harvard Medical School, Boston (Dr Chernow).
Footnotes
The opinions expressed herein are the private views of the authors and are not to be construed as reflecting the views of the Navy Department, the Naval Service at large, or the Department of Defense.
Reprint requests to the Department of Anesthesiology, Massachusetts General Hospital, Boston, MA 02114 (Dr Chernow).
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