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Previous Volume 351:362-369 July 22, 2004 Number 4 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text PDF PDA Full Text Perspective by Stewart, A. F. Letters Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear PubMed Citation

A complex homeostatic system involving the interplay of the bones, the kidneys, and the intestines has evolved to maintain extracellular calcium concentrations within a relatively narrow range.¹ The primary regulator of this system is parathyroid hormone, the release of which is initiated by signals from the calcium-sensing receptor. Overproduction of parathyroid hormone gives rise to hypercalcemia by stimulating the efflux of calcium from bone, increasing the reabsorption of urinary calcium, and promoting the uptake of dietary calcium by means of the activation of vitamin D.¹ Parathyroid hormone–dependent hypercalcemia is commonly caused by parathyroid adenomas and hyperplasia.² Rarer causes of parathyroid . . . [Full Text of this Article]

Case Report

Methods

Results

Response of Hyperparathyroidism to Glucocorticoid Therapy

Parathyroid Hormone Levels after Subtotal Parathyroidectomy

Autoantibodies to the Calcium-Sensing Receptor

Treatment

Discussion

Source Information

From the Departments of Endocrinology (J.C.P., D.S.) and Medicine (J.C.P., Y.-B.C.), Massachusetts General Hospital; and the Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women's Hospital, Harvard Medical School (O.K., E.M.B.) — all in Boston.

Address reprint requests to Dr. Pallais at the Department of Medicine, Massachusetts General Hospital, 55 Fruit St., GRB 740, Boston, MA 02114, or at jpallais@partners.org.

Related Letters:

Hypocalciuric Hypercalcemia and Autoantibodies against the Calcium-Sensing Receptor
Rickels M. R., Mandel S. J., Shakibai N., Pallais J. C., Brown E. M.
Extract | Full Text | PDF  
N Engl J Med 2004; 351:2237-2238, Nov 18, 2004. Correspondence

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