Volume 1, Issue 5 pp. 475-483
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Parathyroid cell surface autoantibodies that inhibit parathyroid hormone secretion from dispersed human parathyroid cells

James T. Posillico Ph.D.

Corresponding Author

James T. Posillico Ph.D.

Endocrine-Hypertension Unit, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115

Endocrine-Hypertension Unit Brigham and Women's Hospital 75 Francis St. Boston, MA 02115Search for more papers by this author
Jacobo Wortsman

Jacobo Wortsman

Department of Medicine, Southern Illinois University, School of Medicine, Springfield, IL. 62708

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Sath Srikanta

Sath Srikanta

Department of Medicine, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02115

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George S. Eisenbarth

George S. Eisenbarth

Department of Medicine, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02115

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Lawrence E. Mallette

Lawrence E. Mallette

The Medical Service, Veterans Administration Medical Center and Baylor College of Medicine, Houston, TX 77211

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Edward M. Brown

Edward M. Brown

Endocrine-Hypertension Unit, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115

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First published: October 1986
Citations: 53

Abstract

Serum autoantibodies directed toward antigenic determinants on the surface of human parathyroid cells (PTAb-CS) have been demonstrated in a subset (8 of 23) of adult patients with idiopathic hypoparathyroidism (IHP). In sera from 3 of 8 patients with PTAb-CS, binding of these autoantibodies to their respective parathyroid cell surface antigen(s) resulted in marked inhibition of parathyroid hormone (PTH) secretion in an in vitro dispersed human parathyroid cell (dPTC) system. In 1 subject evaluated longitudinally, circulating levels of PTAb-CS, and the magnitude of the inhibitory effect on PTH secretion, temporally correlated with the clinical course of the hypoparathyroidism. These findings suggest a causative role for antibodies directed against cell surface antigens in parathyroid dysfunction in some cases of “autoimmune” hypoparathyroidism.

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