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Journal of Clinical Endocrinology & Metabolism, Vol 72, 1226-1228, Copyright © 1991 by Endocrine Society
ARTICLES |
RL Prince, DT MacLaughlin, RD Gaz and RM Neer
Department of Medicine, University of Western Australia, Sir Charles Galrdner Hospital, Nedlands.
It has been hypothesized that estrogen may have a direct effect to reduce the set-point for PTH secretion which may be implicated in its hypocalcemic action. If this is so, estrogen receptors should be demonstrable within parathyroid tissue. Seven human parathyroid adenomas and five samples of normal bovine parathyroid tissue were examined using classical hormone-binding techniques. In no case was there evidence of displaceable estrogen binding of high affinity and low capacity. To exclude the presence of receptors within a small subset of the cells, five of the human adenomas were further studied by immunohistochemistry using a monoclonal antibody to the human estrogen receptor. In no case was there evidence of estrogen receptors. We conclude that the hypocalcemic action of estrogen replacement is unlikely to be mediated via a classical estrogen receptor within the parathyroid, although normal parathyroid tissue was not studied.
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