Mechanism of estrogenic action in acromegaly

Ernest Schwartz; Elsa Echemendia; Martin Schiffer; Vincent A. Panariello

doi:10.1172/JCI105982

^{Metabolic Unit, Veterans Administration Hospital, Bronx, New York 10468}

^{Department of Medicine, Cornell University Medical College, New York}

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^{Metabolic Unit, Veterans Administration Hospital, Bronx, New York 10468}

^{Department of Medicine, Cornell University Medical College, New York}

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^{Metabolic Unit, Veterans Administration Hospital, Bronx, New York 10468}

^{Department of Medicine, Cornell University Medical College, New York}

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^{Metabolic Unit, Veterans Administration Hospital, Bronx, New York 10468}

^{Department of Medicine, Cornell University Medical College, New York}

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Published in Volume 48, Issue 2 on February 1, 1969
J Clin Invest. 1969;48(2):260–270. https://doi.org/10.1172/JCI105982.
© 1969 The American Society for Clinical Investigation

Published February 1, 1969 - Version history

In four acromegalic patients, estrogen therapy did not significantly alter the mean values of basal radioimmunoassayable plasma growth hormone. In two patients, estrogen therapy did not qualitatively alter the lack of reduction of plasma growth hormone levels after oral administration of glucose, nor did it reduce in these patients the response of plasma growth hormone to insulin-induced hypoglycemia. In one of the patients, insulin sensitivity with respect to glucose and the hypoglycemia-induced growth hormone rise seemed greater during estrogen therapy. Despite the absence of demonstrable reductions inplasma growth hormone level under varying experimental circumstances, the administration of estrogen resulted in reduction of urinary calcium and hydroxyproline excretion, in reduction of radiocalcium bone accretion rates and exchangeable pools, in reduction of serum phosphorus, and in more negative nitrogen balances. The experimental data therefore suggest that estrogen may be a peripheral antagonist of the effects of excessive growth hormone secretion in acromegaly.