Estrogenic Antagonism of Metabolic Effects of Administered Growth Hormone

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Abstract
In 3 mildly osteoporotic male patients, human growth hormone administration produced increased urinary calcium and hydroxyproline excretion without reduction of fecal calcium, effects considered compatible with increased bone resorption. During growth hormone therapy, the serum phosphorus rose without definite reduction of urinary phosphorus excretion, suggesting a possible nonrenal origin of the hyperphosphatemic action of growth hormone. The expected anabolic effects of growth hormone were also observed, including reduction of blood urea nitrogen and of urinary nitrogen excretion. Superimposed estrogen therapy reduced the elevations of urinary calcium, urinary hydroxyproline, and of serum phosphorus, and antagonized the nitrogen-retaining effects of growth hormone. While there was no significant reduction in urinary phosphorus excretion during growth hormone therapy, concomitant estrogen administration appeared to produce detectable phosphaturia in 2 patients. The favorable effect of estrogen upon growth-hormone-induced hypercalciuria and hydroxyprolinuria may in part reflect estrogenic antagonism of excessive bone resorption caused by growth hormone. Although estrogen appeared to be a general peripheral antagonist of several growth hormone actions, the sites of antagonism do not seem to share an obvious final common pathway.

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