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Abstract
Under the effect of all these agents, serum 17-beta-estradiol also increased. [...]the abnormality of testicular steroidogenesis and resulting hyperestrogenism caused functional suppression of the hypothalamic-pituitary axis, which could be overcome by competitive inhibition of the suppressive estrogen action at the hypothalamic level by means of direct stimulation of the release of luteinizing hormone or by exogenous human chorionic gonadotropin. In all these cases, serum testosterone was decreased. [...]it appears that steroidogenesis in those patients proceeded from 4-androstenedione via the alternative pathway through 19-hydroxy-4-androstenedione to estrone and 17-beta-estradiol.





