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The responses of plasma testosterone to gonadotropin stimulation (HCG), estrogen and dexamethasone suppression, and clomiphene citrate therapy were studied in 4 patients with virilization. The pattern of response in 1 patient with an ovarian tumor (arrhenoblastoma) aided in tumor localization. Dexamethasone administration in another patient with an adrenocortical carcinoma caused paradoxical elevation of plasma androstenedione, while plasma testosterone was suppressed. In 1 patient with probable polycystic ovarian disease, HCG stimulation increased plasma testosterone levels, while cyclical clomiphene citrate produced normal levels. In 1 patient with virilization and primary amenorrhea (benign adrenal hyperplasia), no alteration in plasma testosterone occurred during stimulation or suppression studies; however, after ACTH administration, urinary 17-ketosteroids were disproportionately increased relative to 17-OH steroid excretion. During clomiphene therapy, plasma testosterone remained unchanged.
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Samaan et al. (1975) studied this question.
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