Normalization of Androgen and Sex Hormone-Binding Globulin Levels after Treatment of Hyperprolactinemia
- 1 March 1983
- journal article
- research article
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 56 (3) , 562-566
- https://doi.org/10.1210/jcem-56-3-562
Abstract
Twenty-eight women with amenorrhea, galactorrhea and hyperprolactinemia without hirsutism, were studied before and after bromocriptine therapy for 2 mo. Compared to 15 euprolactinemic controls, hyperprolactinemic women had elevated levels of dehydroepiandrosterone sulfate and androstenedione and lower levels of total testosterone (T), androst-5-ene-3.beta.,17.beta.-diol (Adiol) and 17.beta.-estradiol (P < 0.05). Unbound T and unbound Adiol were significantly elevated, while sex hormone-binding globulin binding capacity was decreased (P < 0.05) and corticosteroid-binding globulin binding capacity was normal. After treatment with bromocriptine, dehydroepiandrosterone sulfate and androstenedione decreased to control levels, as did unbound Adiol, while 17.beta.-estradiol and sex hormone-binding globulin binding capacity levels increased significantly (P < 0.05). Five hyperprolactinemic women underwent ACTH stimulation tests before and after treatment, and the results were compared to those of 7 controls. Steroid ratios in response to ACTH suggested normal 3.beta.ol-dehydrogenase isomerase, 17-20-desmolase and 17.beta.-hydroxysteroid dehydrogenase enzymatic activities in hyperprolactinemia. Basal steroid ratios of T to (5.alpha.-androstane-17.beta.-01-3-one) (DHT) and of unbound T to unbound dihydrotestosterone were elevated (P > 0.05), suggesting reduced 5.alpha.-reductase activity in hyperprolactinemia which is normalized after treatment. Hirsutism was not present in these patients with hyperprolactinemia despite elevated levels of unbound T and Adiol, and may be explained by reduced 5.alpha.-reductase activity. Apparently the increased levels of androgens in these patients result from the hyperprolactinemia.Keywords
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