Syndrome Characterized by Gynecomastia, Aspermatogenesis without A-Leydigism, and Increased Excretion of Follicle-Stimulating Hormone1

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Abstract
Nine cases are presented of a syndrome characterized by gynecomastia, and small testes with aspermatogenesis but without a-leydigism. The follicle-stimulating hormone (FSH) excretion in the urine was increased to a degree comparable to that found in castrates. Estrin excretion was not increased. The 17-ketosteroid excretion level and the development of the accessory sexual organs varied from apparently normal to definitely subnormal. Testicular biopsies were obtained on 7 patients and showed hyalinization of the seminiferous tubules and normal appearing interstitial cells. Breast tissue was examined on 4 patients and showed some ductal hyper-plasia with marked proliferation of the periductal connective tissue. These studies support the point of view that the testis produces 2 hormones; androgen from the Leydig cells, and X-hormone (inhibin) from the tubules. Inhibin is probably analogous and very similar to estrin. The increased FSH excretion which is found in certain types of hypogonadism may depend primarily upon lack of inhibin and only to a lesser degree upon lack of androgen; indeed the action of testosterone in inhibiting FSH may depend upon its conversion into estrin. The gynecomastia is probably not due to hyperestrinism, not to androgen alone, but possibly to the combination of androgen and lack of inhibin.