Andropause: Incidence and Pathogenesis

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Abstract
One hundred forty-five male volunteers, 60 to 91 years old, without any hepatic, renal, or metabolic pathology, and not under any steroid therapy for at least 1 year were studied. Plasma luteinizing hormone (LH), Follicle Stimulating hormone (FSH), Testosterone (T), 17-β Estradiol (E2), Androstenedione (A), Maximal increase (MI) of LH and FSH after luteinizing hormone releasing hormone (LHRH) (50-γ iv), and pulsations (P) of LH and FSH over a 3 hr period were measured by radioimmunoassay (RIA). The patients were divided in four groups according to LH and T levels. Group I: (46% of our subjects) showed no signs of hypogonadism with normal LH, T, E2, A, MI of LH and FSH, and normal P-LH, P-FSH. Group II: (15%) with high LH but normal T, showed high FSH, MI-LH, MI-FSH, P-LH, and P-FSH, but normal A and E2, Group III: (22%) with classical signs of hypergonadotropic hypogonadism (high LH and low T) showed high FSH, MI-LH, MI-FSH, and P-FSH, normal P-LH and E2, but low A. Group IV: (16.5%) with signs of hypogonadotropic hypogonadism (low LH and low T) had also low MI-LH, MI-FSH and A, but normal FSH, P-LH, P-FSH, and E2. Contrarily to menopause in women, andropause is not an obligatory event in men, and when it does occur, its pathogenesis and hormonal aspects are very variable.