Effect of human pituitary luteinizing hormone administration on plasma levels of dehydroepiandrosterone, androstenediol and their sulphates and testosterone in women with secondary amenorrhoea.

Abstract

Human pituitary LH (1200 i.u.) was infused for 4 h (from 10.00 to 14.00 h) into six women with anorexia nervosa and into five women with polycystic ovarian disease (PCO). Plasma dehydroepiandrosterone sulphate (DHAS), androstenediol sulphate, dehydroepiandrosterone (DHA), androstenediol and testosterone were estimated by gas-liquid chromatography in blood samples taken every 2 h from 10.00 to 20.00 h. The values were compared with those obtained at the same times on the previous control day. There were no significant changes in the plasma levels of DHAS and androstenediol sulphate in response to LH at any of the sampling times in either the anorexia nervosa or the PCO patients. In the anorexia nervosa women, plasma DHA levels were significantly increased at 16.00 (P less than 0.001), 18.00 (P less than 0.001) and 20.00 h (P less than 0.05) after LH infusion. In the PCO women, DHA levels increased significantly at 14.00 (P less than 0.01), 16.00 (P less than 0.001), 18.00 (P less than 0.001) and 20.00 h (P less than 0.001) in response to LH infusion. Plasma androstenediol levels increased significantly in the anorexia nervosa patients at 12.00 (P less than 0.001), 14.00 (P less than 0.01) and 16.00 h (P less than 0.01) in response to LH. Similar increases were also found in the PCO patients at 12.00 (P less than 0.01), 14.00 (P less than 0.001) and 16.00 h (P less than 0.01). Plasma testosterone decreased progressively in the anorexic women in response to LH, becoming significant at 16.00 (P less than 0.05), 18.00 (P less than 0.05) and 20.00 h (P less than 0.01). A similar progressive decrease in plasma testosterone was seen in the PCO women, the levels being significantly lower than controls at 16.00 (P less than 0.05), 18.00 (P less than 0.05) and 20.00 h (P less than 0.05). The results represent the first experimental evidence for a direct regulatory role for LH on androgen secretion in women. In addition, the data have a significant bearing on the pathogenesis of the PCO syndrome and the development of hirsutism which may be directly related to the high androgen levels in PCO women in whom the levels of LH are normally raised. The data may also offer an explanation for the mechanisms responsible for the low androgen levels in anorexia nervosa patients in whom there is a gonadotrophin deficiency.