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Gonadal Dysfunction and Changes of Sex Hormones in Postnecrotic Cirrhotic Men

壞死後肝硬化病人性腺功能異常及血清性激素變化之研究

摘要


To evaluate the gonadal dysfunction and change of sex hormones in male patients with postnecrotic cirrhosis, 27 patients with hepatitis B virus (HBV) related postnecrotic cirrhosis were studied. The severity of cirrhosis was graded according to Pugh's modification of Child's grading, 9 patients were in each Pugh's grade (A,B and C) respectively. None had a history of ethanol consumption. Simultaneously, 30 age matched males who were admitted for physical check-up were served as normal controls. Each subject was asked to complete a questionnaire concerning the male sexual dysfunction and received plasma sex hormone assays. Sixteen of the 27 (59%) cirrhotics had a history of impotence. The cirrhotic patients had significantly lower basal testosterone level, but higher estradiol and prolactin levels than controls did (p<0.05). Moreover, the degree of reduced testosterone level correlated to the severity of liver cirrhosis. Despite the low testosterone concentrations, basal levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) were not increased in the cirrhotics. Both patients and controls had normal FSI-I and LH responses to the stimulation of exogenous gonadotropin releasing hormone. Based upon these results, we conclude that: (1) Impotence and low testosterone levels are not infrequent findings in patients with HB V related postnecrotic cirrhosis, especially in those with decompensated liver function. (2) The liver disease per se is important for the development of gonadal dysfunction. (3) The derangement of hypothalamic-pituitary function may play a role for sexual dysfunction and changes of sex hormones in male patients with postnecrotic cirrhosis.

並列摘要


To evaluate the gonadal dysfunction and change of sex hormones in male patients with postnecrotic cirrhosis, 27 patients with hepatitis B virus (HBV) related postnecrotic cirrhosis were studied. The severity of cirrhosis was graded according to Pugh's modification of Child's grading, 9 patients were in each Pugh's grade (A,B and C) respectively. None had a history of ethanol consumption. Simultaneously, 30 age matched males who were admitted for physical check-up were served as normal controls. Each subject was asked to complete a questionnaire concerning the male sexual dysfunction and received plasma sex hormone assays. Sixteen of the 27 (59%) cirrhotics had a history of impotence. The cirrhotic patients had significantly lower basal testosterone level, but higher estradiol and prolactin levels than controls did (p<0.05). Moreover, the degree of reduced testosterone level correlated to the severity of liver cirrhosis. Despite the low testosterone concentrations, basal levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) were not increased in the cirrhotics. Both patients and controls had normal FSI-I and LH responses to the stimulation of exogenous gonadotropin releasing hormone. Based upon these results, we conclude that: (1) Impotence and low testosterone levels are not infrequent findings in patients with HB V related postnecrotic cirrhosis, especially in those with decompensated liver function. (2) The liver disease per se is important for the development of gonadal dysfunction. (3) The derangement of hypothalamic-pituitary function may play a role for sexual dysfunction and changes of sex hormones in male patients with postnecrotic cirrhosis.

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