Hypophyseal-Gonadal Dysfunction in Men with Non-Alcoholic Liver Cirrhosis

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Abstract
Seven males with liver cirrhosis associated with hepatitis and 1 with schistosomal live fibrosis were studied for hypophyseal gonadal dysfunction and compared to 6 age matched controls. Cirrhotics as a group had higher serum 17.beta. estradiol levels (22.1 .+-. 6.3 vs. 7.8 .+-. 0.8 pg/ml, P < 0.05) which did not rise after 4 days of human chorionic gonadotropin (hCG) stimulation. There was an adequate rise in serum testosterone level after hCG stimulation (332.8 .+-. 99.7 ng/dl baseline to 887.6 .+-. 67.1 ng/dl, P < 0.01). Compared to the controls, cirrhotics had lower baseline serum FSH (3.6 .+-. 1.7 vs. 10.2 .+-. 1.5 mIU/ml, P < 0.02) and higher serum prolactin (13.5 .+-. 2.5 vs. 6.8 .+-. 1.0 ng/ml, P < 0.05). Pituitary dynamic function testing in cirrhotics revealed blunted response of luteinizing hormone (LH) and FSH, to LHRH in 4 out of 8 subjects tested. The mechanism of hypogonadism in non-alcoholic cirrhosis is mostly hypogonadotropic in origin rather than primary gonadal injury which is common is alcoholic cirrhosis.