HYPOGONADISM IS NOT RELATED TO THE ETIOLOGY OF LIVER-CIRRHOSIS

We investigated the clinical and laboratory findings of hypogonadism a nd feminization in male patients with viral or alcoholic cirrhosis to determine whether chronic liver disease plays a primary role in the de velopment of sexual dysfunction and hormonal changes. Two groups of ma le patients with liver cirrhosis (23 alcoholic, 33 viral) age- and Chi ld's grade-matched, and 20 age-matched healthy men, as a control group , were included in this study. Clinical signs of hypogonadism and femi nization were examined in the cirrhotic patients. Follicle-stimulating hormone, luteinizing hormone, prolactin, testosterone, free testoster one, estradiol, androstenedione, dehydroepiandrosterone sulfate, and s ex hormone-binding globulin were estimated in all groups. Seminal flui d was also analyzed in 7 alcoholic and 15 viral cirrhotics. Serum leve ls of estradiol, androstenedione, and sex hormone-binding globulin wer e significantly higher, and free testosterone and dehydroepiandrostero ne sulfate levels were significantly lower in both groups of cirrhotic s compared with the control group. Child's C patients in both groups; of cirrhotics were found to have higher estradiol and lower free testo sterone levels than child's A and B patients. Alcoholic and viral cirr hotics had markedly reduced sperm motility and density. The difference s between alcoholic and viral cirrhotic patients in the clinical signs of hypogonadism, serum levels of sex steroids, and the results of sem inal fluid analysis were not statistically significant. These findings suggest that liver cirrhosis per se, independent of etiology, causes hypogonadism and feminization, and that the degree of hypogonadism and feminization correlates well with the severity of liver failure.