EFFECT OF POSTNECROTIC AND ALCOHOLIC HEPATIC CIRRHOSIS ON DEVELOPMENTOF BENIGN PROSTATIC HYPERPLASIA

BACKGROUND. The object of this study was to investigate the effects of hepatic cirrhosis on the development of benign prostatic hyperplasia and consequent effects un prostatic volume, serum prostate-specific an tigen (PSA), and prostatism symptoms. METHODS. Sixty patients with pos tnecrotic cirrhosis and alcoholic cirrhosis at age 10 and over, and 20 voluntary subjects in the same age group with normal hepatic function s, were evaluated with prostatic volume calculation by transrectal ult rasound, symptom scoring according to American Urology Association (AU A) criteria, measurement of serum prostate-specific antigen (PSA), ser um total testosterone (TT), free testosterone (FT)estradiol (E2), and calculation of E2/FT ratios, and the results were analyzed statistical ly by the Mann-Whitney U-test. RESULTS. Serum FT and TT levels were si gnificantly lower in the hepatic cirrhosis group compared to the contr ol group (P = 0.0000 and P = 0000, respecti\fl!). Though mean serum E2 level was a little higher in cirrhotic patients compared to controls, the difference was not significant; however fr, the higher E2/FT rati o in the cirrhotic group was statistically significant (P = 0.27 and P = 0.0002, respectively). In the cirrhotic group, the decrease in FT a nd TT levels was greater, as tl-ie disease advanced. While E2 and E2/F T ratio increase, correlate with poor prognosis, no statistically sign ificant differences were found. Mean prostatic volume, serum PSA level , and total symptom score were significantly higher in the control gro up, compared to the cirrhotic group (P = 0.0001, P= 0.0006, and P = 0. 002, respectively). Prostatic volume decreased parallel, to severity o f disease in cirrhotic patients. CONCLUSIONS. The main reason for the decrease in mean prostatic volume in cirrhotic patients compared to su bjects in the same age group with normal hepatic functions was the dec rease in serum ET and TT levels, and the secundary cause was the incre ase in E2/FT ratio, indicating estrogenic predominance. (C) 1998 Wiley -Liss, Inc.