Gynecomastia occurs in about 30% to 50% of patients with cirrhosis of the liver. Since estrogens stimulate breast tissue whereas androgens antagonize these effects, gynecomastia has log been considered the result of an imbalance between these
hormones.
Several mechanisms may operate to produce a relative estrogen excess in hepatic disorders, especially alcoholic cirrhosis. We have studied the prevalence of gynecomastia and measured the estrogen/testosterone ratio in cirrhotic subjects and
control.
Twenty male patients with hepatic cirrhosis were identified from the medical inpatients services of our institution and ten nonobese healthy medical students with no history or physical findings of liver disease composed the noncirrhotic control
group.
The mean BMI in the control subjects was 21.3±0.8kg/㎡and that in the group with cirrhosis was 22.1±1.1kg/㎡. Therefore, no statistical significance was present in 30% of the control subjects and 25% of the cirrhotic subject. No significant
correlation existed between breast tissue diameter and the BMI in the subjects with cirrhosis. In the control group, TT concentrations were higher and TE concentrations were lower than the cirrhostic groups, therefore the ratio of TE/TT were more
decreased compared with the subjects with cirrhosis. In contrast, the mean total and free serum testosterone concentrations were considerably lower and the mean total estrogen concentrations were higher in cirrhotic patients with gynecomastia
compared
with those without gynecomastia as were the ratio of TE/FT, E2/FT, TE/TT and E2/TT.
In conclusion, the prevalence of gynecomastia in cirrhotic patients was 25%. Total and free serum testosterone concentrations did not differ statistically significant in the cirrhotic men with and without gynecomastia. Neither the TE-FT ratio nor
the
E2-FT ratio was statistically increased in cirrhotic subjects with gynecomastia compared with those without gynecomastia. These findings imply that factors other than the estrogen-testosterone ratio may play a role in the development of
gynecomastia in
both cirrhotic and control subjects. (Korean J Gastroenterol 1994 ; 26 : 842-849).
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