Our findings of a more significant reduction of inflammatory cytokines such as TNF-α, IL-1β, Il-6 and metabolic markers such as visfatin and leptin seem to indicate that amelioration of fluid overload in cirrhotic subjects with refractory ascites could be accompanied by parallel changes of inflammatory and metabolic pathways probably associated with an adipocite-inflammatory dysfunction that represents the metabolic substrate in subjects with decompensated liver cirrhosis. This evidence concerns the gene LEP and cirrhosis of liver.