Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis

The natural history of chronic liver diseases is characterized by the progression of fibrosis and nodule formation leading to the development of cirrhosis. Once cirrhosis is established, patients progress from a frequently asymptomatic compensated stage to a decompensated stage, marked by the development of clinical complications of portal hypertension and liver failure. While the risk of mortality is very low in the compensated stage, it markedly increases upon decompensation (1). Therefore, prognostic markers of progression to clinical decompensation are needed in patients with compensated cirrhosis. In this population serum albumin, MELD (Model of End stage Liver Disease) score and the degree of portal hypertension, as determined by the hepatic venous pressure gradient (HVPG) are independent predictors of first clinical decompensation (2). Obesity is a growing epidemic worldwide, involving 20-35% of the population in Western countries (3, 4). In addition to known deleterious health consequences outside the liver(5), obesity is a frequent cause of chronic liver disease that can progress to cirrhosis (6-8). Recent data from a cohort study of middle aged women in the UK suggested that an estimated 17% of liver cirrhosis is attributable to excess body weight (9). Moreover, patients with cirrhosis due to obesity-related liver disease have a lower survival than patients with viral cirrhosis (10), and there is increasing evidence of a deleterious effect of obesity on pre-existing chronic liver disease due to hepatitis C, hepatitis B or alcoholic disease. In these settings obesity has been associated with more advanced fibrosis in cross-sectional studies (11, 12) and with faster histological and/or clinical progression in longitudinal studies of patients with chronic hepatitis C (13, 14). Taken together, these data strongly support that obesity per se is a risk factor for progression in the natural history of cirrhosis. Therefore, it can be hypothesised that increased body weight could be an additional risk factor for the transition from compensated to decompensated cirrhosis. However, this aspect has not been adequately evaluated so far, which was the objective of this study.