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

Abstract

Obesity is associated with an aggressive course in chronic viral hepatitis; however, its impact in the development of clinical decompensation (CD) in patients with established cirrhosis is uncertain. We evaluated the role of obesity, in relationship to other recognized predictors, in the development of CD in patients with compensated cirrhosis. The study population, a subset of patients included in a randomized trial of beta-blockers in the prevention of varices in whom data on body mass index (BMI) was available, consisted of 161 patients with compensated cirrhosis. Laboratory tests and portal pressure (assessed by the hepatic venous pressure gradient or HVPG) were assessed on inclusion. Patients were followed until CD (ascites, hepatic encephalopathy, or variceal hemorrhage), or until September 2002. Altogether, 29% had a normal BMI, 40% were overweight, and 30% were obese. In a median follow-up of 59 months, CD occurred in 48/161 (30%) patients with an increasingly higher rate according to BMI group (15% in those with normal BMI; 31% in overweight; 43% in obese patients, P=0.011). The actuarial probability of developing CD was significantly higher in the abnormal BMI groups (P=0.022). In a multivariate model that included parameters previously identified as being predictive of CD (HVPG, albumin, Mayo endstage liver disease score), etiology, and treatment group, BMI (hazard ration 1.06; 95% confidence interval 1.01-1.12), P=0.02] was an independent predictor of decompensation, together with HVPG and albumin.

Conclusion: Obesity has a deleterious effect on the natural history of compensated cirrhosis of all etiologies, independent of portal pressure and liver function. Weight reduction may be a valuable therapeutic measure in this patient population.

Figure 1

Panel A. Proportion of patients developing first clinical decompensation according to BMI group. As shown, obesity was associated with a significantly higher proportion of clinical decompensation in a median follow-up of 59 months. Panel B. Probability of first clinical decompensation of cirrhosis according to BMI group. As shown, obese patients had the highest probability of decompensation and patients with a normal BMI had the lowest probability of decompensation, with overweight patients having an intermediate probability. Differences among groups were statistically significant (Log-Rank 7.60, p=0.022).

Figure 1

Panel A. Proportion of patients developing first clinical decompensation according to BMI group. As shown, obesity was associated with a significantly higher proportion of clinical decompensation in a median follow-up of 59 months. Panel B. Probability of first clinical decompensation of cirrhosis according to BMI group. As shown, obese patients had the highest probability of decompensation and patients with a normal BMI had the lowest probability of decompensation, with overweight patients having an intermediate probability. Differences among groups were statistically significant (Log-Rank 7.60, p=0.022).

Figure 2

Change in HVPG after 1 year of follow-up according to BMI group (normal BMI n= 30, overweight n=47, obese n=41). Change is expressed as percentage, and bars represent mean change; vertical lines over bars indicate standard errors of the mean. As shown, patients with normal BMI and overweight patients had a decrease of HVPG at 1 year, while in obese patients the HVPG did not decrease (p=0.004 vs. normal BMI; p=0.015 vs. overweight).

Figure 3

Probability of remaining free of first clinical decompensation of cirrhosis in the 161 patients included in this study and in the 52 patients of the original RCT that were excluded from the study because of missing BMI. Differences between groups were not significant (Log-Rank 0.54, p=0.816), suggesting that no inclusion bias exists in the present analysis.