From Medscape Medical News
Obesity Linked to Risk for Decompensation of Cirrhosis
Laurie Barclay, MD
Authors and Disclosures
July 29, 2011 — Obesity is an independent risk factor for clinical decompensation (CD) in patients with cirrhosis, according to the results of a prospective observational study from the Portal Hypertension Collaborative Group reported online June 26 and to appear in the August print issue of Hepatology.
"Given the prior evidence of the detrimental effects of obesity on chronic liver disease, we hypothesized that increased BMI [body mass index] may increase the risk of transition from compensated to decompensated cirrhosis," said second author Guadalupe Garcia-Tsao, professor of medicine at Yale University School of Medicine in New Haven, Connecticut, in a news release.
Although obesity was previously known to be associated with an aggressive course in patients with chronic viral hepatitis, its effect on patients with established cirrhosis has been undetermined. The investigators therefore assessed the effect of obesity in patients with compensated cirrhosis, in conjunction with that of other known risk factors, on the development of CD.
The study sample consisted of 161 patients with compensated cirrhosis in whom data on BMI were available and who were enrolled in a randomized trial of beta-blockers to prevent varices. At study enrollment, participants underwent laboratory testing and measurement of portal pressure with use of the hepatic venous pressure gradient (HVPG). Follow-up continued until development of CD, defined as ascites, hepatic encephalopathy, or variceal hemorrhage, or until September 2002. Median duration of follow-up was 59 months.
At enrollment, 29% of participants had a normal BMI, 40% were overweight, and 30% were obese. CD occurred in 48 (30%) of 161 patients during follow-up. Rate of CD increased with increasing BMI: 15% in those with a normal BMI, 31% in the overweight group, and 43% in the obese group (P = .011). The groups with an abnormal BMI had a significantly higher actuarial probability of the development of CD (P = .022).
BMI was an independent predictor of CD (hazard ratio, 1.06; 95% confidence interval, 1.01 - 1.12; P = .02), as were HVPG and albumin, in a multivariate model that included factors previously determined to predict CD (HVPG, albumin level, Mayo end-stage liver disease score), cause, and treatment group.
"Patients who are overweight or obese are at greater risk of accelerating the progression of cirrhosis," Dr. Garcia-Tsao said. "Weight reduction may improve patient outcomes in this high-risk population and studies addressing this specific issue are warranted."
Limitations of this study include the fact that the original trial was not performed with the objective of evaluating the impact of obesity on CD.
"[I]ncreased BMI is an independent predictor of clinical decompensation in patients with compensated cirrhosis of various etiologies, suggesting that obesity accelerates the progression of cirrhosis and that its correction could be a valuable nonpharmacological measure to improve prognosis in this patient population," the study authors conclude.
The National Institutes of Health and the Instituto de Salud Carlos III supported this study. The study authors have disclosed no relevant financial relationships.
Hepatology. 2011;54:555-561.
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