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Obesity is an independent risk factor for clinical decompensation in patients with cirrhosis
Author(s) -
Berzigotti Annalisa,
GarciaTsao Guadalupe,
Bosch Jaime,
Grace Norman D.,
Burroughs Andrew K.,
Morillas Rosa,
Escorsell Angels,
GarciaPagan Juan Carlos,
Patch David,
Matloff Daniel S.,
Groszmann Roberto J.
Publication year - 2011
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.24418
Subject(s) - medicine , cirrhosis , decompensation , gastroenterology , overweight , body mass index , portal venous pressure , hazard ratio , ascites , population , obesity , hepatic encephalopathy , risk factor , portal hypertension , confidence interval , environmental health
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. (H EPATOLOGY 2011;)