Diet, exercise reduced portal hypertension in obese cirrhotic patients




BOSTON – A 16-week diet and exercise program reduced body weight and portal pressure in a prospective pilot study of 50 obese patients with cirrhosis and portal hypertension.

Twenty-six patients achieved a clinically relevant weight loss of at least 5%, compared with baseline weight (52% of the cohort). The hepatic venous pressure gradient (HVPG) decreased by at least 10% in 21 patients (42%), compared with baseline, Dr. Annalisa Berzigotti and her associates reported at the annual meeting of the American Association for the Study of Liver Diseases.

Dr. Annalisa Berzigotti Sherry Boschert/Frontline Medical News

Dr. Annalisa Berzigotti

Obesity has been shown to increase the risk of clinical decompensation in patients with compensated cirrhosis and portal hypertension, possibly by increasing portal hypertension, said Dr. Berzigotti of the Networked Research Center for Hepatic and Digestive Diseases (CIBERehd), Barcelona.

“An intensive 16-week program of tailored diet and moderate exercise can be safely recommended to obtain weight loss,” she said.

Dr. Berzigotti and her associates at two Spanish centers put patients through a 16-week program of a normoproteic, hypocaloric diet supervised by nutritionists. It followed a personalized decrease of 500-1,000 kcal/day, with 20%-25% of the diet consisting of proteins. The exercise intervention consisted of 60 minutes per week of supervised, moderately-intense physical activity in small groups plus personalized advice and use of a daily physical activity log.

Patients had a baseline HVPG of at least 6 mm Hg with or without esophageal varices and regardless of whether they were receiving nonselective beta-blocker medications.

The investigators recruited 60 patients, 50 of whom completed the study and were included in the analysis.

The lifestyle intervention decreased the mean body weight by 5 kg and the median body weight by 5%, which was associated with significant decreases in waist circumference and percentage body fat. Eight patients achieved at least a 10% reduction in body weight (16%), she reported.

The mean HVPG decreased significantly from 13.9 mm Hg at baseline to 12.3 mm Hg after treatment, with an average 11% reduction. The HVPG decreased by at least 20% in 12 patients (24%).

Four patients who lost at least 5% of their body weight reduced their HVPG to below 10 mm Hg. Patients who lost at least 10% of body weight reduced their HVPG to a greater degree than did patients who lost less than 10% of body weight, with 24% and 8% reductions in HVPG, respectively.

Changes in body weight and HVPG were more subtle in patients with diabetes than in those without diabetes. Results did not differ significantly across other subgroups based on cirrhosis etiology, clinically significant portal hypertension and esophageal varices, treatment with nonselective beta-blockers, history of variceal bleeding, or medical center.

No patients clinically decompensated during the study. Patients’ Child-Pugh scores and Model for End-Stage Liver Disease scores did not change.

Patients who lost weight kept it off for 6 months, with average weights of 86 kg at 16 weeks and 85 kg at a 6-month follow-up.

Patients had a mean age of 56 years and 62% were male. The etiologies of cirrhosis were viral in 36% of patients, alcoholic in 38%, and nonalcoholic steatohepatitis in 26%. Patients had an average body mass index of 33 kg/m2, and 72% had an HVPG of at least 10 mm Hg at baseline. Thirty percent of patients had a previous variceal hemorrhage but currently were compensated. Sixty-two percent of patients had a history of esophageal varices and 60% were on nonselective beta-blockers.

Dr. Berzigotti reported having no financial disclosures. One of her associates reported financial associations with Falk, Gilead, Norgine, Ono Pharma USA, Intercept Pharmaceuticals, Exalenz Bioscience, Almirall, and Conatus Pharmaceuticals.

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