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BMI AND WEIGHT ARE NOT PREDICTORS OF RESPONSE TO ANTIVIRAL TREATMENT IN CHRONIC HEPATITIS C (HCV) INFECTION AT 4 WEEKS
NC Ravindran, I Ahmed, H Yusuf, EJL Heathcote
University of Toronto, Toronto, ON
AIM: Does BMI/weight influence rate of rapid virologic response (RVR, defined as undetectable HCV RNA (<50 IU/mL) at 4 weeks into antiviral treatment) in patients with chronic hepatitis C?
METHODS: A retrospective review of all patients at a single centre with chronic hepatitis C started on peginterferon (PegIFN)-alpha and ribavirin (RVN) combination therapy from August 2005 to July 2007 was conducted. Information abstracted for the study database included age, sex, HCV genotype, baseline viral load, cirrhosis (based on liver biopsy fibrosis score or clinical evidence of cirrhosis), type 2 diabetes (DM2), BMI, weight, and HCV RNA (qualitative Roche Amplicor HCV RNA assay version 2.0) at 4 weeks into treatment and at 6 months post cessation of therapy. Sustained virologic response (SVR) was defined as undetectable HCV RNA (qualitative) at 6 months post cessation of therapy. Only individuals who took 80% or more of the prescribed dose of antiviral therapy were included. Treatment duration ranged from 12-48 weeks, depending on genotype and viral response. Patients were excluded if predetermined clinical characteristics were unavailable. Logistic regression was used to examine the above variables.
RESULTS: A total of 140 patients fulfilled the above criteria (10% of the 156 patients treated were excluded). Treatment was with PegIFN alpha-2a (180 mcg/wk) or PegIFN alpha-2b (1.5 mcg/kg/week) and weight-based RVN (800, 1000 or 1200 mg/d). Fifty patients had no SVR data as they had not yet reached 6 months post treatment follow-up. Genotype 1 comprised 55% of patients, genotype 2, 15.7%, genotype 3, 25.7% and genotypes 4 and 6, 3.5%. High baseline viral load, cirrhosis and genotype 1 infection were independent negative predictors of RVR. BMI and weight did not affect percentage with RVR but higher body weight was associated with lack of SVR. As in previous studies, lower body weight (<85 kg), genotype 2 and 3 infection and absence of cirrhosis were positively associated with SVR.
CONCLUSIONS: These results indicate that neither BMI nor weight influence RVR. Nevertheless, lack of SVR is associated with being overweight. Failure to achieve SVR in overweight patients despite an RVR suggests weight may be a risk factor for lack of sustained viral loss.