BACKGROUND: Because high serum low-density lipoprotein (LDL) and total cholesterol concentrations before treatment have been found to be significant positive prognostic factors for a sustained virological response to HCV therapy in monoinfected patients, the aim of this study was to assess this relationship in HIV-HCV-coinfected patients. METHODS: Pretreatment fasting lipid parameters (in particular total cholesterol, LDL, high-density lipoprotein [HDL], apolipoprotein B [apoB] and triglycerides [TG]) were assessed in 315 patients from the French National Agency for Research on AIDS and Viral Hepatitis (ANRS) HC02-Ribavic therapeutic trial. RESULTS: There was a significant correlation between pretreatment lipid parameters and steatosis (total cholesterol r=-0.23, P<0.0001; LDL r=-0.23, P<0.0001; HDL r=-0.28, P<0.0001; and TG r=0.18, P=0.002), but not with fibrosis. None of these lipid parameters were significant predictors of a sustained virological response to HCV therapy, even after adjustment for the type of interferon treatment and for the main known prognostic factors for a response to HCV therapy. CONCLUSIONS: The possible effect of lipid metabolism on virological response is outweighed by other prognostic factors that affect response to HCV therapy in the ANRS HC02-Ribavic study.
RCT Entities:
BACKGROUND: Because high serum low-density lipoprotein (LDL) and total cholesterol concentrations before treatment have been found to be significant positive prognostic factors for a sustained virological response to HCV therapy in monoinfected patients, the aim of this study was to assess this relationship in HIV-HCV-coinfectedpatients. METHODS: Pretreatment fasting lipid parameters (in particular total cholesterol, LDL, high-density lipoprotein [HDL], apolipoprotein B [apoB] and triglycerides [TG]) were assessed in 315 patients from the French National Agency for Research on AIDS and Viral Hepatitis (ANRS) HC02-Ribavic therapeutic trial. RESULTS: There was a significant correlation between pretreatment lipid parameters and steatosis (total cholesterol r=-0.23, P<0.0001; LDL r=-0.23, P<0.0001; HDL r=-0.28, P<0.0001; and TG r=0.18, P=0.002), but not with fibrosis. None of these lipid parameters were significant predictors of a sustained virological response to HCV therapy, even after adjustment for the type of interferon treatment and for the main known prognostic factors for a response to HCV therapy. CONCLUSIONS: The possible effect of lipid metabolism on virological response is outweighed by other prognostic factors that affect response to HCV therapy in the ANRS HC02-Ribavic study.