Reuters Health Information (2008-06-23): LDL cholesterol level predicts HCV therapy response in patients with HIV coinfection
LDL cholesterol level predicts HCV therapy response in patients with HIV coinfection
Last Updated: 2008-06-23 15:53:24 -0400 (Reuters Health)
NEW YORK (Reuters Health) - Patients coinfected with hepatitis C virus (HCV) and HIV who have high pretreatment LDL cholesterol levels are more likely to respond to HCV therapy than are similar patients with low LDL cholesterol levels, according to a report in the May 11th issue of AIDS.
Previous studies have shown better responses to anti-HCV treatment in patients with higher LDL cholesterol levels, the authors report, but it has not been determined whether this holds true for patients coinfected with HCV and HIV.
Dr. Juan A. Pineda from Hospital Universitario de Valme in Sevilla, Spain and colleagues studied the relationship between baseline lipid levels and the response to pegylated interferon and ribavirin treatment in 260 patients with both virus infections. Treatment was given for either 24 or 48 weeks, depending on the HCV genotype.
At 12 weeks of treatment, 62% of patients showed a virologic response. At the completion of treatment, 45% of patients had undetectable plasma HCV-RNA levels. The main outcome variable - a sustained virologic response, defined as undetectable plasma HCV-RNA 24 weeks after completion of treatment - was achieved in 39% of patients.
All three endpoints tended to be more common among patients with baseline LDL cholesterol levels equal to or higher than 100 mg/dL, the report indicates.
LDL cholesterol levels at or above 100 mg/dL were significantly associated with a sustained virologic response on multivariate analysis.
"This study shows for the first time that higher serum LDL cholesterol levels prior to therapy with pegylated interferon and ribavirin are associated with a sustained virologic response in HIV/HCV-coinfected patients, as in HCV monoinfection," the investigators say.
They postulate that their results, and those reported in HCV-monoinfected patients, "support the idea that the interference with HCV entry via blockade of LDL receptors may play a role in the therapy of HCV infection."