title: Correlation between beta-lipoprotein levels and outcome of hepatitis C treatment.
abstract: The low-density lipoprotein receptor (LDLR) has been proposed as a candidate receptor for the hepatitis C virus (HCV). Competitive inhibition of HCV binding to the LDLR by low-density lipoprotein (LDL) has been shown in vitro. If similar inhibition occurs in vivo, an elevated serum concentration of beta-lipoproteins may reduce the efficiency of infecting hepatocytes with HCV by competitively inhibiting HCV viral receptor binding. We investigated the role of baseline lipid values in influencing the outcome of HCV treatment. We conducted a retrospective chart review of patients treated with an interferon-based regimen at our liver and gastroenterology clinics between 1998 and 2004. Of 99 patients enrolled in the study, 49 (49.5%) had HCV genotype 1 (LDL 100.2 +/- 30.2 mg/dL [mean +/- SD]), and 50 patients (50.5%) had genotype 2 or 3 (LDL 110.1 +/- 40 mg/dL) infection. Early viral response (EVR), end-of-treatment response (ETR), and sustained viral response (SVR) were documented in 99, 88, and 77 patients, respectively. LDL and cholesterol levels prior to treatment were found to be higher in patients with positive EVR, ETR, and SVR. This difference remained significant independent of age. Multivariate analysis controlling for genotype and age showed that the higher the cholesterol and LDL levels prior to treatment, the greater the odds of responding to treatment. In conclusion, having higher serum LDL and cholesterol levels before treatment may be significant prognostic indicators for treatment outcome of those with chronic hepatitis C infection, particularly in genotypes 1 and 2.
authors.affiliation: Beth Israel Medical Center, Albert Einstein College of Medicine, New York, NY 10003, USA.
authors.forename: Kavitha
authors.initials: K
authors.lastname: Gopal
authors.forename: Timothy C
authors.initials: TC
authors.lastname: Johnson
authors.forename: Saraswathi
authors.initials: S
authors.lastname: Gopal
authors.forename: Aaron
authors.initials: A
authors.lastname: Walfish
authors.forename: Christine T
authors.initials: CT
authors.lastname: Bang
authors.forename: Pauline
authors.initials: P
authors.lastname: Suwandhi
authors.forename: Helene N
authors.initials: HN
authors.lastname: Pena-Sahdala
authors.forename: David J
authors.initials: DJ
authors.lastname: Clain
authors.forename: Henry C
authors.initials: HC
authors.lastname: Bodenheimer
authors.forename: Albert D
authors.initials: AD
authors.lastname: Min
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D004279:DNA, Viral / Q000235:genetics; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D016174:Hepacivirus / Q000187:drug effects / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000188:drug therapy / Q000821:virology; D006801:Humans; D007372:Interferons / Q000627:therapeutic use*; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012254:Ribavirin / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers; D004279:DNA, Viral; D008077:Lipoproteins, LDL; D012254:Ribavirin; D007372:Interferons