title: Sustained virological response rate to pegylated interferon plus ribavirin for chronic hepatitis C in African Americans: results in treatment-naïve patients in a university liver clinic.
abstract: OBJECTIVE
  The sustained virological response (SVR) to non-pegylated interferon-based regimens for chronic hepatitis-C virus (HCV) has been lower among African Americans compared to Caucasians, a finding attributed to the high proportion of genotype-1 infections in African Americans. To determine whether such a difference in SVR is still present with pegylated interferon and ribavirin regimens, we analyzed SVR rates among treated racial groups according to genotype.
  
  
  METHODS
  Consecutive treatment-naïve patients of multiethnic and racial backgrounds attending a university liver clinic received either Peg alfa-2a or -2b plus ribavirin 1-1.2 g based on body weight for 24-48 weeks, depending on genotype. HCV RNA titers were analyzed at 0, six or 12 months, and six months posttreatment.
  
  
  RESULTS
  Among the first 193 patients eligible for treatment, 73 received therapy [24 African Americans (genotype 1 in 88%); 49 non-African Americans (genotype 1 in 59%)]. Of the 120 patients not treated (33% African-American and 67% non-African-American), most either had mild hepatitis on biopsy, normal ALT values, an untreated psychiatric condition or had a low expectation of treatment efficacy. SVR results for the 73 patients who completed treatment indicate that African Americans and non-African Americans with genotype 1 have similarly low rates of SVR (19% in African Americans compared with 24% in non-African Americans, p=NS).
  
  
  CONCLUSIONS
  Sustained viral response rates in our open-access liver clinic are similar for genotype-1 African Americans compared to non-African Americans receiving pegylated interferon and ribavirin. The predominance of genotype 1 among African-American patients likely accounts for the lower response rates, but genotype 1 in other racial groups is associated with a proportionately lower SVR as well as a risk for delayed relapse after SVR.
authors.affiliation: Division of Gastroenterology, Georgetown University Hospital, Washington, DC 20007, USA.
authors.forename: Savita
authors.initials: S
authors.lastname: Srivastava
authors.forename: Maria
authors.initials: M
authors.lastname: Bertagnolli
authors.forename: James H
authors.initials: JH
authors.lastname: Lewis
mesh_terms: D000328:Adult; D001741:Black or African American / Q000235:genetics*; D000483:Alleles; D000998:Antiviral Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000208:ethnology / Q000235:genetics*; D006630:Hispanic or Latino / Q000235:genetics; D006785:Hospitals, University; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use*; D011446:Prospective Studies; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use*; D012307:Risk Factors; D013997:Time Factors; D044465:White People / Q000235:genetics
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C417083:peginterferon alfa-2b; C100416:peginterferon alfa-2a