title: The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: a long-term retrospective cohort study.
abstract: In this study we analyzed the influence of human immunodeficiency virus (HIV) infection on the course of chronic hepatitis C through multivariate analysis including age, alcohol consumption, immune status, and hepatitis C virus (HCV)-related virologic factors. Eighty HIV-positive and 80 HIV-negative injection drug users included between 1980 and 1995 were matched according to age, gender, and duration of HCV infection and followed-up during 52 months. The progression to cirrhosis was the primary outcome measure. The impact of HIV on HCV-RNA load, histologic activity index, response to interferon therapy, and liver-related death was also considered. In HIV-positive patients, chronic hepatitis C was characterized by higher serum HCV-RNA levels (P =.012), higher total Knodell score (P =.011), and poorer sustained response to interferon therapy (P =.009). High serum HCV-RNA level was associated with low CD4-lymphocyte count (P =.001). Necroinflamatory score was higher in HIV-positive patients (P =.023) independently of the CD4-lymphocyte count, whereas increased fibrosis was related to decreased CD4-lymphocyte count (P =.011). The progression to cirrhosis was accelerated in HIV-positive patients with low CD4 cell count (RR = 4.06, P =.024) and in interferon-untreated patients (RR = 4.76, P =.001), independently of age at HCV infection (P =.001). Cirrhosis caused death in 5 HIV-positive patients. The risk of death related to cirrhosis was increased in heavy drinkers (RR = 10.8, P =.001) and in HIV-positive patients with CD4 cell count less than 200/mm(3) (RR = 11.9, P =.007). In this retrospective cohort study, HIV coinfection worsened the outcome of chronic hepatitis C, increasing both serum HCV-RNA level and liver damage and decreasing sustained response to interferon therapy. Age and alcohol were cofactors associated with cirrhosis and mortality. Interferon therapy had a protective effect against HCV-related cirrhosis no matter what the patient's HIV status was.
authors.affiliation: Service d'Hépatologie, INSERM U481 et Centre de Recherche Claude Bernard sur les Hèpatites Virales, Hôpital Beaujon, Clichy, France.
authors.forename: V
authors.initials: V
authors.lastname: Di Martino
authors.forename: P
authors.initials: P
authors.lastname: Rufat
authors.forename: N
authors.initials: N
authors.lastname: Boyer
authors.forename: P
authors.initials: P
authors.lastname: Renard
authors.forename: F
authors.initials: F
authors.lastname: Degos
authors.forename: M
authors.initials: M
authors.lastname: Martinot-Peignoux
authors.forename: S
authors.initials: S
authors.lastname: Matheron
authors.forename: V
authors.initials: V
authors.lastname: Le Moing
authors.forename: F
authors.initials: F
authors.lastname: Vachon
authors.forename: C
authors.initials: C
authors.lastname: Degott
authors.forename: D
authors.initials: D
authors.lastname: Valla
authors.forename: P
authors.initials: P
authors.lastname: Marcellin
mesh_terms: D000328:Adult; D018791:CD4 Lymphocyte Count; D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D015658:HIV Infections / Q000209:etiology* / Q000503:physiopathology; D018023:HIV Seronegativity; D016174:Hepacivirus / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D006801:Humans; D007107:Immune System / Q000503:physiopathology; D007372:Interferons / Q000627:therapeutic use; D008099:Liver / Q000473:pathology; D008103:Liver Cirrhosis / Q000209:etiology; D008297:Male; D012189:Retrospective Studies; D015819:Substance Abuse, Intravenous / Q000150:complications*; D016019:Survival Analysis; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D007372:Interferons