The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: A long-term retrospective cohort study

In this study we analyzed the influence of human immunodeficiency virus (HI V) infection on the course of chronic hepatitis C through multivariate anal ysis including age, alcohol consumption, immune status, and hepatitis C vir us (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 mo nths. The progression to cirrhosis was the primary outcome measure. The imp act of HIV on HCV-RNA load, histologic activity index, response to interfer on therapy, and liver-related death was also considered. In HIV-positive pa tients, chronic hepatitis C was characterized by higher serum HCV-RNA level s (P =.012), higher total Knodell score (P =.011), and poorer sustained res ponse to interferon therapy (P =.009). High serum HCV-RNA level was associa ted with low CD4-lymphocyte count (P =.001). Necroinflamatory score was hig her in HIV-positive patients (P =.023) independently of the CD4-lymphocyte count, whereas increased fibrosis was related to decreased CD4-lymphocyte c ount (P =.011). The progression to cirrhosis was accelerated in HIV-positiv e patients with low CD4 cell count (RR 4.06, P =.024) and in interferon-unt reated 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 de ath related to cirrhosis was increased in heavy drinkers (RR = 10.8, P =.00 1) 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 wors ened the outcome of chronic hepatitis C, increasing both serum HCV-RNA leve l and liver damage and decreasing sustained response to interferon therapy. Age and alcohol were cofactors associated with cirrhosis and mortality. In terferon therapy had a protective effect against HCV-related cirrhosis no m atter what the patient's HIV status was.