Background:  HIV has a negative effect on the natural history of hepatitis C virus (HCV). While immune dysfunction may explain this observation, there are many potential confounders that have yet to be adequately assessed. We evaluated the contribution of various addictions, lifestyle and physiologic factors on hepatic fibrosis in HIV/HCV co-infection.

Methods:  We used a prospective cohort of HCV/HIV-co-infected patients who completed questionnaires and provided blood for biochemical, serologic, virologic, and immunologic studies every 6 months. The APRI = [(AST /ULN)/platelet count (10⁹/L)] X 100), a recently validated surrogate for significant fibrosis in HCV disease was used to study potential risk factors for fibrosis at baseline. Only HCV real-time polymerase chain reaction (RT-PCR)⁺ were studied. Multivariate logistic regression models were used to evaluate the association of various baseline factors with significant fibrosis.

Results:  Of 162 patients who were recruited and followed for an average of 1 year; 22 were excluded for HCV PCR^­ and 13 for missing APRI. At baseline, 81% male with mean age 43 years; CD4, 378 cells/mL and HIV RNA, 2.6 log copies/mL; 70% currently receiving HAART. Mean time since first potential HCV exposure was 17 years; 70% HCV genotype 1; 7% HBsAg⁺. The following substances were used at baseline/ever: injection drugs (35%/79%), alcohol (58%/86%), marijuana (54%/85%), and cigarettes (71%/91%). The median APRI was 0.66 (0.16 to 49.5), 24% had APRI >1.5 (cutoff for significant fibrosis). In multivariate analyses with HBsAg⁺ excluded, higher CD4 cell count (OR 0.43/100 cells; 95%CI, 0.2 to 0.9, p = 0.03) and higher cholesterol (OR 0.18; 95%CI, 0.04 to 0.85, p = 0.03) were protective and ever having used alcohol (OR 9, 95%CI, 0.96 to 85, p = 0.03) was associated with hepatic fibrosis. Past or present injection drug use, cigarette and marijuana smoking were not associated with fibrosis nor was current HAART use.

Conclusions:  In this cross-sectional analysis, impaired immunity was associated with fibrosis as expected. In addition, we found that any amount of alcohol use was associated with fibrosis, however no contribution of other addictions or lifestyle factors was observed. The observation that low cholesterol was associated with fibrosis may be an indication of decreased synthetic function in advanced liver disease versus its association to HCV replication.