Background:  Few data are available regarding the prevalence of significant liver fibrosis among HIV-infected patients without viral hepatitis and among coinfected patients not referred to liver clinics. We estimated the prevalence of significant fibrosis in this population using the AST to platelet ratio index (APRI) which has been validated in HIV-infected patients.   

Methods:  We evaluated markers of liver fibrosis in 4052 patients followed in the Johns Hopkins HIV clinic who had complete data available. We determined the prevalence of significant hepatic fibrosis (Ishak stage ≥F3) according to APRI (AST /ULN)*100/platelet count.). We further examined univariate associations between significant fibrosis, defined by APRI >1.5, and clinical and laboratory variables using χ²-tests for categorical variables, Mann–Whitney tests for continuous variables; significant variables were considered in multivariate analysis.

Results:  Population characteristics:  male 67%; black 76%; age >35 years, 64%; active or past alcohol abuse, 27%; active or past injection drug use, 44%; weight, 71 kg; no current ART, 72%; hepatitis C virus (HCV) antibody⁺, 42%, HBsAg⁺, 9%; CD4 >200 cells/mm³, 55%; HIV RNA <400 copies/mL, 27%; glucose >140 mg/dL, 6.3%. The prevalence of significant fibrosis is shown in the table. By multivariate logistic regression, significant fibrosis was independently associated with:  black race, AOR, 0.74 (95%CI 0.55 to 1.0); alcohol abuse, 1.6 (1.4 to 2.3); CD4 >50 cells/mm³, 0.31 (0.3 to 0.4); current ART, 1.41 (1.0 to 1.95); glucose >140 mg/dL, 2.5 (1.8 to 3.4); chronic HBV, 2.7 (2.0 to 3.6); chronic HCV 2.9 (2.4 to 3.6).

Conclusions:  Consistent with estimates derived from liver biopsy cohorts, the prevalence of significant fibrosis by APRI was relatively high among patients with chronic viral hepatitis, particularly among those tri-infected with HBV and HCV. Additionally, ~7% of patients with HIV alone had significant fibrosis, indicating that research is needed to define the prevalence and histologic features (e.g, steatosis) of liver disease in HIV-mono-infected patients in the era of effective ART. These data also suggest that strategies to prevent liver disease (e.g., HCV- or HBV-treatment and alcohol cessation) should be implemented in similar settings.