Background:  The true rate of hepatic fibrosis secondary to viral hepatitis co-infection and the effect of HAART on mitigating it are not known and difficult to measure due to the need for repeated liver biopsy. Non-invasive measures of liver fibrosis could aid in the longitudinal evaluation of hepatic complications. APRI ([AST /upper limit of normal)/platelet count (10⁹/L)] X 100) of > 1.5 has been shown to be a good surrogate for significant liver fibrosis. We evaluated the evolution of the APRI and it determined its predictive value for hepatic outcomes in HIV⁺ patients with chronic hepatitis B (HBV) and C (HCV) co-infection.

Methods:  A retrospective cohort study from a tertiary care HIV clinic:  621 HIV⁺ patients without liver complications at baseline (437 HIV only, 117 HCV⁺, 53 HBV⁺) were followed between 1991 and 2004. Data for 6-month intervals were extracted from a computerized database. We excluded 14 who had triple infection. The trend in APRI over time was estimated using repeated measures multiple linear regression. Ln APRI was used in regression models which were adjusted for age, sex, time from HIV diagnosis, HAART, CD4 cell count, and HIV RNA. Liver outcomes included cirrhosis, hepatic encephalopathy, ascites, and death due to liver failure.

Results:  Patients were followed for a median of 4.3 years (2894 person-years):  77% were male with mean age 38 years, CD4 293 ± 249 cells/µL and log HIV RNA 3.88 ± 1.29. At baseline, both HCV⁺ and HBV⁺ had higher APRI compared with HIV⁺ (0.96, 0.94, respectively, vs 0.54, p < 0.001). Male sex, lower CD4, and higher HIV RNA were associated with APRI. The change in ln APRI over time was only significantly different from 0 in HCV⁺ (adjusted β = 0.43/5 years; p < 0.001) although a trend was observed in HBV⁺. This translated to an estimated time to develop significant fibrosis from baseline in HCV⁺ of 5 years. Liver complications were developed in 6 of 117 (5%) of HCV⁺ and 4 of 53 (8%) HBV⁺ compared with 5 of 437 (1%) HIV⁺. Baseline APRI and change in APRI predicted liver complications in HCV⁺ (adjusted HR: 2.0, 95% CI 1.01 to 5.3). Neither baseline nor cumulative HAART was protective against progression of fibrosis in HCV infection (β = –0.028/year of HAART; p = 0.34).

Conclusions:  APRI can be used as a marker for progression of liver disease especially in HCV co-infection and is useful in predicting complications. HAART was not protective in slowing the progression to fibrosis in HCV co-infection.

Keywords: Hepatitis C; Hepatitis B; Hepatic fibrosis