Long-term fibrosis and viral level progression among treated and untreated patients with chronic hepatitis B
Li J, Gordon SC, Rupp LB, Zhang T, Boscarino J, Trinacty C, Schmidt M, Moorman A, Holmberg S, Lu M. Long-term fibrosis and viral level progression among treated and untreated patients with chronic hepatitis B. J Hepatol 2016; 64(2 Suppl):S371.
Background and Aims: The temporal relationship between HBV DNA viral load and liver fibrosis progression remains controversial. Using data from in the Chronic Hepatitis Cohort Study (CHeCS), a longitudinal study of patients from four large US health systems,we investigated long-term trajectories of viral load and FIB4 among HBV patients with and without antiviral therapy.
Methods: Observation for each patient commenced at the“indexdate,” either the date of first treatment initiation (treated) or the earliest date of viral load measurement (untreated). Median FIB4scores and viral load levels derived from routine testing were summarized in 30-day intervals for up to 5 years after index.Propensity scores for inverse probability of treatment weighting (IPTW) were used to control for bias in treatment selection. The propensity scores were derived using multiple logistic regression with a large selection of baseline covariates. Changes in FIB4 and viral load over time were modeled using a bivariate piecewise linear spline mixed effects model.
Results:1,126 untreated and 928 treated patients were included. The five-year dynamics of viral load and FIB4 exhibited a bi-phasic pattern. Viral load declined 31% (p < 0.001) per month for the first 5months after treatment initiation, then slowed to a 2.3% (p < 0.001)decline per month thereafter. A non-significant viral load decline was observed for untreated patients. FIB4 began to decline 0.4%per month (p < 0.001) at 5 months post-treatment initiation and stabilized at 28 months. Starting at approximately 28 months after index, FIB4 significantly increased by 0.6% per month (p < 0.001)among untreated patients. FIB4 trajectories were consistent across baseline FIB4 levels.
Conclusions: Antiviral therapy results in a rapid HBV DNA viral load decline followed by a delayed decline in FIB4. In untreated patients,viral load remains stable and significantly higher than in treated patients, and FIB4 gradually increases over time, suggesting fibrosis progression.