Long‐term progression of viral load and serum markers of fibrosis among treated and untreated patients with chronic hepatitis B

Abstract

Background and Aims Antiviral therapy for patients with hepatitis B (HBV) infection is generally deferred for “immune inactive” patients, although longitudinal changes in viral load and liver fibrosis remain understudied in this population. Likewise, in treated patients, the temporal relationship between changes in viral load and liver fibrosis is not well characterized. Using data from the chronic hepatitis cohort study, the study investigated viral load and the Fibrosis-4 index (FIB4, a serum-based marker of liver fibrosis) trajectories in both untreated and treated HBV patients. Materials and Methods We applied a bivariate, piecewise, linear spline, mixed-effects modeling approach to data from 766 HBV patients (342 untreated, 424 treated). Treatment selection bias was adjusted using propensity scores. Multiple sensitivity analyses were used to confirm results in untreated patients. Results Among all untreated patients, FIB4 began to increase by 0.9% per month (11% per year; P < 0.05) at 28 months post-index date, suggesting fibrosis progression. Significant FIB4 progression was also observed in a subgroup analysis of “immune inactive” untreated patients. In treated patients, viral load declined 31.8% per month (P < 0.05) for the first 5 months after treatment initiation, and 1.4–1.7% per month (P < 0.05) thereafter. At 5 months after treatment initiation, FIB4 began to decline 0.5% per month (P < 0.05), stabilizing at 28 months. Conclusion Among untreated HBV patients, FIB4 gradually increases over time, suggesting fibrosis progression, even in those patients designated as immune inactive. In treated patients, antiviral therapy results in a rapid decline in viral load followed by a delayed decline in markers of liver fibrosis.

Sex and FOXP3 gene rs2232365 polymorphism may be associated with the clinical and pathological aspects of chronic viral diseases

“…It seems counterintuitive to associate an anti-in ammatory factor with the risk of tissue aggression; however, these ndings corroborate previous studies that suggest that variant T favors the persistence of viral infection in patients with brosis (10). With the increase in VL, there is a long-term pro-brogenic tendency induced by chronic in ammation and continuous response to healing (11), resulting in the uctuation of pre-cirrhotic biomarkers (12), such as GGT. The transaminase ratio was stable between genotypes and sexes, indicative of chronic infection, but not relevant for estimating the stage of brosis (13).…”

Serum autotaxin is a useful liver fibrosis marker in patients with chronic hepatitis B virus infection

“…Liver biopsy provides essential information regarding the severity of necro‐inflammatory activity and liver fibrosis but is often limited by invasiveness, pain, sampling error, and interobserver disparity . Thus, simple and reliable non‐invasive methods to estimate liver fibrosis and HBV progression are needed, such as the newly proposed Wisteria floribunda agglutinin‐positive Mac‐2 binding protein (WFA + ‐M2BP), hyaluronic acid (HA), type IV collagen 7S, aspartate aminotransferase (AST)‐to‐platelet ratio index (APRI), and fibrosis index based on four factors (FIB‐4) index . However, the diagnostic ability of these markers remains under scrutiny due to their significant, but moderate, accuracies …”

NGF (−198C > T, Ala35Val) and p75NTR (Ser205Leu) gene mutations are associated with liver function in different histopathological profiles of the patients with chronic viral hepatitis in the Brazilian Amazon

“…The viral load (a) and liver damage markers (b, c and d) were altered in individuals with the SerSer variant with A2-A3 inflammation. e Clustering trends were not inferred from the heatmap graph of inflammation and subsequent fibrogenic activity (Nallagangula et al, 2017), which can occur long term (Li et al, 2017).…”