Fibrosis regression following hepatitis C antiviral therapy

Abstract

Hepatitis C virus (HCV) infection is one of the most common causes of liver pathology. It is a major etiological factor of continuous liver injury by triggering an uncontrolled inflammatory response, causing liver fibrosis and cirrhosis. Liver fibrosis is a dynamic process that can be reversible upon timely cessation of the injurious agent, which in cases of HCV is represented by the sustained virological response (SVR) following antiviral therapies. Direct-acting antiviral therapy has recently revolutionized HCV therapy and minimized complications. Liver fibrosis can be assessed with variable invasive and non-invasive methods, with certain limitations. Despite the broad validation of the diagnostic and prognostic value of non-invasive modalities of assessment of liver fibrosis in patients with HCV, the proper interpretation of liver stiffness measurement in patients after SVR remains unclear. It is also still a debate whether this regression is caused by the resolution of liver injury following treatment of HCV, rather than true fibrosis regression. Regression of liver fibrosis can possess a positive impact on patient's quality of life reducing the incidence of complications. However, fibrosis regression does not abolish the risk of developing hepatocellular carcinoma, which mandates regular screening of patients with advanced fibrosis.

Skeletal muscle mass increases after viral eradication with direct‐acting antivirals in patients with chronic hepatitis C: A longitudinal study

“…In line with previous studies, a dynamic reduction of non‐invasive markers of fibrosis was identified in our research. The improvement of liver function might be due to reduced inflammation rather than substantial fibrosis regression 74 ; therefore, its relationship to necroinflammatory improvement cannot be excluded. These data highlight the role of muscle‐liver‐immune crosstalk as a potential pathway implicated in restoring inflammatory response after HCV eradication by DAA.…”

Evaluation of Long-Term Outcomes of Direct Acting Antiviral Agents in Chronic Kidney Disease Subjects: A Single Center Cohort Study

“…Previous studies also aimed to identify potential predictors of fibrosis decline. Both host factors, such as the presence of liver cirrhosis, old age of the patient, alcohol consumption, diabetes mellitus or BMI, and viral factors (genotype, viral load) were investigated, but the results remained inconclusive [50,51].…”

Prevention in Hepatology

“…The risk factors for post-SVR HCC development include age, male gender, lower baseline albumin, higher bilirubin levels, an FIB-4 score > 3.25, hepatitis B coinfection, and liver stiffness post-SVR ≥ 20 kPa [39]. Some studies have examined the impact of SVR achieved with DAAs on hepatic fibrosis in patients with chronic hepatitis C. These studies found that fibrosis improved by at least one stage in 56% of patients after a 15-month follow-up, and, notably, cirrhosis reversed in 29% of patients [40].…”

“…It is essential to recognize the potential for fibrosis reversal, particularly in high-risk patients (those with advanced liver fibrosis-F3 or cirrhosis-at the time of DAA treatment). Doing so can lead to improved clinical outcomes, including a reduction in hepatic decompensation and complications, and a decreased risk of HCC development [40].…”