Entecavir Antiviral Therapy, Eryptosis, and Anemia in HBV-Related Liver Cirrhosis: Current Evidence and Potential Mechanistic Links

Chronic hepatitis B virus (HBV) infection is a significant cause of progressive liver disease and cirrhosis, often accompanied by hematological complications, including anemia. Evidence increasingly indicates that eryptosis—the programmed death of erythrocytes—may play a role in disrupting red blood cell balance in chronic liver conditions. Eryptosis is characterized by phosphatidylserine externalization, intracellular calcium accumulation, oxidative stress, and ceramide-dependent signaling pathways. Entecavir, a highly effective antiviral medication, is used to consistently suppress HBV replication in patients with chronic hepatitis B and HBV-related cirrhosis. Entecavir-induced viral suppression is associated with improved hepatic function, biochemical markers, and clinical outcomes. However, direct evidence on the effects of HBV suppression on red blood cell survival, eryptosis, and anemia is lacking. In this review, we summarize current knowledge of eryptosis in HBV-related liver cirrhosis, focusing on its molecular mechanisms, biomarkers, and potential role in anemia. We also review the documented effects of entecavir on virological, biochemical, and hematologic parameters, and discuss possible indirect links between viral suppression, restored hepatic function, and erythrocyte homeostasis. Direct evidence linking entecavir therapy to changes in eryptosis remains scarce, underscoring the need for prospective clinical and experimental studies.