Abstract
Anemia is a common complication in patients with liver cirrhosis, especially those with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Besides gastrointestinal bleeding, hypersplenism, and nutritional deficiencies, recent evidence highlights changes in erythrocyte membrane biology as an underrecognized factor contributing to anemia. Phosphatidylserine (PS) externalization on the surface of circulating red blood cells (RBCs) is a key feature of eryptosis, the programmed cell death of erythrocytes. This review explores the pathophysiological mechanisms by which PS externalization leads to early RBC clearance in cirrhotic patients, focusing on HBV-and HCV-related cirrhosis. We discuss the molecular triggers of eryptosis, the impact of oxidative stress and inflammatory cytokines, the clinical effects of PS exposure, and potential therapeutic implications. Understanding this process could provide new insights into managing anemia in cirrhotic patients, encouraging a focus on red cell biology alongside traditional causes.