Research advances in hemolytic anemia in liver diseases

There is a bidirectional relationship between liver diseases and hemolytic anemia. Liver diseases may cause or aggravate erythrocyte destruction through abnormalities in erythrocyte membrane lipids， copper toxicity， oxidative stress， mechanical injury， and immune dysregulation； conversely， some primary hemolytic diseases may initially present with abnormalities in the hepatobiliary system due to jaundice， bile pigment stones， splenomegaly， or thrombosis of the splanchnic veins. Hemolysis is classified into intravascular hemolysis and extravascular hemolysis according to the predominant site of erythrocyte destruction； however， the two processes may coexist and may change with disease stage or treatment. Hemolysis associated with Wilson’s disease and acute liver failure， paroxysmal nocturnal hemoglobinuria， and some cases of hemolysis after transjugular intrahepatic portosystemic shunt are characterized by intravascular destruction； spur cell anemia， hereditary erythrocyte membrane disorders， and warm-antibody autoimmune hemolytic anemia are mainly characterized by extravascular destruction； Zieve syndrome， glucose-6-phosphate dehydrogenase deficiency， some cases of autoimmune hemolytic anemia， and passenger lymphocyte syndrome after liver transplantation may involve both pathways of hemolysis. With the site of hemolysis as the primary framework and the immune versus non-immune mechanisms as a supplementation， this article reviews hemolysis associated with liver diseases and primary hemolytic disorders that may present with hepatobiliary abnormalities and proposes a therapeutic approach based on stratified diagnosis and etiology.