Malarial anemia: an interplay between impaired erythropoiesis and uninfected erythrocyte clearance

Malaria-associated anemia is a major cause of morbidity and mortality, affecting young children and pregnant women in endemic regions. This review synthesizes current evidence on the pathophysiological mechanisms underlying malaria-associated anemia, emphasizing impaired erythropoiesis and increased destruction of uninfected erythrocytes. Ineffective erythropoiesis may result from the presence of parasites within the bone marrow, hemozoin accumulation, inflammatory cytokine responses, and altered iron availability. Persistent inflammation and oxidative stress promote erythrocyte shrinkage, with consequent eryptosis and premature clearance by splenic macrophages. Plasmodium-induced immune responses promote anti-erythrocyte antibody production, which further contributes to erythrocyte removal. Malaria-associated anemia arises from interconnected alterations in erythrocyte production, survival, and clearance, highlighting its multifactorial nature and the need for more integrated studies to better characterize these mechanisms.