Abstract
Acquired hemolytic anemias are produced by an early destruction of circulating red blood cells. The bone marrow responds by increasing red cell production. As a consequence, reticulocytes are increased in peripheral blood smear, along with other typical laboratory findings: increased indirect serum bilirubin and serum lactate dehydrogenase (LDH) and decreased serum haptoglobin. Immune hemolytic anemias are the most frequent ones. There are three remarkable forms to bear in mind: autoimmune hemolytic anemia (most of them are warm antibody-mediated, sometimes secondary to lymphoproliferative disorders), aloimmune hemolytic anemia (post-transfusional hemolytic reaction and new-born hemolytic disease) and drug-mediated hemolytic anemia. The most severe ones are thrombotic thrombocytopenic purpura (TTP), which is a thrombotic microangiopathy related to Von Willebrand factor, and paroxysmal nocturnal hemoglobinuria (PNH), characterized by complement-induced intravascular hemolytic anemia.
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