In hemolytic anemias, the RBCs have a shortened life span; thus, the number of RBCs in circulation is reduced. Fewer RBCs result in decreased in available oxygen causes hypoxia, which in turn stimulates an increase in erythropoietin release from the kidney. The erythropoietin stimulates the bone marrow to compensate by producing new RBCs and releasing some of them into the circu-lation somewhat prematurely as reticulocytes. If the RBC de-struction persists, the hemoglobin is broken down excessively; about 80% of the heme is converted to bilirubin, conjugated in the liver, and excreted in the bile.
The mechanism of RBC destruction varies, but all types of he-molytic anemia share certain laboratory features: the reticulocyte count is elevated, the fraction of indirect (unconjugated) bilirubin is increased, and the supply of haptoglobin (a binding protein for free hemoglobin) is depleted as more hemoglobin is released. As a result, the plasma haptoglobin level is low. If the marrow cannot compensate to replace the RBCs (indicated by a decreased reticu-locyte count), the anemia will progress.
Hemolytic anemia has various forms. Among the inherited forms are sickle cell anemia, thalassemia and thalassemia major, G-6-PD deficiency, and hereditary spherocytosis. Acquired forms include autoimmune hemolytic anemia, nonimmune-mediated paroxysmal nocturnal hemoglobinuria, microangiopathic hemo-lytic anemia, and heart valve hemolysis, as well as anemias asso-ciated with hypersplenism.
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