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Hemolytic anemia due to drugs and toxins

Stanley L Schrier, MD
Section Editor
William C Mentzer, MD
Deputy Editor
Jennifer S Tirnauer, MD


Hemolytic anemia is defined as an anemic state due primarily to an increased rate of destruction of red blood cells (RBCs), resulting in a RBC survival of less than 100 days (normal: approximately 120 days). (See "Diagnosis of hemolytic anemia in the adult".)

This process is caused by one of two mechanisms:

Intrinsic abnormalities arising from within the RBC and/or its membrane (intracorpuscular defects). These are usually congenital (eg, sickle cell anemia, thalassemia, glucose-6-phosphate dehydrogenase (G6PD) deficiency, hereditary spherocytosis), but may rarely be acquired, as in paroxysmal nocturnal hemoglobinuria.

Extrinsic abnormalities in the environment of the RBC. These processes are, by definition, extracorpuscular, and the ensuing hemolysis is called extrinsic hemolytic anemia.

Extrinsic hemolytic anemia is often due to immune mechanisms, as in warm and cold agglutinin hemolytic anemia. (See "Diagnosis of hemolytic anemia in the adult", section on 'Conceptual framework'.) However, there are many nonimmune causes including systemic diseases, mechanical destruction (ie, fragmentation hemolysis), increased destruction within an enlarged spleen (hypersplenism), and the action of drugs and toxins that interfere with metabolic pathways in the red cell.


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Literature review current through: Sep 2016. | This topic last updated: Oct 8, 2015.
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