DRUG-INDUCED HEMOLYTIC ANEMIAS
By Aaron Han,MD, PhD Chief, Department of Pathology, American Hospital, Dubai, UAE
INTRODUCTION Immune mediated anemias are not infrequently encountered in clinical practice. Drug induced anemias can be marked by production abnormality or by hemolysis and destruction of red cells. Lack of production may be further sub-classified as megaloblastic, sideroblastic or aplastic. Hemolysis can also be subdivided into those that are immune related versus non-immune.
IMMUNE ANEMIAS Drug induced immune anemias occur through three known mechanisms: hapten- induced drug adsorption, immune complex, or autoantibody formation. Penicillin and certain cephalosporins cause hapten formation and is cleared by extravascularly by IgG antibodies. Autoantibody formation is also via an extravascular clearance, and L-dopa and aldomet are classic drugs that cause anemia through this mechanism. Whereas IgM-C3 immune complex formation leads to intravascular hemolysis and is typical for quinine-induced hemolysis. These three types can usually be discriminated on Coombs testing by whether hapten or C3 is required for hemolysis.
NON-IMMUNE ANEMIAS G6PD deficiency and ribavirin can cause red cell hemolysis through membrane damage. G6PD deficiency is an x-linked trait and can be induced by drugs, fava beans, infection and stress. It is the most common enzyme deficiency and found often in Africa, Middle East, and South Asia. The enzyme deficiency results in increased susceptibility of red cells to oxidative stress. Fragmented red cells and ‘bite cells’ are common in peripheral smears of affected patients. Ribavirin used to treat hepatitis can concentrate in red
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