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Drug-induced hemolytic anemia
Last reviewed: 23.04.2024
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Drug hemolytic anemia develops as a result of the effects of many drugs that cause hemolysis. There are 3 mechanisms of development of drug (immune) hemolytic anemia.
The first mechanism of hemolysis development is that the drug causes the formation of antibodies of IgG class to erythrocyte antigens (often related to Rh antigens). As a result, autoimmune hemolytic anemia with thermal agglutinins develops. A similar mechanism for the formation of anti-erythrocyte antibodies has been described with the use of many drugs, in particular, methyldopa, teniposide, and certain NSAIDs.
To realize the second mechanism of hemolysis development, it is necessary to bind the drug or its metabolite to the membrane proteins of erythrocytes, as a result of which the complex formed reacts with the corresponding antibodies. This so-called haptenic mechanism is typical for certain antibiotics (penicillins, cephalosporins, tetracycline), especially when used in high doses.
The third mechanism for the development of hemolysis is due to the fact that antibodies of the IgM class react with the drug in the bloodstream and the immune complex is attached to the erythrocyte for a short time, resulting in the activation of complement and intravascular hemolysis.
Treatment of drug hemolytic anemia
Treatment of drug hemolytic anemia is:
- in the elimination of the etiologic factor (drug withdrawal);
- in the appointment of a specific treatment aimed at eliminating hemolysis;
- in symptomatic treatment.
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