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Drug-induced hemolytic anemia

Alexey Kryvenko, medical expert
Last reviewed: 07.07.2025

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Drug-induced hemolytic anemia develops as a result of exposure to many drugs that cause hemolysis. There are 3 known mechanisms for the development of drug-induced (immune) hemolytic anemia.

The first mechanism of hemolysis development is that the drug causes the formation of IgG antibodies to erythrocyte antigens (often related to Rh antigens). As a result, autoimmune hemolytic anemia with warm agglutinins develops. A similar mechanism of formation of anti-erythrocyte antibodies has been described with the use of many drugs, in particular, methyldopa, teniposide, and some NSAIDs.

For the second mechanism of hemolysis development to be realized, the drug or its metabolite must bind to the membrane proteins of erythrocytes, as a result of which the resulting complex reacts with the corresponding antibodies. This so-called hapten mechanism is typical for some antibiotics (penicillins, cephalosporins, tetracycline), especially when used in high doses.

The third mechanism of hemolysis development is associated with the fact that IgM class antibodies react with a drug in the bloodstream and the resulting immune complex attaches to the erythrocyte for a short time, resulting in complement activation and the development of intravascular hemolysis.

Treatment of drug-induced hemolytic anemia

Treatment of drug-induced hemolytic anemia consists of:

in eliminating the etiological factor (discontinuing the drug);
in the appointment of specific treatment aimed at eliminating hemolysis;
in symptomatic treatment.

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