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Figure 1 Mechanisms of drug-induced immune cytopenia Drug-induced antibodies may react with the drug-receptor com plex (drug-dependent antibody) or with the drug receptor atone (drug-independent autoantibody). Both types of antibody may be present at the same time.

Receptor

Figure 1 Mechanisms of drug-induced immune cytopenia Drug-induced antibodies may react with the drug-receptor com plex (drug-dependent antibody) or with the drug receptor atone (drug-independent autoantibody). Both types of antibody may be present at the same time.

drawn. The direct antiglobulin test (DAT) is likely to become strongly positive during the hemolytic phase, the patient's red cells being agglutinated by antibodies to complement and sometimes by anti-immunoglobulin G (IgG).

Drugs that have been shown to cause hemolysis by this mechanism include quinine, quini-dine and rifampicin, as well as chlorpropamide, hydrochlorothiazide, nomifensine, phenacetin, salicylazosulfapyridine, the sodium salt of p-aminosalicylic acid and stibophen. 2. Extravascular hemolysis. This is brought about by IgG antibodies that usually do not activate complement, or if they do, not beyond C3. The direct antiglobulin test will be positive with anti-IgG, and sometimes also with antibodies to complement.

The hemolytic anemia associated with prolonged high-dose penicillin therapy is caused by this mechanism, and other penicillin derivatives, as well as cephalosporins and tetracycline, may cause hemolysis in a similar fashion. Hemolysis ceases when the offending drug has been identified and withdrawn.

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