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A patient developed immune hemolysis and thrombocytopenia while receiving quinidine. In vitro testing showed that antiquinidine antibodies of the IgG class were active against both cell lines. Complement- and drug-dependent platelet lysis occurred with either the patient’s serum or his IgG fraction; there was no reaction with his IgM fraction. Drug-dependent red cell antibodies were studied by antiglobulin testing and analysis of the interaction of sensitized red cells with human monocytes in vitro. Antiglobulin testing revealed the presence of cell-adherent IgG, IgM, and complement; however, IgG-type red cell antibodies were of prime importance in producing red cell ingestion by monocytes. Donor red cells incubated with the drug and the patient’s serum readily adhered to and were ingested by monocytes. The majority of antibody activity was found in the IgG fraction, whereas only a minor degree of phagocytosis was seen with the patient’s IgM complement fraction. Using the monocyte system, IgG antibodies were detected on the cells, even after extensive washing. This suggests that red cell destruction in this syndrome may occur by a mechanism other than the innocent-bystander type.
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Zeigler et al. (1979) studied this question.
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