Immune hemolytic anemia and thrombocytopenia secondary to quinidine: in vitro studies of the quinidine-dependent red cell and platelet antibodies.

A patient developed immune hemolysis and thrombocytopenia while receiving quinidine. In vitro testing showed that antiquinidine antibodies of the lgG class were active against both cell lines. Complementand drug-dependent platelet lysis occurred with either the patient’s serum or his lgG fraction; there was no reaction with his 1gM 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 lgG. 1gM, and complement; however. lgG-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 lgG fraction, whereas only a minor degree of phagocytosis was seen with the patient’s 1gM complement fraction. Using the monocyte system. lgG 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.

[1]  S. Ballas,et al.  Quinidine‐induced Hemolytic Anemia: Immunohematologic Characterization , 1978, Transfusion.

[2]  F. Gardner,et al.  Microscopic platelet size and morphology in various hematologic disorders. , 1978, Blood.

[3]  J. Atkinson,et al.  Receptors for immunoglobulin and complement on human alveolar macrophages. , 1975, Journal of immunology.

[4]  F. Gardner,et al.  Post-transfusion purpura: a heterogeneous syndrome. , 1975, Blood.

[5]  Petz Ld,et al.  Immunologic mechanisms in drug-induced cytopenias. , 1975 .

[6]  A. Zipursky,et al.  The ingestion of IgG-sensitized erythrocytes by abnormal neutrophils. , 1974, Blood.

[7]  B. Korbitz,et al.  Quinine‐induced Thrombocytopenic Purpura Due to an IgM and an IgG Antibody , 1972, Transfusion.

[8]  S. Karpatkin,et al.  Use of the megathrombocyte as an index of megakaryocyte number. , 1971, The New England journal of medicine.

[9]  T. Mcneill,et al.  Antibody Production to the Factor in Human Urine Stimulating Colony Formation In Vitro by Bone Marrow Cells , 1970, British journal of haematology.

[10]  R. Aster,et al.  A platelet and granulocyte membrane defect in paroxysmal nocturnal hemoglobinuria: usefulness for the detection of platelet antibodies. , 1969, The Journal of clinical investigation.

[11]  M. Polley,et al.  Human Monocytes: Distinct Receptor Sites for the Third Component of Complement and for Immunoglobulin G , 1968, Science.

[12]  H. Huber,et al.  Receptor sites of human monocytes for IgG. , 1968, International archives of allergy and applied immunology.

[13]  C. M. Weerdt,et al.  Thrombocytopenia Due to Quinidine or Quinine , 1967 .

[14]  N. Shulman Immunoreactions involving platelets. I. A steric and kinetic model for formation of a complex from a human antibody, quinidine as a haptene, and platelets; and for fixation of complement by the complex. , 1958 .

[15]  N. Shulman IMMUNOREACTIONS INVOLVING PLATELETS , 1958, The Journal of experimental medicine.

[16]  E. Brody,et al.  Hemolytic anemia due to quinidine: observations on its mechanism. , 1956, The American journal of medicine.

[17]  J. Harris Studies on the mechanism of a drug-induced hemolytic anemia. , 1956, The Journal of laboratory and clinical medicine.

[18]  F. G. Bolton,et al.  Observations on Cases of Thrombocytopenic Purpura Due to Quinine, Sulphamezathine, and Quinidine , 1953, Journal of clinical pathology.