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http://dx.doi.org/10.1016/0030-4220(81)90004-9 | DOI Listing |
Arch Intern Med
January 2004
Genetech Inc, South San Francisco, CA 94080-4990, USA.
Clin Lab Haematol
October 2001
Finnish Red Cross Blood Transfusion Service, Helsinki, Finland Jorvi Hospital, Espoo, Finland.
In autoimmune thrombocytopenia, platelet-associated IgG (PA-IgG) frequently displays specificity against glycoprotein (GP) IIbIIIa and/or GP IbIX. Because in a high proportion of patients positive PA-IgG may not be explained by these GP specificities, studies on other target proteins are needed. We studied the presence of GP V-specific PA-IgG by direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA) with the monoclonal antibody SW16.
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August 2000
Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University Giessen, Germany.
Drug-induced immune thrombocytopenia (DITP) is a serious complication of drug treatment. Previous studies demonstrated that most drug-dependent antibodies (DDAbs) react with the platelet membrane glycoprotein (GP) complexes IIb/IIIa and Ib/IX/V. We analyzed the sera from 5 patients who presented with DITP after intake of carbimazole.
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December 1994
Department of Laboratory Medicine, Hamilton Civic Hospitals (General Division), Ontario, Canada.
Heparin-induced thrombocytopenia is characterized by moderate thrombocytopenia and thrombotic complications, whereas quinine/quinidine-induced thrombocytopenia usually presents with severe thrombocytopenia and bleeding. Using flow cytometry and assays of procoagulant activity, we investigated whether sera from patients with these immune drug reactions could stimulate normal platelets to generate platelet-derived microparticles with procoagulant activity. Sera or purified IgG from patients with heparin-induced thrombocytopenia stimulated the formation of platelet-derived microparticles in a heparin-dependent fashion.
View Article and Find Full Text PDFBr J Haematol
January 1992
Finnish Red Cross Blood Transfusion Service, Helsinki.
We have studied the clinical course of quinidine-induced thrombocytopenia in relation to the presence of drug-dependent (dd-ab:s) and drug-independent antibodies in 14 patients. Thrombocytopenia was reversible in 9 d after discontinuation of quinidine treatment in 10 patients. In four it lasted more than 1 month.
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