Document Type

Article

Department

Haematology and Oncology, East Africa

Abstract

D rugs may cause thrombocytopenia by three principal mechanisms: suppression of platelet production, direct platelet toxicity, or antibody-mediated platelet destmction (1). With the advent of assays specifically capable of detecting and quantifying IgG on the platelet surface (2), it has become increasingly possible to recognize cases of drug-induced immune thrombocytopenia based on the detection of elevated levels of platelet surface bound IgG in association with ingestion of causative dmgs. Consequendy, dmg-induced immune thrombocytopenia is no longer a disease diagnosed primarily by exclusion. The occurrence of quinidine-induced thrombocytopenia, though uncommon, was documented as early as 1965 (3) and has been thought to be immune in origin (4,5). The platelets themselves may serve as innocent bystanders (6,7) or partial immunogens (8). We discuss six cases of clinically documented quinidine-induced thrombocytopenia, outlining the mode of diagnosis as well as therapeutic considerations. The '^^I-labeled monoclonal anti-IgG assay (2) is used for the quantitation of IgG on the platelet surface. We discuss the role of this assay in diagnosing drug-induced immune thrombocytopenia and address its diagnostic and prognostic value.

Comments

This work was published before the author joined Aga Khan University.

Publication (Name of Journal)

Henry Ford Hospital Medical Journal

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