Drug-induced
immune thrombocytopenia (DIIT) is a relatively uncommon adverse reaction caused by
drug-dependent
antibodies (DDAbs) that react with
platelet membrane glycoproteins only when the implicated
drug is present. Although more than 100 drugs have been associated with causing DIIT, recent reviews of available data show that
carbamazepine,
eptifibatide,
ibuprofen,
quinidine,
quinine,
oxaliplatin,
rifampin,
sulfamethoxazole,
trimethoprim, and
vancomycin are probably the most frequently implicated. Patients with DIIT typically present with
petechiae, bruising, and
epistaxis caused by an acute, severe drop in platelet count (often to <20,000 platelets/pL). Diagnosis of DIIT is complicated by its similarity to other non-
drug-induced
immune thrombocytopenias, including
autoimmune thrombocytopenia,
posttransfusion purpura, and
platelet transfusion refractoriness, and must be differentiated by temporal association of exposure to a candidate
drug with an acute, severe drop in platelet count. Treatment consists of immediate withdrawal of the implicated
drug. Criteria for strong evidence of DIIT include (1) exposure to candidate
drug-preceded
thrombocytopenia; (2) sustained normal platelet levels after discontinuing candidate
drug; (3) candidate
drug was only
drug used before onset of
thrombocytopenia or other drugs were continued or reintroduced after resolution of
thrombocytopenia, and other causes for
thrombocytopenia were excluded; and (4) reexposure to the candidate
drug resulted in recurrent
thrombocytopenia. Flow cytometry testing for DDAbs can be useful in confirmation of a clinical diagnosis, and
monoclonal antibody enzyme-linked
immunosorbent assay testing can be used to determine the
platelet glycoprotein target(s), usually GPIIb/IIIa or GPIb/IX/V, but testing is not widely available. Several pathogenic mechanisms for DIIT have been proposed, including
hapten,
autoantibody, neoepitope,
drug-specific, and
quinine-type
drug mechanisms. A recent proposal suggests weakly reactive platelet
autoantibodies that develop greatly increased affinity for
platelet glycoprotein epitopes through bridging interactions facilitated by the
drug is a possible mechanism for the formation and reactivity of
quinine- type
drug antibodies.