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Immune thrombocytopenia (ITP) is an acquired immune disorder in which antiplatelet antibodies cause shortened platelet survival and suppress megakaryopoiesis leading to thrombocytopenia and increased bleeding risk.1 Etiologies of ITP include idiopathic (primary), associated with coexisting conditions (secondary), or drug induced.
Adult primary ITP has an incidence of 3.3 cases per 10 persons.2
- In primary ITP, autoantibodies bind to platelet surface antigens and cause premature clearance by the reticuloendothelial system in addition to immune-mediated suppression of platelet production.
- Secondary ITP occurs in the setting of systemic lupus erythematosus (SLE), antiphospholipid antibody syndrome (APS), HIV, hepatitis C virus (HCV), Helicobacter pylori, and lymphoproliferative disorders.1
- Drug-dependent ITP results from drug–platelet interactions prompting antibody binding.3 Medications linked to thrombocytopenia include quinidine and quinine; platelet inhibitors abciximab, eptifibatide, tirofiban, and ticlopidine; antibiotics linezolid, rifampin, sulfonamides, and vancomycin; the anticonvulsants phenytoin, valproic acid, and carbamazepine; analgesics acetaminophen, naproxen, and diclofenac; cimetidine; and chlorothiazide.4