Heparin-induced thrombocitopenia (HIT): A case report

Numerous medications are known to cause clinically significant thrombocytopenia by one of two mechanisms—inhibition of megakaryocyte proliferation and destruction of platelets in the peripheral blood. In the former situation, all myeloid elements are usually affected, leading to pancytopenia. However, a few agents are relatively specific for megakaryocytes. In the second group of conditions, antibodies are usually the cause of platelet destruction, but a few drugs appear to act directly on megakaryocytes and/or platelets without involvement of the immune system. Drugs appear to cause antibody-mediated platelet destruction by at least nine different mechanisms, each of which is reviewed in detail. Laboratory tests capable of determining whether thrombocytopenia is drug-induced and which drug is responsible can be of considerable value in the clinic. Available assays, although improved over those previously available, yield an unequivocal diagnosis only in a minority of cases, highlighting the need for further work to improve the sensitivity and specificity of assays for drug-dependent antibodies. Recent studies indicate that drug metabolites can induce sensitization leading to immune thrombocytopenia. It is likely that testing for metabolite-dependent antibodies will improve diagnostic yield. Drug-induced immune thrombocytopenia should be considered in any patient who develops acute thrombocytopenia of uncertain etiology since failure to entertain this possibility can lead to inappropriate treatment and risk of recurrence upon re-exposure to the sensitizing medication.