Drug-induced thrombocytopenia (DIT) may be a life-threatening adverse drug reaction due to bleeding, indicated by a decrease in platelet count. DIT is defined as a platelet count less than 150 000 / mm³ with a severe status of less than 50 000 / mm³. Many DIT patients experience moderate-to-severe thrombocytopenia, reaching nadir platelet counts of less than 20 000 / mm³.
 
In DIT, up to 9% of patients experience major bleeding, while fatal bleeding happens in 0.8%. Another 30% of patients have overt but minor bleeding, while an additional 40% experience trivial bleeding or purpura.

Drugs can cause thrombocytopenia through several mechanisms, including nonimmune dose-dependent myelosuppression and immune-mediated destruction of platelets. In the former, some antineoplastic drugs used in myelosuppressive therapy (alkylating agents, antimetabolites, and cytotoxic drugs) have the known consequence of marrow suppression leading to DIT. In the latter, thrombocytopenia resulting from immune platelet destruction occurs due to drug-dependent antibodies (DDAbs).

Immune-mediated DIT occurs through at least 6 antibody types that have been identified according to their binding mechanisms. Gold causes an antibody that reacts with autologous platelets in the absence of the drug, while quinine-type drugs (quinine, sulfonamide antibiotics, NSAIDs) induce an antibody that binds to membrane protein in the presence of the sensitizing drug. Other binding mechanisms include hapten-dependent DDAbs, fiban-type DDAbs, drug-specific DDAbs, and immune complex. 

Over 300 drugs have been thought to cause DIT. The drug most commonly cited to induce DIT through immune platelet destruction is quinidine; other frequent offenders include quinine, gold, trimethoprim-sulfamethoxazole, vancomycin, penicillin, piperacillin, rifampin, acetaminophen, carbamazepine, mirtazapine, tirofiban, abciximab, eptifibatide, danazol, heparin, and methyldopa. 

Drug reactions may begin from 1 day to 3 years after the start of a drug, although usually within 5-10 days of the offending medication. Early onset of DIT, which can present within hours of exposure, may happen when induced by chimeric GPIIb / IIIa antagonists due to natural antibodies that have preformed against murine compounds found in monoclonal antibodies.