Clopidogrel bisulfate was recently approved by the US Food and Drug Administration for the reduction of ischemic events in patients with recent myocardial infarction, stroke, and peripheral arterial disease, with no added risk for neutropenia.1 We report an initial case of severe febrile pancytopenia after clopidogrel use.
A 90-year-old woman was monitored for cardiac failure and atrial fibrillation and treated with digoxin and aspirin since 1997. In December 1999, she presented with recurrent episodes of ischemic stroke, so clopidogrel treatment (75 mg/d) was initiated (aspirin treatment was stopped). Twenty days after the introduction of clopidogrel, she was admitted to a hospital because of somnolence and fever (temperature, >39°C) with chills. There was no clinical evidence of focal sepsis. Hematologic findings disclosed severe pancytopenia (hemoglobin, 85 g/L; neutrophil count, 0.9 × 109/L; and platelet count, 100 × 109/L). Laboratory test results revealed an inflammation (C-reactive protein >180 mg/L). Blood cultures and cerebral fluid were sterile. Other pertinent laboratory data, including liver and renal function test results, serologic test results for viral infection (human immunodeficiency virus, hepatitis B and C, or parvovirus B19), and serum levels of vitamin B12 and folic acid were normal. Bone marrow examination findings showed a hypocellular picture suggestive of drug-induced bone marrow suppression. The patient was treated with cefotaxime sodium (3 g/d) and enoxaparin sodium (80 mg/d) (clopidogrel treatment was stopped). Hematological abnormalities were resolved on the eighth day of hospitalization. She was well at 2 months of follow-up treatment with pindione sodium. Excluding other causes, clopidogrel-associated pancytopenia was considered.2