Case Presentation:
A 52‐year‐old woman presented to the emergency department (ED) with the chief complaint of scattered bruises and petechiae on both legs beginning 5 days prior to presentation, and a platelet count of 6, 000 cells per micro liter (K/uL). She was prescribed daily clopidogrel 75 mg and aspirin 81 mg 2 days prior to the onset of the above symptoms.
Her past medical history is significant for a right posterior communicating artery aneurysm three years prior, requiring coil embolization; repeat angiography two months prior to this presentation demonstrated re‐canalization of the aneurysm. She was started on dual antiplatelet therapy with the plan of coil embolization and stent placement one week later.
She was also taking atenolol for hypertension; the remainder of her history was unremarkable. Physical exam was significant for petechiae on both legs and on her hard and soft palate; no other areas of bleeding were noted.
Her labs on admission revealed a normal white blood cell count, hemoglobin, and renal function. No schistocytes were noted on peripheral blood smear review; coagulation profile was normal. Review of outside labs 2 months prior to admission revealed a platelet count of 249 K/uL.
Aspirin and clopidogrel were stopped; she was given platelet transfusions and oral prednisone. Her platelet count increased to 75 K/uL but gradually trended downwards. She underwent bone marrow biopsy that revealed normocellular marrow for age, with increased mega‐karyocytes. She was given 2 doses of intravenous immune globulin with a rise in her platelet count to 14 K/uL; because of no symptoms or signs of bleeding she was discharged home.
She was re‐admitted again shortly with a platelet count of 4 K/uL to an outside hospital. She was given rituximab with improvement in her platelet count to the mid 200's. Repeat platelet count on follow up 4 months later was 272 K/uL.
Discussion:
Autoimmune thrombocytopenia involves the peripheral destruction of platelets by autoantibodies. To our knowledge this case represents the third published report of clopidogrel induced autoimmune thrombocytopenia. The patient had no manifestations of TTP. The temporal relationship between the drug exposure and the appearance of the syndrome suggests potential causality, and the dramatic response with rituximab therapy supports an autoimmune etiology.
The critical lab value, the purpuric eruption and bleeding will lead most of these patients to the ED; hence we need to increase awareness among the inpatient specialists.
Conclusion:
It is increasingly recognized that rare side effects of a drug become apparent only after a large segment of the population has been exposed to it. Inpatient specialists need to be aware of the potential for profound isolated thrombocytopenia developing shortly after a patient is exposed to clopidogrel. The role of monoclonal antibodies in treating this disorder warrants further studies.
Author Disclosure Block:
W. Saber, None; C. Whinney, None.