Clopidogrel-induced neutropenia in an 80-year-old patient with chronic kidney disease who underwent percutaneous coronary intervention: a case report and literature review

Abstract

Background Clopidogrel is a widely-used antiplatelet and acts as an adenosine diphosphate receptor inhibitor. Neutropenia is a rare but serious adverse effect of clopidogrel. It is unknown whether this adverse effect has any association with impaired kidney function. Case presentation An 80-year-old male with chronic kidney disease was diagnosed with non-ST elevation myocardial infarction and underwent percutaneous coronary intervention. During hospitalization, the patient was diagnosed with contrast-induced nephropathy, treated symptomatically, and discharged with a back-to-baseline creatinine level. Two weeks later, the patient presented to the emergency department with fever and chills. Complete blood count showed leukopenia (0.84 × 103/mm3) and severe neutropenia (0.13 × 103/mm3). Blood cultures were positive for Pseudomonas aeruginosa. Clopidogrel was stopped immediately and switched into ticagrelor. Imipenem and granulocyte colony-stimulating factor were administered to the patient. The patient’s white blood cell and absolute neutrophil count were within the normal range after four days of treatment. The patient was discharged after a 10-day hospitalization, and his complete blood counts were normal during further follow-ups. Conclusions Clopidogrel was the most likely primary cause of neutropenia in our case. The incidence of clopidogrel-induced neutropenia is low and the exact mechanism is not fully explained. We provide suggestions on the management of clopidogrel-associated neutropenia, and summarize all five cases of clopidogrel-induced neutropenia in patients with impaired kidney function.

Identifying causative medications for agranulocytosis: A case report of an older adult with cerebral infarction

“…Several studies have reported clopidogrelinduced agranulocytosis. [1][2][3] Additionally, stem cell activity is elevated after cerebrovascular events. 4,5 Wu et al 2 proposed a possible mechanism for clopidogrelinduced agranulocytosis, suggesting a toxic reaction that impairs the growth of myeloid colonies.…”

“…In this case, we believe that agranulocytosis was believed to result from a complex interplay between (1) bone marrow hematopoietic toxicity and (2) allergic reactions. Several studies have reported clopidogrel‐induced agranulocytosis 1–3 . Additionally, stem cell activity is elevated after cerebrovascular events 4,5 .…”

“…Several studies have reported clopidogrel‐induced agranulocytosis. 1 , 2 , 3 Additionally, stem cell activity is elevated after cerebrovascular events. 4 , 5 Wu et al.…”