Abstract
Introduction: Clopidogrel is used for secondary prevention of coronary artery disease, stroke, and peripheral vascular disease. Increased doses has been associated with increased odds of gastrointestinal (GI) complications (gastritis, gastric ulcer and bleeding). Effectiveness of clopidogrel is dependent on its conversion to active metabolite by liver enzyme CY2C19. Hypothesis: Clopidogrel metabolizer status impacts the incidence of GI bleed. Methods: Patients aged >18 years, on clopidogrel and known CYP2C19 status were included in the study. Based on functional copies of CYP2C19 they were divided into two groups slow (poor or intermediate) and adequate metabolizers (normal, rapid, ultra-rapid) and were retrospectively analyzed for documented diagnosis of GI bleed after initiation of clopidogrel. Results: A total of 3778 patients were included in the study who were on clopidogrel and had known CYP2C19 status. Of these patients, 74.2% were adequate and 25.8% were slow metabolizers. Overall, there were 332 patients (8.8%) with a documented diagnosis of GI bleed following initiation of clopidogrel. There was no significant difference observed in incidence of GI bleed among slow and adequate metabolizers (8% vs 9.1%, p=0.313). Conclusions: Our study demonstrates that the clopidogrel metabolizer status does not appear to have any significant impact on incidence of GI bleeding, which further strengthens the fact that GI bleed is a multi-factorial pathology.
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