Aspirin, as an anti-platelet medication, has been increasingly prescribed to elderly patients for primary and secondary prevention of cardio--and cerebro--vascular events. Nonetheless, aspirin's effectiveness in such disease prevention is limited by the risk of gastrointestinal (GI) complications such as ulceration, hemorrhage and perforation. Aspirin administration is associated with 2-fold increase in GI risk in middle-aged users without prior history of peptic ulcer and without concomitant medications. However, the GI risk increases dramatically in patients with a prior history of peptic ulcer disease, advanced age, and concomitant use of NSAIDs, corticosteroids, clopidogrel, or anticoagulants. Mechanisms of aspirin-induced GI injury are believed to be through local effects within the GI mucosa that cause topical injury and through systemic inhibition of cyclo-oxygenase (CO) resulting in depletion of mucosal protective prostaglandins. Herein, we focus on the role of proton pump inhibitor (PPI) in the strategy to prevent and to treat aspirin-induced peptic ulcerations and their complications, based on the scientific evidence.
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