Hiraishi Hideyuki, Shimada Tadahito
Department of Gastroenterology, Dokkyo Medical University.
Nihon Rinsho. 2010 Nov;68(11):2096-101.
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.
阿司匹林作为一种抗血小板药物,越来越多地被开给老年患者用于心脑血管事件的一级和二级预防。尽管如此,阿司匹林在这类疾病预防中的有效性受到胃肠道(GI)并发症风险的限制,如溃疡、出血和穿孔。在没有消化性溃疡病史且未同时服用其他药物的中年使用者中,服用阿司匹林会使胃肠道风险增加两倍。然而,在有消化性溃疡病史、高龄以及同时使用非甾体抗炎药、皮质类固醇、氯吡格雷或抗凝剂的患者中,胃肠道风险会急剧增加。阿司匹林引起胃肠道损伤的机制被认为是通过胃肠道黏膜内的局部作用导致局部损伤,以及通过对环氧化酶(CO)的全身抑制导致黏膜保护性前列腺素的消耗。在此,我们基于科学证据,重点探讨质子泵抑制剂(PPI)在预防和治疗阿司匹林引起的消化性溃疡及其并发症策略中的作用。