Hochain P, Capet C, Colin R
Groupe de recherche sur l'appareil digestif, hôpital Charles-Nicolle, Rouen, France.
Rev Med Interne. 2000 Mar;21 Suppl 1:50s-59s. doi: 10.1016/s0248-8663(00)88725-1.
This review focuses on aspirin-related gastrointestinal side-effects and the mechanism by which aspirin causes gastrointestinal damage.
Aspirin causes direct gastric damage by topical irritant effects and indirect damage via systemic inhibition of cyclooxygenase synthesis and microcirculation injury. The question of a possible synergistic relation between the presence of Helicobacter pylori infection and aspirin use on gastric damage is not resolved. The pathogenesis of small intestinal and colonic damage is less well understood; an increase in intestinal permeability and free radical synthesis are suggested. Gastric damage predominates. Gastroduodenal lesions from aspirin have been documented in endoscopy studies. The lesions occur rapidly, even for low-dose aspirin. The association of aspirin consumption with upper gastrointestinal bleeding has been well established. The main risk factors are advanced age, concomitant use of nonsteroidal antiinflammatory drugs and history of ulcer. Low-dose aspirin are associated with increased risk of gastrointestinal bleeding and this risk is dose-dependant. Chronic aspirin consumption can cause iron deficiency anaemia. Uncomplicated gastric ulcer (but not uncomplicated duodenal ulcer) is associated with aspirin use, with relative risk 3. Other upper gastrointestinal complications have been reported: stenosis and perforation. Aspirin can also damage other areas of the gastrointestinal tract. Oesophageal injuries (oesophagitis and stricture) have been reported. Aspirin is associated with variceal bleeding episodes in patients with cirrhosis. The adverse effects of aspirin on the small bowel are perforation, bleeding, increasing permeability. The adverse effects of aspirin on the large intestine are perforation, bleeding, collagenous colitis and anorectal stenosis with suppositories containing aspirin. Direct clinical data regarding prophylaxis with co-administration of a protective drug are not yet available for aspirin.
Patients should be made aware of adverse gastrointestinal effects due to aspirin. Further studies regarding prophylactic therapy of low-dose aspirin induced gastroduodenal lesions, which identify a subset of patients who may be at higher risk than the low-dose aspirin population as a whole, are warranted.
本综述聚焦于阿司匹林相关的胃肠道副作用以及阿司匹林导致胃肠道损伤的机制。
阿司匹林通过局部刺激作用直接造成胃损伤,并通过对环氧合酶合成的全身抑制和微循环损伤间接造成损伤。幽门螺杆菌感染与阿司匹林使用对胃损伤可能存在协同关系这一问题尚未解决。小肠和结肠损伤的发病机制了解较少;有人提出肠道通透性增加和自由基合成增加。胃损伤占主导。内镜研究已记录到阿司匹林导致的胃十二指肠病变。这些病变出现迅速,即使是低剂量阿司匹林也是如此。阿司匹林服用与上消化道出血的关联已得到充分证实。主要危险因素是高龄、同时使用非甾体抗炎药和溃疡病史。低剂量阿司匹林与胃肠道出血风险增加相关,且这种风险呈剂量依赖性。长期服用阿司匹林可导致缺铁性贫血。单纯性胃溃疡(而非单纯性十二指肠溃疡)与阿司匹林使用相关,相对风险为3。还报告了其他上消化道并发症:狭窄和穿孔。阿司匹林也可损伤胃肠道的其他部位。已报告有食管损伤(食管炎和狭窄)。阿司匹林与肝硬化患者的静脉曲张出血发作有关。阿司匹林对小肠的不良反应有穿孔、出血、通透性增加。阿司匹林对大肠的不良反应有穿孔、出血、胶原性结肠炎以及含阿司匹林栓剂导致的肛管狭窄。关于联合使用保护药物进行预防的直接临床数据在阿司匹林方面尚不可用。
应让患者了解阿司匹林导致的胃肠道不良反应。有必要进一步开展关于低剂量阿司匹林所致胃十二指肠病变预防治疗的研究,以确定可能比整个低剂量阿司匹林人群风险更高的患者亚组。