非甾体类抗炎药致胃溃疡药学分析

目的：探讨非甾体类药（NSAIDs）相关性溃疡的发病机理、相关因素、预防治疗。方法：从NSAIDs致溃疡临床表现、分析发病机理、相关因素和预防治疗。结果：根据患者情况，合理选用NSAIDs药物和其它药物可减少NsAIDs致胃溃疡的风险，防止胃溃疡发生。结论：NSAIDs是诱发消化性溃疡的重要病因，需长期服用NSAIDs的高危患者，要同时服用两种以上NSAIDs或与糖皮质激素同服者应给予预防性治疗，可减少NSAIDs致胃溃疡的风险，防止胃溃疡发生。     

非甾体抗炎药的胃肠损害及其预防

非甾体抗炎药（NSAIDs）在临床上广泛用于风湿性疾病及心血管疾病的治疗。NSAIDs的常见不良反应为胃肠道不适、恶心，严重不良反应有消化性溃疡、胃肠道出血或穿孔。胃肠损伤发生的原因是由于NSAIDs抑制了环氧酶（COX）系统而阻断了前列腺素的合成，因此干扰了正常黏膜保护机制导致局部受损。NSAIDs致胃肠道损伤的危险因素为高龄、有消化性溃疡或出血史。预防NSAIDs所致胃肠损伤的措施有：应用预防溃疡的药物，选择新一代高选择性COX-2抑制剂，根据患者情况应用抗幽门螺杆菌疗法，依据患者相关的危险因素采用不同的治疗方案。     

非甾体抗炎药相关消化性溃疡出血患者的临床特点及药学监护

目的:总结非甾体抗炎药(NSAIDs)相关消化性溃疡出血患者的临床特点,探讨其实施药学监护的要点。方法:收集3家医院2013年5-12月非静脉曲张性上消化道出血住院患者282例的临床资料,根据入院前2周内有无NSAIDs服用史将患者分为NSAIDs组(59例)和非NSAIDs组(223例),对两组患者的年龄、性别、吸烟史、饮酒史、既往胃病史、消化道临床症状和服药情况进行分析比较,并提出药学监护要点:建立新入院患者药学评估制度、药师查房、个体化用药教育、预防NSAIDs相关性消化性溃疡的用药建议、随访。结果:NSAIDs组患者年龄(63.79±10.94)岁,≥65岁37例(62.7%),22例患者(37.3%)有消化道症状;非NSAIDs组患者年龄(50.03±12.95)岁,≥65岁82例(36.8%),151例(67.7%)有消化道症状。两组患者年龄、高龄患者所占比例、出血前有消化道症状的比例比较,差异有统计学意义(P<0.05),而性别、吸烟史、饮酒史、既往胃病史比较,差异无统计学意义(P>0.05)。结论:NSAIDs相关消化性溃疡出血在高龄患者中多见,起病隐匿;长期服用阿司匹林或其他NSAIDs、合并使用其他易致溃疡的药物、空腹服药者更常见。临床药师应掌握NSAIDs相关消化性溃疡出血患者的临床特点,对NSAIDs相关消化性溃疡出血高危患者实施重点药学监护。     

消化性溃疡合并上消化道出血影响因素分析

目的探讨消化性溃疡合并上消化道出血的影响因素。方法收集笔者所在医院315例消化性溃疡合并上消化道出血患者为研究组;同期门诊选取656例消化性溃疡无上消化道出血并发症的患者为对照组。再根据研究组中HP阳性者根除HP后随访2年,观察上消化道再出血情况。所有入选患者均统计幽门螺杆菌检测结果、NSAIDs服用、性别、年龄、饮酒史、血小板计数等情况。结果 NSAIDs对消化性溃疡合并上消化道出血的差异有统计学意义(P<0.05);年龄对消化性溃疡合并上消化道出血的差异有统计学意义(P<0.01);合用不同种类NSAIDs对消化性溃疡合并上消化道出血的差异有统计学意义(P<0.05)。结论 NSAIDs增加消化性溃疡合并上消化道出血的风险;年龄与消化性溃疡合并上消化道出血相关,大于60岁的老龄消化性溃疡患者更易合并上消化道出血;合用不同种类NSAIDs较单用NSAIDs者消化性溃疡更易合并上消化道出血。     

老年人非甾体抗炎药相关性消化性溃疡出血的临床探讨

目的探讨老年人非甾体抗炎药（NSAIDs）相关性消化性溃疡出血的临床特点。方法回顾性分析118例老年消化性溃疡出血的临床资料,并根据出血前10d内是否服用过NSAIDs将患者分为NSAIDs组42例与非NSAIDs组76例,并对2组临床资料进行比较。结果 2组在临床症状方面、溃疡类型差异均有统计学意义（P〈0.05）。结论加强对老年人非甾体抗炎药相关性消化性溃疡出血的临床特点认识,合理用药并采取相应措施,降低使用NSAIDs引起消化性溃疡出血的风险。     

老年人上消化道出血的病因及临床特点分析

目的 探讨老年人上消化道出血的主要病因及临床特点,为临床诊疗提供依据.方法 回顾性分析248例上消化道出血老年患者的出血病因、发病诱因、临床表现及伴随全身慢性疾病,并与同期174例中青年患者比较.结果 老年人上消化道出血病因主要为消化性溃疡,以胃溃疡居多,其次为上消化道肿瘤,所占比例较中青年患者高.老年人服用非甾体类抗炎药（NSAIDs）药物引起的上消化道出血较中青年患者多,无痛性黑便常为老年人上消化道出血的首发症状,上消化道出血伴随全身慢性疾病较中青年患者多.结论 老年人上消化道出血中,消化性溃疡、上消化道肿瘤是主要病因,服用NSAIDs药物是主要诱因,以无痛性黑便为其首发症状及伴随多种慢性疾病是主要的临床特点.     

非甾体类抗炎药致上消化道出血56例临床分析

目的探讨非甾体抗炎药（NSAIDs）致上消化道出血的临床特点。方法调查我科2007年1月至2010年4月,因服用NSAIDs致上消化道出血收住入院的56例患者的临床资料,对患者年龄、服药种类、临床表现、内镜特点及临床治疗等方面进行分析。结果 NSAIDs致上消化道出血以老年人尤为多见（62.5%）,年龄越大症状越重,且疗效亦差。起病隐匿,主要表现为糜烂出血性胃炎及消化性溃疡。停用NSAIDs或对确需继续服用者换用小剂量、对胃肠损害小的药物,是治疗和预防NSAIDs胃肠黏膜损伤的关键。结论 NSAIDs是一把双刃剑,我们利用其治疗作用的同时,应加强对NSAIDs相关性上消化道出血临床特点的认识,尽量减少NSAIDs的不良反应。     

非甾体抗炎药相关性上消化道出血的临床特征

目的探讨非甾体抗炎药（NSAIDs）相关性上消化道出血的临床特点。方法回顾性分析80例NSAIDs相关性上消化道出血患者临床资料,观察基本情况、既往史、服药史、临床症状;与同期溃疡病及黏膜糜烂所致上消化道出血340例进行对比。结果NSAIDs相关性上消化道出血占上消化道出血的15.4%（80/520）,出血多发生在服药1周内,NSAIDs为预防或治疗剂量;两组比较,服药组患者年龄偏大、多有心脑血管病史;出血前消化道症状不明显;血红蛋白水平低;胃溃疡和复合性溃疡、多发黏膜病损的情况在服药组更多见;但两组患者Hp阳性率差异无显著性。结论老年心脑血管病史者更易发生NSAIDs相关性上消化道出血,无腹痛性消化道出血是其临床表现的特点。     

泮托拉唑治疗老年NSAIDs相关消化性溃疡出血的效果观察

目的观察泮托拉唑治疗老年非甾体类抗炎药（NSAIDs）相关消化性溃疡出血的临床效果。方法随机选取在我院就诊的老年NSAIDs相关消化性溃疡出血患者100例,分为观察组和对照组。对照组使用法莫替丁静脉滴注,观察组使用泮托拉唑静脉滴注。对比两组止血效果、再出血及不良反应情况。结果经一个疗程治疗,观察组止血总有效率为94％,对照组总有效率为82％,两组止血效果差异有统计学意义（P〈0．05）;观察组再出血率为6％,显著低于对照组的22％,差异有统计学意义,P〈0．05。结论泮托拉唑治疗老年NSAIDs相关消化性溃疡出血安全有效,并发症少。     

胃及十二指肠溃疡的致病因素及临床有效性分析

目的探讨胃及十二指肠溃疡致病因素以及临床有效性。方法筛选2014年1月至2015年1月我院收治的胃及十二指肠溃疡患者156例,作为研究对象。所有患者均经临床检查以及胃镜检查确诊为胃、十二指肠溃疡,对所有患者临床症状、伴随疾病、X线表现、年龄、病因进行回顾性分析,总结胃及十二指肠溃疡的致病因素以及其有效性。结果基础资料调查结果显示患者吸烟饮酒史、胃酸、胃蛋白酶、遗传、胃十二指肠动力异常以及服用非甾体抗炎药(NSAIDs)和幽门螺杆菌(Hp)感染等与胃及十二指肠发病密切相关,有效性分析显示服用NSAIDs与Hp感染OR值明显高于其他分组,P<0.05,具有统计学意义。结论药物因素、遗传因素、胃肠肽的作用、精神因素和环境因素等可直接致病胃及十二指肠溃疡,其中与服用NSAIDs与Hp感染关系最为密切,临床应准确掌握为胃及十二指肠溃疡病因,积极对症对因的针对性治疗,提供消化性溃疡的临床治愈率。     

引起消化性溃疡复发的危险因素分析及预防措施

目的探讨引起消化性溃疡复发的危险因素分析及预防措施。方法对2007年1月至2008年12月间邳州市东方医院诊治的经胃镜检查确诊是消化性溃疡患者愈合后通过门诊复诊、电话随访等,将胃镜复查确诊复发者设为观察组,按照1∶2比例选择未复发者作为对照组,比较两组患者在性别构成、年龄、不良生活方式、服NSAIDs、精神因素、复发季节、溃疡愈合质量等方面的差异。结果消化性溃疡患者220例,随访(14.5±4.6)个月;复发60例占27.3%,复发危险因素:男性、存在不良生活方式、服NSAIDs、精神因素、春秋季节,溃疡S1期愈合。结论消化性溃疡的复发与多种因素有关,应通过保持良好生活方式、心理行为干预、提高溃疡愈合质量、对于需长期服用NSAIDs时宜选用选择性COX-2抑制剂,应给予PPI预防性治疗来预防或减少复发。     

Treatment of peptic ulcer disease in the arthritic patient

Dyspepsia associated with arthritis and non-steroidal anti-inflammatory drugs (NSAIDs) is a common clinical problem. Up to 80% of deaths attributable to peptic ulceration may be associated with NSAID usage. The problem is foremost in the elderly population, in which there has been an increase both in the incidence of peptic ulcers and in the use of NSAIDs. Although the development of duodenal ulceration is not clearly associated with NSAIDs, it is accepted that these drugs increase the risk of gastric ulceration and the occurrence of peptic ulcer complications. Asymptomatic peptic ulceration is common, and patients taking NSAIDs are often asymptomatic prior to presentation with life-threatening complications. The key principle in management of this problem is prevention through careful selection of patients for NSAID use, adequate treatment of peptic ulceration and maintenance of remission. A variety of effective drugs are available for the treatment of peptic ulcers, including H2-receptor antagonists, pirenzepine, sucralfate and colloidal bismuth subcitrate. However, it is recognised that peptic ulceration is a chronic disease with a relapsing-remitting course, often with asymptomatic ulcer episodes. The knowledge that current ulcer-healing strategies do not significantly alter this natural history has lead to increasing efforts to prevent relapse with effective 'maintenance' therapy.     

Should NSAID/low‐dose aspirin takers be tested routinely for H. pylori infection and treated if positive? Implications for primary risk of ulcer and ulcer relapse after initial healing

Helicobacter pylori infection and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) can each result in gastric or duodenal ulcer(s) and ulcer complications. Together, H. pylori infection and NSAIDs account for approximately 90% of peptic ulcer disease. In 2003, the results of studies suggest, and guidelines recommend, the careful selection of anti-inflammatory drugs - NSAIDs or selective COX-2 inhibitors (coxibs) based upon patients gastrointestinal history and use of aspirin therapy. Testing for, and cure of, H. pylori infection is recommended in patients prior to the initiation of NSAID therapy and in those who are currently receiving NSAIDs and have a history of dyspepsia, peptic ulcer or ulcer complications. For patients who present with peptic ulcer bleeding but require NSAIDs long-term, H. pylori eradication therapy should be considered, followed by continuous proton pump inhibitor prophylaxis to prevent re-bleeding, regardless of which kind of NSAID (nonselective NSAID /coxib) is being prescribed. Routine testing for, and eradication of, H. pylori infection has not been recommended for current takers of NSAIDs with no or low risk of complications. The management of patients taking low-dose aspirin is complex, but eradication of H. pylori infection alone in those with a past history of bleeding does not guarantee complete protection and therefore a proton pump inhibitor should also be given. The success of eradication therapy should always be confirmed, because of the risk of ulcer recurrence and bleeding in H. pylori-infected patients who require anti-inflammatory treatments.     

拉呋替丁联合奥美拉唑治疗非甾体抗炎药引起的消化性溃疡的疗效观察

目的:观察拉呋替丁联合奥美拉唑治疗非甾体抗炎药(NSAIDs)引起的消化性溃疡的疗效与安全性。方法:将67例NSAIDs引起的消化性溃疡患者随机分成2组,治疗组34例,对照组33例。治疗组采用拉呋替丁联合奥美拉唑治疗,对照组单用奥美拉唑治疗,2组疗程均为4周。观察2组治疗效果及安全性。结果:2组患者临床总有效率分别为97.06%和75.75%,治疗组明显优于对照组(P<0.05)。2组均未见严重不良反应发生。结论:拉呋替丁联合奥美拉唑治疗NSAIDs引起的消化性溃疡,作用更迅速,溃疡愈合质量高,安全性较好。     

非甾体抗炎药致老年人消化性溃疡的临床特点分析

目的:分析非甾体抗炎药(NSAIDs)所致的老年人消化性溃疡的临床特点。方法:回顾性调查上海市金山区亭林医院1999年1月至2006年12月间因消化性溃疡和(或)合并出血入院治疗的491例老年病人的临床资料,根据入院前1周内有无服用NSAIDs史将病人分为两组,对两组病人的临床资料进行分析比较。结果:服药组105例,未服药组386例。与未服药组比较,服药组病人的贫血更明显(P<0.05);复合溃疡和多发溃疡在服药组更多见(P<0.05)。服药组幽门螺杆菌的感染率为67.6%(71/105),未服药组为58.3%(225/386),两组间差别无统计学意义(P>0.05)。结论:应加强对老年人使用NSAIDs所致消化性溃疡的临床特点的认识,减少NSAIDs的不良反应。     

Proton pump inhibitors for preventing non-steroidal anti-inflammatory drug induced gastrointestinal toxicity: a systematic review

Objective: Proton pump inhibitors (PPIs) are recommended for preventing gastrointestinal lesions induced by non-steroidal anti-inflammatory drugs (NSAIDs). We performed this study: (1) to evaluate the effectiveness and safety of PPIs, (2) to explore the association between effectiveness and potential influential factors, and (3) to investigate the comparative effect of different PPIs.

Methods: MEDLINE, EMBASE, and the Cochrane Library were searched to identify randomized controlled trials comparing different classes of PPIs, or comparing PPIs with placebo, H₂ receptor antagonists or misoprostol in NSAIDs users. Both pairwise meta-analysis and Bayesian network meta-analysis were performed.

Results: Analyses were based on 12,532 participants from 31 trials. PPIs were significantly more effective than placebo in reducing ulcer complications (relative risk [RR]?=?0.29; 95% confidence interval [CI], 0.20 to 0.42) and endoscopic peptic ulcers (RR?=?0.27; 95% CI, 0.22 to 0.33), with no subgroup differences according to class of NSAIDs, ulcer risk, history of previous ulcer disease, Helicobacter pylori infection, or age. To prevent one ulcer complication, 10 high risk patients and 268 moderate risk patients need PPI therapy. Network meta-analysis indicated that the effectiveness of different PPIs in reducing ulcer complications and endoscopic peptic ulcers is generally similar. PPIs significantly reduced gastrointestinal adverse events and the related withdrawals compared to placebo; there is no difference in safety between different PPIs.

Conclusions: PPIs are effective and safe in preventing peptic ulcers and complications in a wide spectrum of patients requiring NSAID therapy. There is no major difference in the comparative effectiveness and safety between different PPIs.     

Review article: the effect of Helicobacter pylori infection on nonsteroidal anti-inflammatory drug-induced upper gastrointestinal tract injury

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of peptic ulcers. This article reviews the interaction of H. pylori and NSAIDs on the development of gastric mucosal histological changes, endoscopically confirmed ulcers, and ulcer complications, and assesses whether underlying H. pylori infection potentiates (or mitigates) the development of NSAID-induced ulcer disease. The weight of evidence does not suggest that H. pylori infection potentiates the risk of ulcer formation or ulcer complications in NSAID users. If such an effect occurs, it is likely to be relatively small. Some data even suggest that H. pylori may be protective against NSAID-induced gastric ulcers. Limited data raise the possibility that H. pylori infection, however, may potentiate the effect of low-dose aspirin with respect to ulcer bleeding. Both NSAIDs and H. pylori are independent risk factors for ulcer disease. Therefore, in an individual patient with an ulcer, one cannot be certain which factor is responsible for the ulcer, and both risks should be removed if possible.