非甾体抗炎药致胃肠道黏膜损伤的研究进展

随着非甾体抗炎药(NSAIDs)在临床的广泛应用,其对胃肠道黏膜的损害已受到越来越多的关注。笔者就NSAIDs胃肠道黏膜损害的发病机制、临床表现和防治等做一综述。     

非甾体类抗炎药致上消化道出血366例临床分析

目的探讨非甾体类抗炎药（NSAIDs）诱发上消化道出血（PU）的临床流行病学特点。方法调查中山大学孙逸仙纪念医院2002年1月至2009年1月间因上消化道出血收住院治疗366例患者,根据入院前1周内有无服用NSAIDs,将患者分为服药组（103例）及未服药组（263例）,对两组患者的临床资料进行分析比较。结果服药组患者的年龄较未服药组更高,血红蛋白在服药组下降更明显（P〈0.01）;胃溃疡和复合溃疡、多发溃疡在服药组更多见（P〈0.01）,服药组幽门螺杆菌（Hp）的感染率与未服药组的感染率有显著差异,分别为65.05%和26.24%,（P〈0.05）。结论应加强对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。     

非甾体类抗炎药致老年人上消化道出血的临床分析

目的 分析老年人服用非甾体类抗炎药(NSAIDs)致上消化道出血的临床特征。方法 回顾性分析92例60岁以上消化性溃疡出血住院患者的临床资料,依据出血前10 d内是否服用过NSAIDs将患者分为NSAIDs组(40例)和非NSAIDs组(52例),并对两组患者的临床资料进行分析比较。结果 在性别方面,NSAIDs组与非NSAIDs组比较差异无统计学意义(P>0.05);在心脑血管病史、血红蛋白含量、消化道溃疡等方面NSAIDs组与非NSAIDs组比较差异有统计学意义 (P<0.05)。结论 与非NSAIDs相比,NSAIDs组老年人更易合并心血管疾病,Hb较低,胃溃疡较常见、糜烂少见。NSAIDs服用时间越长,形成溃疡出血的几率越高。     

非甾体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。方法回顾性总结2006年1月至2010年12月我院收治因NSAIDS引起上消化道出血的56例病人的临床资料。结果 56例应用NSAIDS均发生不同程度上消化道出血。结论 NSAIDS可诱发或导致上消化道出血,应合理应用,对需长期用药者,采取预防性措施,尤其是老年患者。     

老年人非甾体类抗炎药致上消化道出血的临床特征分析

目的探讨老年人应用非甾体抗炎药(NSAIDs)致上消化道出血的临床特征。方法回顾性分析我院消化内科收治的NSAIDs相关性上消化道出血患者616例,按年龄分为老年组(≥60岁)416例和中青年组(<60岁)200例,分析两组临床特征的差异。结果老年组应用NSAIDs以阿司匹林为主,占55.8%(232/416),高于中青年患组(37.0%,74/200),两组比较差异有统计学意义(P<0.05);其血液常规及凝血常规指标与中青年组相比较差异无统计学意义(P>0.05);老年组服用NSAIDs药物后近期出血率(21.2%)低于中青年组(63.0%),两组比较差异有统计学意义(P<0.05)。老年组及中青年组上消化道出血患者的溃疡病史及Hp感染史比较差异无统计学意义(P>0.05)。结论老年NSAIDs相关上消化道出血的临床特征与青年患者不同,需予以个体化治疗。     

非甾体类抗炎药致上消化道出血98例

目的研究非甾体类抗炎药（NSAIDs）致上消化道出血患者的临床特点。方法收集412例经胃镜及实验室检查证实上消化道出血患者,其中98例出血前10d内有服用NSAIDs史,分为老年组（122例）和中青年组（290例）进行研究。结果老年组NSAIDs相关性上消化道出血发生率明显高于中青年组（P〈0.01）;老年组服用药物以阿司匹林为主,中青年组以布洛芬为主;伴随疾病老年组以心脑血管疾病为主,青年组以上感或关节疾病为主;老年组消化道出血以溃疡性病变为主,中青年组以黏膜糜烂为主。Hp感染老年组略低于中青年组差异无统计学意义（P〉0.05）,但2组内NSAIDs相关性与非相关性比较,差异有统计学意义（P〈0.01）。结论老年人患NSAIDs相关性上消化道出血具有其自身特点,不同于中青年患者,对于长期服用NSAIDs的老年患者应加强监测。     

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。     

非甾体抗炎药致上消化道出血的临床特征分析

目的分析非甾体抗炎药致上消化道出血的临床特征。方法选取天津市第一中心医院2012年10月—2015年6月消化道出血的住院患者110例,对其临床资料进行分析统计。按照出血前10 d内是否服用过非甾体抗炎药为标准对患者进行分组,比较两组的临床特征。结果两组患者在急性胃黏膜病变、胃底和胃窦胃溃疡、心血管病史以及前壁和后壁十二指肠溃疡方面存在显著差异,两组比较具有统计学意义(P0.05)。其中用药组的急性胃黏膜病变、胃底和胃窦胃溃疡、心血管病史所占比例大于非用药组,而用药组的前壁和后壁十二指肠溃疡所占比例小于非用药组。结论在临床治疗过程中,需要采取适当的措施有效地降低非甾体抗炎药所致的上消化道出血等不良反应。     

非甾体抗炎药致老年人上消化道出血26例临床分析

目的减少老年患者盲目服用非甾体抗炎药(NSAIDs)所致的损害,针对病因,通过采取积极预防,重视健康教育,避免NSAIDs所引起的严重不良反应。方法回顾性分析26例老年患者服非甾体类抗炎药患者所致上消化道出血的原因、临床症状。结果 26例患者经过7～14d的治疗后,症状均消失,大便潜血转阴性,临床治愈出院。结论老年人长期盲目服用NSAIDs可引起上消化道出血,症状隐匿,易危及生命,应引起临床的高度重视。     

非甾体抗炎药致上消化道出血70例的临床分析

目的探讨非甾体抗炎药致上消化道出血的临床特点。方法选择非甾体抗炎药致上消化道出血患者70例作为观察组,其他原因造成的上消化道出血患者70例作为阳性对照组,服用非甾体抗炎药未出现上消化道出血的患者70例作为阴性对照组。分析疾病的危险因素和临床特征。结果非甾体抗炎药致上消化道出血的发生与性别、饮食习惯呈负相关,与年龄、酗酒、焦虑抑郁呈正相关;观察组年龄55岁及以上、女性患者、血红蛋白(Hb)水平降低、糜烂病变、多发病变、胃部病变的例数明显多于阳性对照组,有消化道症状、幽门螺旋杆菌(HP)阳性例数明显少于对照组。结论女性、规律饮食是疾病的保护因素,高龄、酗酒、焦虑抑郁情绪是危险因素,且非甾体抗炎药致上消化道出血多为糜烂、多发的胃部病变。     

泮托拉唑治疗非甾体抗炎药所致老年人上消化道出血的临床分析

目的：探讨泮托拉唑治疗非甾体药物致老年人上消化道出血的临床疗效。方法：选取本院2009年3月~2010年9月收治的62例老年上消化道出血患者的临床资料,所有患者均有服用非甾体抗炎药物史,随机分为治疗组（31例）和对照组（31例）,治疗组患者应用泮托拉唑治疗,对照组患者应用雷尼替丁予以对照,比较两组患者止血效果。结果：治疗组患者止血效果好,与对照组患者比较,差异有统计学意义（P〈0.05）。结论：泮托拉唑治疗非甾体抗炎药致上消化道出血,止血效果好,是治疗上消化道出血的理想药物,值得临床推广。     

非甾体类抗炎药相关性上消化道出血的临床特点

目的探讨非甾体类抗炎药相关性上消化道出血的临床特点。方法选择因呕血或黑便就诊并行胃镜检查确诊的216例患者,分为NSAIDs组和非NSAIDs组,比较两组患者临床特点、内镜特点及幽门螺杆菌（HP）感染情况。结果结果显示两组患者的性别、出血方式比较差异无显著性（P〉0．05）;而年龄、出血前消化道症状、心血管病史、HP感染及内镜特点两组比较差异有显著性（P〈0．05）。结论非甾体类抗炎药相关性上消化道出血多见于老年人,有心血管病史,以粘膜糜烂及胃溃疡居多,HP感染增加了NSAIDs相关性胃黏膜损害。     

非甾体类消炎药致消化道出血的临床分析

目的探讨非甾体类消炎药（NSAIDs）致消化道出血的临床特点。方法回顾性分析广东省东莞市东坑人民医院收治的经病理证实存在消化道出血及在出血前10d内有服用NSAIDs史的患者100例的临床资料,将其分为老年组62例和中青年组38例,按照使用NSAIDs的不同和患者的年龄进行研究。结果老年组NSAIDs相关性上消化道出血发生率明显高于中青年组（P〈0·01）,老年组服用的NSAIDs药物以阿司匹林为主显著高于中青年组（P〈0·01）;中青年组以布洛芬为主显著高于老年组（P〈0·01）;老年组消化道出血以溃疡性病变为主,中青年组以黏膜糜烂为主。两组患者的Hp感染差异无统计学意义（P〉0·05）。结论老年人患NSAIDs相关性上消化道出血具有其自身特点,不同于中青年患者,应该进行个体化的预防和治疗。     

Upper gastrointestinal disorders induced by non-steroidal anti-inflammatory drugs

Aims: We examined the characteristics of upper gastrointestinal disorders induced by non-steroidal anti-inflammatory drugs (NSAIDs). Methodology: The questionnaire investigation was performed over a five year period. Results: A study was performed on 354 patients (161 men and 193 women with mean ages of 66.0 and 70.7 years, respectively) who developed NSAIDs associated upper GI disorders: 21 patients had AGML, 212 had gastric ulcer, 63 had duodenal ulcer, 17 had gastroduodenal ulcers and 41 other cases. About 75 % of patients received NSAIDs for orthopedic conditions. Sixty percent of gastric disorders induced by NSAIDs affected the antrum or angulus of the stomach. The incidence of disorders of the gastric antrum was significantly higher in women than in men whilst the incidence of disorders on the gastric angulus was significantly higher in men than in women (p < 0.05). The proportion of patients with abdominal pain was significantly lower in patients over 65 years old than in those under 65 years old, and the proportion of patients with hematemesis or melena was significantly higher in patients over 80 years old than in those under 80 years old (p < 0.05). The time taken to achieve the healing stage was significantly longer in patients with greater than 3 months NSAIDs ingestion compared to patients that had received NSAIDs for less than 3 months (p < 0.05). Conclusions: Patients 65 years old and over with continuous NSAIDs use had asymptomatic ulcers, and patients 80 years old and over had hemorrhagic ulcers. Received and accepted 20 September 2006     

非甾体类消炎药不良反应的相关研究

目的分析比较几种常用的非甾体类消炎药（布洛芬、双氯芬酸、美洛昔康）的不良反应。方法将160例骨关节炎、类风湿性关节炎患者随机分成3组,分别予以布洛芬、双氯芬酸、美洛昔康治疗6个月,观察比较其消化道、心血管系统不良反应及血象变化。结果布洛芬组患者消化道损害发生率显著高于美洛昔康组,有统计学意义;三组患者心血管事件的发生率无统计学差异,血象变化亦无统计学差异。结论选择性COX-2抑制剂的消化道损害显著低于非选择性的非甾体类消炎药,但其对于心血管事件的不良影响尚不明确,临床医师用药需谨慎。     

Renal and cardiovascular toxicity of non-steroidal anti-inflammatory drugs

Introduction. In addition to gastro-intestinal side effects, non-steroidal anti-inflammatory drugs (NSAIDs) have been associated with renal and cardiac complications. We review the mechanisms of NSAID-induced renal and cardiac toxicity and the epidemiological evidence regarding the magnitude of these problems. Methods. A Medline search was undertaken, using MESH and keyword terms, specified drug names, and renal/cardiac outcomes. The Cochrane Database was also searched. Results. Renal toxicity may manifest as acute or chronic failure and/or nephropathy, cardiac toxicity, as failure. For the most part, renal and cardiac side effects are consequences of interference by NSAIDs with prostaglandin-dependent processes, including homeostasis and vasodilitation/constrictor balance. Based on the epidemiological evidence, NSAID-induced vasomotor renal failure is fairly uncommon, and is usually identified and treated promptly. Factors increasing the risk include old age, pre-existing renal failure, and NSAIDs with long half-lives. In patients with existing cardiac disease, NSAIDs increase the risk of failure and may account for up to 19% of failure-related hospital admissions. The risk of renal and cardiac toxicity may be highest early in the course of treatment. NSAIDs may increase mean arterial pressure by around 5 mm Hg, an amount clinically significant in those with hypertension. Conclusions. NSAIDs may produce clinically significant renal and cardiac toxicity. Some of the factors increasing susceptibility may be identified easily, thereby permitting prescribers to either choose alternatives or look for evidence of harm in those most at risk.