非甾体类抗炎药物与消化性溃疡出血的关系

目的探讨非甾体类抗炎药物(NSAIDs)诱发消化性溃疡出血的临床流行病学特点。方法回顾分析1991~2004年我院诊治的消化性溃疡出血的临床资料,并用电脑数据库处理分析。结果在694例消化性溃疡并出血患者中,26.80%近期内有服用NSAIDs史。服用NSAIDs组与未服用NSAIDs组比较,服用NSAIDs组前驱症状(腹痛、消化不良等)发生率较低(30.65%比61.42%P<0.01);平均年龄较大[(44.16±13.25)岁比(35.23±11.49)岁,P<0.05];女性比例相对较多(26.34%比15.55%,P<0.01);胃溃疡比例较高(28.50%比20.67%,P<0.01);外科手术率无明显差别(P>0.05);结论NSAIDs是诱发消化性溃疡出血的一常见原因,应加强对NSAIDs胃肠毒副作用的防治。     

非甾体抗炎药引起小肠黏膜损伤机制及其治疗的研究进展

非甾体抗炎药(NSAIDs)是目前临床应用最广泛的药物之一,具有解热、镇痛、抗炎作用。随着NSAIDs的广泛应用,其胃肠道不良反应的报道日趋增多。目前NSAIDs对小肠黏膜损伤的机制未完全阐明。本文就NSAIDs引起小肠黏膜损伤的机制及其治疗的研究进展作一综述。     

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1病历资料患者男,73岁。因反复便血4个月于2011-09-27入我院。入院前4个月(2011年5月)患者进食辛辣食物后出现鲜血便,覆于大便表面,量约数滴。此后间断出现上述情况,自认为痔疮出血,未行诊治。20 d前(2011年9月)上楼时突发头晕、大汗、心悸,休息后缓解,院外查血常规示血红蛋白(Hb)66 g/L,白细胞(WBC)、血小板(PLT)、出凝血时间及肝肾功能正常。     

广东地区上消化道出血病因演变及相关因素分析

目的 探讨近20年来广东地区上消化道出血(UGIB)的病因及死亡率变化.方法 回顾性分析1990年1月至2009年10月广东省人民医院确诊的UGIB患者共3140例,按入院时间顺序及年龄分组,对比UGIB病因的变化及其影响因素.结果 UGIB患者中男性多于女性,性别比为2.5∶1,前后10年性别构成比未发生明显变化;消...     

云母对NSAIDs相关性胃肠病的防治作用

随着非甾体消炎药（NSAIDs）被广泛应用于骨关节炎、类风湿性关节炎以及心脑血管疾病的治疗和预防,其胃肠道不良反应逐渐引发关注。中药云母具有天然层状结构和特殊的物理性质,可吸附于黏膜表面,发挥黏膜保护作用。研究发现云母对NSAIDs相关性胃肠病具有预防和治疗作用,其起效机制可能包括维持胃肠道屏障功能、促进胃肠黏膜损伤修复、抑制和吸附促炎细胞因子以及抗脂质过氧化等。本文对相关内容作一综述。     

非甾体类抗炎药与消化道肿瘤

非甾体类抗炎药(NSAID)对抑制实验动物的结肠癌、胃癌和食管癌有效,多数的流行病学调查也得到类似结论.消化道肿瘤组织中COX-2表达增加,因此COX抑制剂可能通过减少花生四烯酸代谢产物产生、减少免疫抑制性前列腺素的合成、抑制血管形成等途径抑制肿瘤.但NSAID也可以在完全缺乏COX活性的细胞中发挥抗增殖作用,因此激活对转录因子核因子кB的抑制以及抑制包括依赖CAMP的蛋白激酶在内的大量酶类等也可能是其抗肿瘤的作用方式.     

非甾类抗炎药致上消化道出血226例

目的:为了解NSAID引起的胃肠道副作用 。方法:分析1986—1992年因其所致上消化道出血226例。结果:住院比例逐年增高,56.2％发病前无症状,35.4％和14.2％,9例穿孔;69.9％为急性胃十二指肠粘膜麋烂、应激性溃疡出血,30.1％为慢性溃疡出血。结论:①诱发急性慢性溃疡:②不论年龄、使用时间长短均可发生胃十二指肠粘膜损害致严重并发症。     

抗氧化剂及非甾体抗炎药物对大鼠阿尔茨海默病的预保护研究

目的研究预先施加抗氧化剂VirC和VitE及非甾体抗炎药Ibuprofen对阿尔茨海默病(AD)大鼠模型认知功能的预保护作用。方法 SD大鼠72只按体重随机分为6组:其中3个药物干预组包括VitC+VitE组、Ibuprofen组和VitC+VitE+Ibuprofen组;另3组分别为直接造模组、空白对照组和生理盐水组,每组12只。连续给药15周后,分别对各组大鼠进行AD造模。进行Morris水迷宫行为学测试、免疫组织化学染色及海马CA3区病理特征观察。结果与空白对照组和生理盐水组比较,药物干预组和直接造模组大鼠的逃避潜伏期延长,平台所在象限游泳时间缩短,平台所在象限游泳路径长度占总路径长度的百分比降低(P<0.05,P<0.01);空白对照组脑源性神经营养因子阳性细胞率高于其他组(P<0.01),直接造模组低于其他组(P<0.05,P<0.01),VitC+VitE+Ibuprofen组高于VitC+VitE组和Ibuprofen组(P<0.05)。海马CA3区神经细胞受损严重,直接造模组改变最为明显。结论抗氧化剂及非甾体抗炎药物有一定的神经保护作用,可在一定程度上抵抗AD造模对大脑的损害,两者联合使用效果更加显著。     

非类固醇抗炎药物与消化性溃疡出血

非类固醇抗炎药物(NSAIDs)广泛应用于临床,由此引起的胃、十二指肠损害越来越受到人们的关注。我们的研究包括溃疡出血组、消化性溃疡组、住院病人组、健康人组,结果示消化性溃疡组服用NSAIDs明显高于其他组,特别是十二指肠溃疡病人,多数病人在出血前有服NSAIDs历史,且药物频率大于其它组。部分服用NSAIDs病人以出血为首发症状,扑热息痛对消化溃疡出血并无影响。     

Effects of nonsteroidal anti-inflammatory drugs on endogenous gastrointestinal prostaglandins and therapeutic strategies for prevention and treatment of nonsteroidal anti-inflammatory drug-induced damage.

Although nonsteroidal anti-inflammatory drugs (NSAIDs) are effective for pain relief and treatment of arthritis, they can induce gastric and duodenal ulcers and life-threatening complications. The mechanisms of their anti-inflammatory action and their gastroduodenal toxic effects are related, in part, to inhibition of prostaglandin synthesis. This review article discusses prostaglandins, their functions in the gastrointestinal tract, anti-inflammatory actions of NSAIDs, and mechanisms by which NSAIDs produce gastroduodenal ulcers. Also reviewed are risk factors associated with the development of NSAID-related ulcers and pharmacologic strategies for the prevention and treatment of NSAID-induced ulcers.     

Syncope caused by nonsteroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors

A 85-year-old woman with diabetes mellitus and prior myocardial infarction was transferred to the emergency room with loss of consciousness due to marked bradycardia caused by hyperkalemia. The T wave during right ventricular pacing was tall and tent-shaped while the concentration of serum potassium was high, and its amplitude during pacing was decreased after correction of the serum potassium level. Simultaneously with the correction, normal sinus rhythm was restored. The cause of hyperkalemia was considered to be several doses of loxoprofen, a nonsteroidal anti-inflammatory drug (NSAID), prescribed for her lumbago by an orthopedic specialist, in addition to the long-term intake of imidapril, an angiotensin-converting enzyme inhibitor (ACEI), prescribed for her hypertension by a cardiologist. This case warns physicians that the combination of NSAID and ACEI can produce serious side effects in aged patients who frequently suffer from hypertension, diabetes mellitus, ischemic heart disease, and degenerative joint disease.     

Acute renal failure and glomerulopathy caused by nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs are now one of the most common causes of acute renal failure (ARF). To define more clearly the magnitude of the problem, we reviewed all cases of ARF in the Reno (Nev) area from 1972 through 1986. Twenty-seven cases of ARF and seven cases of glomerulopathy were identified, primarily during the last 5 years of the study period. Twenty-three of the cases of ARF and six of the cases of glomerulopathy cleared an average of 23 and 118 days, respectively, after treatment with the nonsteroidal anti-inflammatory drug was stopped. Two cases of ARF persisted, and two patients died. Proteinuria, hematuria, and casts were prominent in both ARF and glomerulopathy but were more pronounced in the glomerulopathies. The treatment of choice is to stop the use of the nonsteroidal anti-inflammatory drug. The role of steroids has not been evaluated.     

The relative gastrointestinal toxicity of the nonsteroidal anti-inflammatory drugs

To assess the relative rate or upper gastrointestinal (UGI) tract bleeding associated with nonsteroidal anti-inflammatory drugs (NSAIDs), we performed a retrospective cohort study using 1980 billing data from all Medicaid patients in the states of Michigan and Minnesota. The rate of UGI tract bleeding in the 30 days following each drug exposure was examined in the 88,044 patients dispensed only one of seven NSAIDs. The rate of UGI tract bleeding differed significantly among users of these drugs. Stratification and logistic regression were used to adjust for multiple potential confounding factors, without substantive changes in the results. An alcohol-drug interaction was found. Sulindac users had the highest rate of UGI tract bleeding, and it was the only drug statistically different from ibuprofen. When the average daily dose of sulindac received was divided by the maximum recommended daily dose, it was notably higher than those for other drugs. Repeated analyses using data from 1982 confirmed these results. We conclude that there are significant and consistent differences in the incidence of UGI tract bleeding associated with the use of NSAIDs in this population.     

The prevention of gastropathy and upper abdominal symptoms caused by nonsteroidal anti-inflammatory drugs

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is increasing, primarily due to arthritis in the aging population. This article reviews current data on the risk of gastrointestinal complications related to NSAIDs and strategies to manage risk in patients taking these agents. Risks of NSAID use include gastrointestinal ulceration, hemorrhage, or perforation; renal dysfunction; death; and dyspepsia. Alternate therapies include use of non-NSAID analgesics; low-dose NSAIDs; and concurrent administration of cytoprotective agents with NSAIDs, acid inhibitors, proton pump inhibitors, and COX-2 agents.     

Novel nonsteroidal anti-inflammatory drugs

The authors first briefly review how the concept of COX-2 selectivity was brought to light, then tested against the known gastrotoxicity ranking of currently used NSAIDs, from the old classics to the most recent. One truly selective COX-2 agent--celecoxib--is now being marketed in an ever increasing number of countries. So far it seems to keep its main promises, i.e. high--albeit not total--safety regarding gastrointestinal adverse effects, and undisturbed platelet function. Association with warfarin drugs seems to raise no problems, but one should still be wary of possible renal side-effects. Efficacy, at least as assessed in osteoarthritis and rheumatoid patients, appears satisfactory. However, treatment of intense inflammatory crises, such as gout or ankylosing spondylitis, has not been assessed, as yet. Another COX-2 agent--rofecoxib--is on the brink of being released. Its even more potent COX-2 selectivity raises new issues. What about some COX-1 activity that several authors detected in rheumatic synovitis? On the other hand, in particular circumstances, organs such as the stomach, the kidney and small blood vessels, seem to have their homeostasis partly controlled by COX-2 mechanisms also. These questions should be answered soon, whilst clinical experience with the COX-2 agent builds up.