不同抗酸药防治非甾体类抗炎药胃黏膜损伤的疗效观察

目的探讨不同抗酸药防治非甾体类抗炎药胃黏膜损伤的临床效果。方法选取2016年9月至2017年9月我院收治的服用非甾体类抗炎药物患者共90例,随机分为A组、B组和C组,A组。患者均接受为期3个月的原治疗方案,服用NSAIDs3个月,A组给予奥美拉唑治疗,B组给予雷尼替丁联合铝碳酸镁咀嚼片治疗,C组给予雷尼替丁治疗,3个月后观察患者疗效。结果 A组和B组的胃黏膜损伤发生率较C组显著降低(P <0.05),患者消化道病症发生率也较C组显著下降(P <0.05)。结论服用非甾体类抗炎药物患者,服用奥美拉唑或雷尼替丁联合铝碳酸镁咀嚼片,能有效防治胃黏膜损伤,降低消化道病症反应,具有积极推广意义。     

奥美拉唑对老年人NSAID相关性胃黏膜损伤的预防作用

目的观察奥美拉唑对老年患者应用非甾体抗炎药引起胃黏膜损伤的预防作用。方法选择服用非甾体抗炎药的老年患者64例,随机分为对照组34例,奥美拉唑组30例。对照组均单独服用非甾体抗炎药,奥美拉唑组在应用非甾体抗炎药治疗的基础上,口服奥美拉唑每日20mg。4周后对患者上消化道症状及上消化道出血的发生率进行比较。结果对照组消化道出血发生率为11.8%,奥美拉唑组未见消化道出血,两组比较差别显著(P<0.05)。对照组上消化道症状发生率为17.6%,奥美拉唑组出现上消化道症状的为13.4%,两组比较无显著差别(P>0.05)。结论老年患者在应用非甾体抗炎药过程中预防性应用奥美拉唑,能减轻消化道症状、预防消化道出血的发生。     

奥美拉唑肠溶片致白细胞减少

39岁女性反流性食管炎、慢性胃窦炎患者,给予奥美拉唑肠溶片20mg,2次/d,以及多潘立酮片和铝碳酸镁咀嚼片。服药2周后,患者出现困倦、乏力、纳差、低热。WBC由6.3×109/L降到3.6×109/L。将奥美拉唑改为雷尼替丁150mg,2次/d,多潘立酮片、铝碳酸镁咀嚼片继续服用,加服利血生20mg,3次/d。3d后,WBC升至4.2×109/L。随访患者血细胞恢复正常。     

铝碳酸镁联合奥美拉唑治疗胃溃疡的疗效观察

目的 观察铝碳酸镁联合奥美拉唑治疗胃溃疡的疗效.方法 将90例胃溃疡患者随机分为A、B、C 3组各30例.A组给予铝碳酸镁20mg口服,每天3次;B组给予奥美拉唑20mg口服,每天1次;C组给予铝碳酸镁20mg口服,每天3次,奥美拉唑20mg口服,每天1次.2个月后观察3组临床疗效.结果 治疗2个月后,A、B和C组总有效率分别为80.0%、83.3%和96.7%,C组高于A组和B组,差异有统计学意义(P＜0.05).3组2个月后无效患者经治疗1年后均痊愈或有效.结论 铝碳酸镁联合奥美拉唑治疗胃溃疡疗效优于单纯应用铝碳酸镁或奥美拉唑,值得临床推广应用.     

铝碳酸镁联合奥美拉唑治疗胃溃疡的疗效观察

目的观察铝碳酸镁联合奥美拉唑治疗胃溃疡的疗效。方法将90例胃溃疡患者随机分为A、B、C3组各30例。A组给予铝碳酸镁20mg口服,每天3次;B组给予奥美拉唑20mg口服,每天1次;C组给予铝碳酸镁20mg口服,每天3次,奥美拉唑20mg121服,每天1次。2个月后观察3组临床疗效。结果治疗2个月后,A、B和c组总有效率分别为80．0％、83．3％和96．7％,C组高于A组和B组,差异有统计学意义（P〈0．05）。3组2个月后无效患者经治疗1年后均痊愈或有效。结论铝碳酸镁联合奥美拉唑治疗胃溃疡疗效优于单纯应用铝碳酸镁或奥美拉唑,值得临床推广应用。     

社区人群非甾体抗炎药、糖皮质激素相关胃肠损伤认知调查及PPI干预效果观察

目的 (1)对长期服用非甾体抗炎药物或糖皮质激素人群进行问卷调查,掌握对胃肠损伤的认知率;(2)评价质子泵抑制剂对非甾体抗炎药物、糖皮质激素胃肠道损伤干预效果。方法 (1)对东莞市麻涌镇社区中心登记长期服用非甾体类抗炎药物及糖皮质激素的人群进行问卷调查。(2)2018年6月1日～2019年5月31日,选取我院及社区门诊长期服用糖皮质激素或非甾体抗炎药物患者各120例,采用随机、单盲方法分别分为安慰剂组、雷尼替丁组与奥美拉唑组。比较各组患者的治疗效果。结果 (1)社区长期服用非甾体抗炎药物或糖皮质激素者对相关胃肠损伤认知率低。(2)奥美拉唑组患者在胃肠黏膜损伤等不良反应发生率方面均少于安慰剂组、雷尼替丁组患者(P 0.05)。结论 (1)提高社区长期服用非甾体抗炎药物或糖皮质激素者对相关胃肠损伤认知率具有重大的社会效益;(2)质子泵抑制剂能减少长期服用非甾体抗炎药、糖皮质激素药胃肠不良反应及预防胃肠出血。     

铝碳酸镁和奥美拉唑联合治疗胃溃疡的比较

目的比较铝碳酸镁和奥美拉唑联合治疗胃溃疡病的疗效。方法 90例经内镜证实的胃溃疡患者,随机平分成铝碳酸镁组、奥美拉唑组和铝碳酸镁联合奥美拉唑组,铝碳酸镁组予以铝碳酸镁,3次/d,20 mg/次;奥美拉唑组给予奥美拉唑1次/d,20 mg/次。铝碳酸镁联合奥美拉唑组同时给予前两组的药物。观察治疗效果。结果铝碳酸镁组、奥美拉唑组和铝碳酸镁联合奥美拉唑组2个月的溃疡愈合有效率分别为86.7%、83.3%和96.7%。铝碳酸镁联合奥美拉唑组的有效率优于其他两组(P<0.05),具有统计学意义。三组的1年愈合有效率均为100%。结论铝碳酸镁联合奥美拉唑治疗胃溃疡有效率优于单纯应用铝碳酸镁或者奥美拉唑,值得临床推广。     

铝碳酸镁在胃溃疡伴胆汁反流的临床效果分析

目的探讨铝碳酸镁在胃溃疡伴胆汁反流的临床效果。方法选择我院胃溃疡伴胆汁反流患者150例,随机分为观察组和对照组(各组患者75例)。对照组患者给予奥美拉唑,餐前30 min口服,第1周,每次口服20 mg(每天2次),而后的第2⁶周,每次服用20 mg,每天服用1次。观察组患者上述用药基础上给予铝碳酸镁治疗,第1周,每次1.0 g,每天服用3次,第26周,每次服用20 mg,每天服用1次。观察组患者上述用药基础上给予铝碳酸镁治疗,第1周,每次1.0 g,每天服用3次,第2⁶周,改为每天用药2次。治疗6周后,对照组患者停止服用奥美拉唑,观察组再给予铝碳酸镁服用,每次1.0 g,每天2次。治疗后评定治疗效果。结果观察组的临床效果总有效率(显效55例、占73.3%;有效16例、占21.3%;无效4例,占5.4%)为94.6%;对照组临床效果总有效率(显效45例、占60.0%;有效17例、占22.7%;无效13例,占17.3%)为82.7%;观察组总有效率高于对照组,差异有统计学意义(P<0.05)。结论铝碳酸镁在胃溃疡伴胆汁反流的临床效果显著,指导借鉴。     

铝碳酸镁治疗胃溃疡伴胆汁反流的疗效观察

目的探讨铝碳酸镁对伴胆汁反流的胃溃疡患者的疗效。方法将80例胃溃疡伴胆汁反流患者随机分为观察组和对照组各40例,第1周两组均给予奥美拉唑胶囊20mg,2次/d,餐前30min温开水送服;观察组同时给予铝碳酸镁片1.0g,3次/d,餐后30min内嚼碎服。第2～6周两组均给予奥美拉唑胶囊20mg,每晨1次,观察组同时给予铝碳酸镁片1.0g,2次/d。第7～8周观察组给予铝碳酸镁片1.0g,2次/d,口服,对照组停药。观察并比较两组患者临床症状积分变化、疗效变化。结果治疗后观察组患者临床症状、胆汁反流积分明显降低（P〈0.01）,组间对比差异亦有统计学意义（P〈0.05）。结论胆汁反流可能参与胃溃疡的形成,铝碳酸镁治疗伴胆汁反流的胃溃疡疗效肯定。     

联合用药治疗胆汁反流性胃炎疗效对比

目的 观察莫沙必利分散片＋铝碳酸镁和莫沙必利分散片＋奥美拉唑联合用药治疗胆汁反流性胃炎（BRG）的疗效差异.方法 150例BRG患者平分为两组,两组均给予口服莫沙必利分散片,3次/d,5 mg/次,餐前30 min温开水送服.观察组联合铝碳酸镁,3次/d,1.0 g/次,餐后1h内嚼服;对照组联合奥美拉唑,2次/d,20 mg/次,口服.四周为一疗程.观察疗效.结果 观察组显效65例（86.7％）,有效7例（9.3％）,无效3例（4.0％）;对照组显效46例（61.3％）,有效12例（16.0％）,无效17例（22.7％）.观察组显效率86.7％和有效率96.0％均明显高于对照组显效率61.3％和有效率77.3％,差异均有统计学意义（P＜0.05）.结论 莫沙必利分散片联合铝碳酸镁治疗BRG,能达到较高的显效率和有效率.     

Meta-analysis: upper gastrointestinal tolerability of valdecoxib, a cyclooxygenase-2-specific inhibitor, compared with nonspecific nonsteroidal anti-inflammatory drugs among patients with osteoarthritis and rheumatoid arthritis

AIM: To compare the incidence of abdominal pain, dyspepsia and/or nausea associated with valdecoxib, nonspecific nonsteroidal anti-inflammatory drugs and placebo in patients with rheumatoid arthritis and osteoarthritis. METHODS: Data from five randomized, double-blind 12-week trials were pooled. Independent risk factors for abdominal pain, dyspepsia and/or nausea were also determined. RESULTS: The final analysis consisted of 4394 patients. Nonspecific nonsteroidal anti-inflammatory drug users (n = 1185) received naproxen 1000 mg/day (n = 766), ibuprofen 2400 mg/day (n = 207) or diclofenac sodium 150 mg/day (n = 212). Valdecoxib users received 10 mg/day (n = 955), 20 mg/day (n = 851) or 40 mg/day (n = 430). A total of 973 patients received placebo. The nonspecific nonsteroidal anti-inflammatory drug group was most likely to report abdominal pain or dyspepsia, while the placebo group reported the highest incidence of nausea. The most important risk factors for abdominal pain, dyspepsia and/or nausea were nonspecific nonsteroidal anti-inflammatory drug use, gastrointestinal history of nonspecific nonsteroidal anti-inflammatory drug-related intolerance or gastroduodenal ulcers, osteoarthritis diagnosis, female gender and age <65 years. CONCLUSION: This pooled analysis demonstrates a clear decrease in dyspepsia and an improvement in upper gastrointestinal tolerability for patients with osteoarthritis and rheumatoid arthritis taking valdecoxib, even at supratherapeutic doses, compared with those taking nonspecific nonsteroidal anti-inflammatory drugs over 12 weeks.     

Further evidence of the antiulcer activity of IAC, a novel free radical scavenger

It has been proposed that free radicals, reactive oxygen species (ROS) and reactive nitrogen species play a critical role in gastric mucosal damage. It is well known that the exposure of gastric mucosa to damaging factors such as stress and nonsteroidal anti-inflammatory drugs produces acute ulcers that are mainly mediated by ROS. The aim of the present study was to investigate the gastroprotective properties of bis(1-hydroxy-2,2,6,6-tetramethyl-4-piperidinyl)decandioate (IAC), a novel nonpeptidyl low-molecular-weight radical scavenger, in two different models of gastric ulcer in rats caused by ROS. IAC was orally administered at the doses of 50 and 100 mg/kg before gastric ulceration induced by indomethacin and water immersion and restraint stress. The number and severity of gastric lesions, following macroscopic inspection of the mucosa, were evaluated and expressed as an ulcer score. Oral administration of IAC dosed at 50 and 100 mg/kg was able to significantly prevent gastric ulceration induced by indomethacin and by stress. The gastroprotective effect of IAC on gastric mucosa could be attributed to its intrinsic antioxidant activity, suggesting it as a novel antiulcer agent.     

Treatment and prevention of nonsteroidal anti-inflammatory drug induced gastrointestinal mucosal injury

It is generally recognized that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can cause varying degrees of gastroduodenal mucosal damage. These agents are most frequently used by physicians for rheumatic diseases because of their high effectiveness in reducing joint pain and swelling. Four classes of drugs, namely histamine (H2) blockers, antacids, sucralfate and prostaglandins are available for treatment of gastric mucosal damage caused by NSAIDs. All these drugs are very effective in healing gastric and duodenal injury if nonsteroidal anti-inflammatory drugs are discontinued. However, current data suggest that if nonsteroidal anti-inflammatory drugs are continued while gastrointestinal damage is present there may be significant differences among these drugs in healing of gastric mucosal damage. Synthetic prostaglandins are therapeutically superior over other forms of treatment when nonsteroidal anti-inflammatory drugs are continued in the presence of gastric mucosal injury. This article is a review of such data from the literature for a) the treatment and b) the prevention of gastrointestinal damage due to aspirin and nonsteroidal anti-inflammatory drugs.     

Prophylaxis of aspirin-induced gastric mucosal bleeding with ranitidine

The ability of ranitidine to protect the human gastric mucosa against aspirin-induced damage was investigated by timed measurements of blood loss collected by gastric washing. Ranitidine (150 mg) 1 h or 5 h before 900 mg aspirin (5 doses of each) over 48 h reduced subsequent mean bleeding from 7.7 microliters/10 min to 2.6 microliters/10 min or 3.4 microliters/10 min, respectively. Both regimens were antisecretory at the time of aspirin administration, as judged by a rise in the pH of the aspirated washings. The prolonged protection against aspirin-induced bleeding achieved with twice daily dosing with ranitidine has clinical potential in the management of patients taking anti-inflammatory drugs.     

Clinical trial: comparison of the gastrointestinal safety of lumiracoxib with traditional nonselective nonsteroidal anti-inflammatory drugs early after the initiation of treatment--findings from the Therapeutic Arthritis Research and Gastrointestinal Event Trial

Background  The large ( n  = 18 325) Therapeutic Arthritis Research and Gastrointestinal Event Trial (TARGET) study demonstrated a significant gastrointestinal benefit with lumiracoxib 400 mg o.d. (4× the recommended dose in osteoarthritis) vs. naproxen 500 mg b.d. or ibuprofen 800 mg t.d.s.
Aim  To investigate how early a reduction in ulcer complications could be detected with lumiracoxib vs. nonselective nonsteroidal anti-inflammatory drugs in TARGET.
Methods  Pointwise 95% confidence intervals were generated for the between-treatment differences in Kaplan–Meier estimates for definite or probable upper gastrointestinal ulcer complications (ulcer complications) and for all ulcers.
Results  In patients not on aspirin, there was a significant reduction in all ulcers by day 8 and in ulcer complications by day 16 with lumiracoxib compared with both nonselective nonsteroidal anti-inflammatory drugs combined, by day 6 (all ulcers) and day 14 (ulcer complications) vs. naproxen and by day 32 (all ulcers) and day 33 (ulcer complications) vs. ibuprofen.
Conclusion  Even with short-term use, there are gastrointestinal safety benefits for lumiracoxib vs. nonselective nonsteroidal anti-inflammatory drugs.     

Ranitidine. An updated review of its pharmacodynamic and pharmacokinetic properties and therapeutic use in peptic ulcer disease and other allied diseases

Ranitidine, a histamine H2-receptor antagonist, is now well established as a potent inhibitor of gastric acid secretion effective in the treatment and prophylaxis of gastrointestinal lesions aggravated by gastric acid secretion. Therapeutic trials involving several thousands of patients with peptic ulcer disease confirm that ranitidine 300mg daily administered orally in single or divided doses is at least as effective as cimetidine 800 to 1000mg daily in increasing the rate of healing of duodenal and gastric ulcers. Similar dosages of ranitidine have been shown to relieve the symptoms of reflux oesophagitis and heal or prevent gastrointestinal damage caused by ulcerogenic drugs. Ranitidine 150mg orally at night maintains ulcer healing in the long term. Ranitidine has also demonstrated good results in the treatment of Zollinger-Ellison syndrome and in the prevention of aspiration pneumonitis when given prior to surgery and to pregnant women at full term. It may also have a place in the management of acute upper gastrointestinal bleeding and in the prevention of stress ulcers in the intensive care setting, although these areas require further investigation. Ranitidine has been used safely in obstetric patients during labour, in children, the elderly, and in patients with renal impairment when given in appropriate dosages. The drug is very well tolerated and is only infrequently associated with serious adverse reactions or clinically significant drug interactions. Even at high dosages, ranitidine appears devoid of antiandrogenic effects. Ranitidine is clearly comparable or superior to most other antiulcer agents in the treatment and prevention of a variety of gastrointestinal disorders associated with gastric acid secretion. With its favourable efficacy and tolerability profiles, ranitidine must be considered a first-line agent when suppression of gastric acid secretion is indicated.     

Comparison in rats of the anti-inflammatory and gastric irritant effects of etodolac with several clinically effective anti-inflammatory drugs

The anti-inflammatory and gastric effects of etodolac were compared in the rat with those of seven clinically established nonsteroidal anti-inflammatory drugs. The anti-inflammatory potency of etodolac was found to lie between that of sulindac and piroxicam. Etodolac was 2.8 times more active than sulindac and 2.2 times less active than piroxicam. Compared to phenylbutazone it was 12.5 times more potent. The irritation produced on the gastric mucosa was less than that of sulindac, although this difference did not reach statistical significance. However, etodolac was significantly (p less than 0.05) less irritant than piroxicam. Of the drugs studied, etodolac showed the highest ratio between the irritant ED50 and the dose which inhibited inflammation by 50%. From these results etodolac is predicted to be a potent anti-inflammatory drug with a high gastric tolerance. Clinical trials appear to confirm these predictions.     

非甾体类消炎药致上消化道出血的临床表现与内镜特征

目的　探讨非甾体类消炎药物导致上消化道出血的临床与内镜特征。方法　回顾性分析 5 6例非甾体类消炎药物导致上消化道出血病人的临床资料。结果　服用非甾体类消炎药物后 5 d内出血 38例 (6 8% ) ,表现为上腹痛 39例 (6 9% ) ,呕血伴黑便 34例 (6 1% ) ,单纯黑便 2 2例 (39% ) ,内镜下表现为弥漫性胃黏膜充血、水肿及多发糜烂 38例 (6 8% ) ,胃溃疡 14例 (2 5 % )。结论　非甾体类消炎药物致上消化道出血的主要临床表现为腹痛、呕血伴黑便或单纯黑便。内镜下为弥漫性胃黏膜充血、水肿 ,多发性糜烂和溃疡。     

A comparative gastroscopic study of lonazolac and indomethacin in healthy subjects

In 9 healthy volunteers the effects of a 14-day treatment with lonazolac 300 mg b.i.d. on gastric and duodenal mucosa have been endoscopically compared with those of indomethacin 75 mg b.i.d. in a double-blind placebo-controlled trial. Lonazolac and indomethacin induced significantly more gastric and duodenal mucosal injuries (1.9 +/- 0.4 and 1.7 +/- 0.3) compared to placebo (0.9 +/- 1.0) (p less than 0.05). The validity of different procedures in predicting the deleterious effects of nonsteroidal antiinflammatory drugs on the human upper gastrointestinal epithelium is discussed.