雷贝拉唑与奥美拉唑对老年人反流性食管炎的抑酸效能及其症状缓解作用比较

目的比较雷贝拉唑和奥美拉唑对老年人反流性食管炎（RE）的抑酸效果及症状缓解作用。方法60例经胃镜检查确诊为反流性食管炎的老年患者,随机分成两组,每天早餐前空腹121服雷贝拉唑10mg或奥美拉唑20mg,疗程均为7d。在用药前和用药后的第1天及第7天对患者的主要反流症状进行症状学评分,比较两组治疗前后症状学评分。每组各选10名患者于服药第1天做24h胃内pH值监测,比较这两种药物胃酸抑制效果。结果服药第1天雷贝拉唑组的症状评分为1．86±1．17,奥美拉唑组为2．53±1．14．P〈0．05。雷贝拉唑组7人症状消失,奥美拉唑组的2人症状消失。至第7天两组的症状评分分别为0．47±0．68和0．63±0．72,症状消失率分别为63．3％和50％,两组差异无统计学意义。服药第1天雷贝拉唑组服药后2h胃内中位pH值为6．10±1．13,高于奥美拉唑组的4．22±2．38,起效时间40．8±24．35．快于奥美拉唑组的112．0±105．46．P值均小于0．05。其余各项指标差异无统计学意义。两组均无明显不良反应事件发生。结论雷贝拉唑和奥美拉唑对老年人RE患者均有良好的抑酸效能及症状缓解作用,但雷贝拉唑起效更快、抑酸作用更稳定。     

雷贝拉唑三联疗法治疗幽门螺杆菌阳性十二指肠溃疡

目的观察雷贝拉唑三联短程疗法治疗幽门螺杆菌(H.pylori)阳性十二指肠溃疡的疗效.方法100例经胃镜检查确诊为十二指肠溃疡并经快速尿素酶实验和病理学检查确定为H.pylori阳性的患者随机分为两组雷贝拉唑组和奥美拉唑组.两组先予以三联疗法雷贝拉唑10mg或奥美拉唑20mg、阿莫西林1g及克拉霉素500mg,每日2次,连续7天,然后给予雷贝拉唑10mg或奥美拉唑20mg,每天1次,连续7天,疗程结束后4周复查胃镜并检测H.pylori,并记录用药后患者症状的改变程度.结果93例完成治疗方案.其中雷贝拉唑组2周溃疡愈合率为93.6%,奥美拉唑组为73.9%,雷贝拉唑组明显高于奥美拉唑组,两组有显著性差异(P＜0.05),雷贝拉唑组第1、3天症状缓解率分别为68.1%、91.4%,奥美拉唑组为39.1%、65.2%,两组比较差异有显著性(P＜0.05);雷贝拉唑H.pylori根除率为91.5%,奥美拉唑组为86.9%,两组间无显著性差异(P＞0.05).结论雷贝拉唑、克拉霉素和阿莫西林三联短程疗法能有效根除H.pylori及提高溃疡愈合率,并能迅速缓解症状,与奥美拉唑三联疗法相比较,在H.pylori根除率上无显著性差异,而在2周溃疡愈合率及症状缓解率方面,雷贝拉唑却明显优于奥美拉唑.     

埃索美拉唑对健康志愿者抑制胃泌酸的药效学研究

目的　比较埃索美拉唑与雷贝拉唑对健康志愿者抑制胃泌酸的效果及安全性。方法　 36名健康志愿者随机分为两组 ,分别口服埃索美拉唑 4 0mg或雷贝拉唑 10mg ,每日 1次 ,连续 5d ,经过14d的洗脱期后 ,交叉口服雷贝拉唑 10mg或埃索美拉唑 4 0mg ,每日 1次 ,连续 5d。分别于服药首日及第 5天连续测定 2 4h胃内 pH ,并以PCR方法鉴定细胞色素 (CYP) 2C19基因型。 结果　埃索美拉唑组服药后首日最初 4、2 4h和第 5天 2 4h胃内pH >4 .0的时间百分比分别为 5 8.9%、73.7%和 84 .2 % ,显著高于雷贝拉唑组 (32 .1%、5 4 .8%和 76 .2 % ,P <0 .0 0 1) ;胃内 pH中位值分别为 4 .2 9、5 .6 0和 6 .38,亦显著高于雷贝拉唑组 (2 .88、4 .2 6和 5 .77,P≤ 0 .0 0 1)。服药后首日及第 5天pH >4 .0超过 16h的志愿者埃索美拉唑组百分率分别为 6 3.9%和 88.9% ,亦显著高于雷贝拉唑 (33.3%和 6 1.1% ,P <0 .0 5 )。36名志愿者中 2 8名CYP 2C19基因型为强代谢型 ,8名为弱代谢型。两药对强代谢型或弱代谢型者胃泌酸的抑制差异无显著性 (P >0 .0 5 )。服药期间两组均未发生明显不良反应。结论　埃索美拉唑和雷贝拉唑均具有较强的抑制胃酸分泌效应 ,但在抑酸速度、抑酸强度和维持时间方面 ,4 0mg埃索美拉唑优于 10mg雷贝拉唑。两药     

雷贝拉唑、阿莫西林二联疗法治疗幽门螺杆菌相关性溃疡

目的 评估雷贝拉唑、阿莫西林二联疗法治疗幽门螺杆菌（Helicobacter pylori，Hp）相关性溃疡的疗效。方法 120例经胃镜检查确诊为胃和十二指肠溃疡并经快速尿素酶法和病理学特染法测定为Hp阳性的病人随机分为两组：雷贝拉唑组和奥美拉唑组。两组分别予以二联疗法；雷贝拉唑10mg或奥美拉唑20mg，1次／d；阿莫西林0．5g，3次／d；连续2周。疗程结束后4周复查胃镜并检测Hp，并记录用药后病人症状的改变程度。结果 雷贝拉唑组溃疡愈合率为94．3％，奥美拉唑组72．0％，两组比较有显著的差异性（P〈0．05）。雷贝拉唑组第1、3d症状缓解率分别为81．4％、94．3％。奥美拉唑组为38．0％、64．0％，两组有显著性差异（P〈0.05）。雷贝拉唑组Hp清除率为91．4％，奥美拉唑组为88．0％，两组无统计学差异（P〉0．05）。结论 雷贝拉唑、阿莫西林二联疗法能提高溃疡愈合率及迅速缓解症状，并能有效根除Hp。与奥美拉唑组相比较，雷贝拉唑组在溃疡愈合率及症状缓解率方面更显优势。     

CYP2C19基因多态性与质子泵抑制剂对消化性溃疡患者抑酸效应的关系

目的: 研究奥美拉唑(OME)、雷贝拉唑(RAB)及埃索美拉唑(ESO)对消化性溃疡患者的抑酸效应及与CYP2C19基因多态性的关系.方法:采用随机、开放和对照研究, 将消化性溃疡患者59例随机分为3组, 分别给予OME肠溶片(n = 19)、RAB肠溶片(n = 20)或ESO肠溶片(n = 20)各20 mg单剂量口服, 动态监测24 h胃内pH, 观察3种药物对患者的24 h和夜间抑酸效应及夜间酸突破(NAB)的影响. 用多聚酶链反应-限制性片段长度多态性(PCR-RFLP)方法测定所有患者的CYP2C19基因型并分为强代谢型(EMs)和弱代谢型(PMs).结果: OME组、RAB组及ESO组EM和PM的比例分别为16/3, 17/3及17/3. OME 24 h抑酸与夜间抑酸效应(胃内pH>4的总时间和时间百分比)在PMs和EMs中的差异有显著性[24 h抑酸: (胃内pH>4的总时间: 10.65±2.3 h vs 7.22±2.1 h, P<0.05;时间百分比: 48.9±15.5 vs 32.5±12.6, P<0.05);夜间抑酸: (胃内pH>4的总时间: 3.67±1.2 h vs 2.25±1.2 h, P<0.05;时间百分比: 38.3±20.6 vs 20.8±18.9, P<0.05)]. 而RAB及ESO组24 h抑酸和夜间抑酸效应在PMs和EMs中的差异无显著性. RAB及ESO组NAB持续时间较OME组短(3.08±2.12 h, 2.98±2.73 h vs 4.50±2.86 h, 均P<0.05), NAB的pH高于OME组(2.15±0.70, 2.45±0.65 vs 1.15±0.31, 均P<0.001). RAB与ESO组间差异无显著性. 结论:奥美拉唑的抑酸效应受患者CYP2C19基因多态性影响;雷贝拉唑和埃索美拉唑的抑酸效应则受CYP2C19基因多态性影响极小, 3种PPIs的日间抑酸效应强于夜间, 雷贝拉唑和埃索美拉唑的抑酸效应优于奥美拉唑.     

雷贝拉唑治疗十二指肠溃疡的临床观察

目的验证与评估雷贝拉唑治疗十二指肠溃疡的临床疗效和安全性.方法将活动期十二指肠溃疡患者随机分为雷贝拉唑(10mg/d)治疗组和奥美拉唑(20mg/d)对照组.服药4周后,胃镜观察溃疡愈合程度并观察有无不良反应出现.结果4周后治疗组和对照组溃疡愈合率分别为95.0%和93.6%,总有效率分别为99.0%和98.9%,两组无显著差异(P＞0.05).在腹痛消失率和消化道症状缓解率方面两组也无显著性差异(P＞0.05),但治疗组腹痛消失更为迅速,治疗组第1天腹痛消失率33.0%,而对照组为18.8%,有显著差异(P＜0.05).结论雷贝拉唑和奥美拉唑治疗十二指肠溃疡具有良好疗效,而雷贝拉唑第1天对腹痛的缓解作用更为明显,且无严重不良反应,值得临床上推广.     

雷贝拉唑钠治疗消化性溃疡的多中心临床研究

目的：评价雷贝拉唑钠10mg/d在消化性溃疡治疗中的疗效及安全性,并与奥美拉唑20mg/d进行比较。方法：采用随机开放对照临床研究,患者随机进入雷贝拉唑钠组（治疗组）或奥美拉唑组（对照组）,共有137例病人完成治疗,其中治疗组70例,对照组67例;治疗组口服雷贝拉唑钠片每次10mg,每日1次;对照组口服奥美拉唑胶囊每次20mg,每日1次。十二指肠球部溃疡疗程为4周,胃溃疡为6周。结果：两组治疗前后疼痛症状的改善及疼痛时间的消失,差异无显著性（P＞0．05）。十二指肠溃疡病人中,治疗组痊愈率和愈合率分别为38．5％和98．1％,对照组分别为26．0％和94．0％,两组间差异无显著性（P均＞0．05）。胃溃疡 病人中,治疗组痊愈率和愈合率分别为50．0％和100．0％,对照组分别为35．3％和94．1％,两组间差异无显著性（P均＞0．05）。整个试验过程中,治疗组和对照组不良反应率分别为4．3％和4．5％,两组间不良反应发生率相似（P＝1．000）。结论：雷贝拉唑钠10mg能安全、有效地治疗消化性溃疡,其缓解疼痛、促进溃疡愈合的疗效与奥美拉唑20mg相当。     

雷贝拉唑与奥美拉唑对消化性溃疡近期疗效比较

目的评价短期应用雷贝拉唑与奥美拉唑对消化性溃疡的治疗作用。方法根据临床症状和胃镜检查结果将80例消化性溃疡患者随机分为两组，A组40例，给予雷贝拉唑10mg／d，B组40例，给予奥美拉唑20mg／d，两组均为po，qd，疗程共7天。于用药前1天，用药后第1、4、7天，按标准对上腹痛、反酸进行评分，记录患者有无出现任何不良反应。结果雷贝拉唑组上腹痛消失率用药后第1天为67．5％，第4天为95．0％；奥美拉唑组上腹痛消失率用药第1天为17．5％，第4天为67．5％，两组比较差异有显著性。服药第7天，雷贝拉唑组上腹痛消失率为97．5％，奥美拉唑组为92．5％，两组比较差异有显著性。所有患者均未发现明显不良反应。结论雷贝拉唑与奥美拉唑均为强效、安全的抑酸药物，但雷贝拉唑起效更快。     

枸橼酸铋雷尼替丁治疗十二指肠球部溃疡的作用及其与夜间酸突破的关系

目的　评价枸橼酸铋雷尼替丁 (瑞倍 )为主三联治疗十二指肠球部溃疡 (DU )的疗效及安全性 ,及与夜间酸突破的关系 ,并与奥美拉唑为主三联进行比较。方法　采用随机对照临床研究 ,68例患者随机进入瑞倍组 (治疗组 )及奥美拉唑组 (对照组 ) ,其中治疗组、对照组各 3 4例 ,疗程为 1周 ,治疗第 5天连续监测胃内 2 4小时pH值。结果　两组治疗前后疼痛症状及内镜下改变的改善 ,差异无显著性 (P >0 .0 5 ) ,两组 pH <4的比例及夜间 pH <4的比例均无显著性差异 (P >0 .0 5 ) ,治疗组无 1例发生夜间酸突破 ,对照组 5例发生夜间酸突破 (14 .71% )。结论　瑞倍为主三联是治疗DU比较理想的方案 ,并可防止夜间酸突破发生     

雷贝拉唑与奥美拉唑对十二指肠溃疡患者症状的短期疗效

目的　评价短期应用雷贝拉唑和奥美拉唑对十二指肠溃疡 (DU)患者症状的治疗作用及其安全性。方法　多中心、随机、双盲、平行对照研究。将活动期DU患者随机分为雷贝拉唑 (1 0mg/d)治疗组和奥美拉唑 (2 0mg/d)对照组。 2组均服药 7d。记录治疗前和用药期间的腹痛、反酸、腹胀和嗳气症状的变化及有无不良反应出现。结果　治疗组和对照组分别完成了 1 0 8例和 1 0 3例患者的观察。治疗组的腹痛平均消失天数为 (3 1± 1 7)d ,与对照组 (3 2± 1 8)d相同。治疗组和对照组服药期间每天的腹痛消失率无明显差异。用药第 1天时治疗组的腹痛缓解率为 56 % ,明显高于对照组的 33 % (P <0 0 5) ,其余各天内 2组间无差异。治疗组患者第 7天的反酸消失率为 1 0 0 % ,明显高于对照组的 83 % (P <0 0 5)。 2组患者的每天腹胀和嗳气的消失率差异均无显著性。 2组均无不良反应发生。结论　雷贝拉唑及奥美拉唑均对DU患者的症状具有良好的治疗作用 ,而雷贝拉唑在服药第 1天对腹痛及第 7天对反酸的缓解作用更为明显。雷贝拉唑短期应用具有良好的安全性     

Effect of a single oral dose of rabeprazole on nocturnal acid breakthrough and nocturnal alkaline amplitude

AIM: To study the effect of rabeprazole (RAB) on nocturnal acid breakthrough (NAB) and nocturnal alkaline amplitude (NAKA) and to compare it with omeprazole (OME) and pantoprazole (PAN).METHODS: By an open comparative study, forty patients with active peptic ulcer were randomly assigned to receive one of the three PPIs (proton pump inhibitor) with a single oral dose. They were divided into RAB group (10 mg), OME group(20 mg) and PAN group (40 mg). Twenty healthy volunteers were enrolled to the control group (without taking any drug). Intragastric pH monitoring was then performed 1 hour before and 24 hours after the dose was given.RESULTS: No clinically undesirable signs and symptoms possibly attributed to the administration of RAB or OME and PAN were recognizable throughout the study period. All subjects completed the study according to the protocol. All data were processed by a computer using the Student ttest or t' test followed by an analysis of covariance. P<0.05 was considered to have statistical significance. The intragastric pH of NAB was significantly higher in RAB group (1.84±0.55) than in either OME group (1.15±0.31) or PAN group (1.10±0.30) (both P<0.01). RAB produced a longer sustaining time (4.65±1.22 h) on NAKA than OME (3.22±1.89 h) (P<0.05),PAN (3.15±1.92 h) (P<0.05), and the sustaining time of NAKA in RAB group was longer than that in the healthy control group (P<0.01) too. In addition, RAB produced a much higher pH on NAKA (6.41±0.45) in comparison with PAN (6.01±0.92) (P<0.05).CONCLUSION: A single oral dose of 10 mg RAB may increase the pH of NAB and shorten the sustaining time of NAB, and it may increase the pH of NAKA as well as prolong the sustaining time of NAKA.     

Comparison of the Effects of Single Morning and Single Bedtime Doses of Famotidine on Intragastric Acidity in Patients with Gastric Ulcer

The effects of single morning and single bedtime doses of famotidine on intragastric acidity were studied by 24-b intragastric pH monitoring in 16 patients with gastric ulcer. The patients were randomly allocated to tbe following regimen: one group (n = 8) received 40 mg famotidine at 8:30 AM and anotber group (n = 8) received tbo same dose at 10 PM. Tbe morning group showed significant inbibition of gastric acidity during the 24-b and daytime measurements, compared to those of the bedtime group (p < 0.05 in 24 h, p < 0.01 in daytime). Conversely, tbe bedtime group sbowed a sig-nificant inbibition of gastric acidity during tbe nocturnal period compared to tbe morning group (p < 0.01). These results indicate that the relative importance of suppression of gastric acidity on tbe gastric ulcer heal-ing process sbould be evaluated in a clinical trial.     

A Double-Blind Randomized Study Comparing Different Dose Regimens of H2-Receptor Antagonists on 24-Hour Gastric Secretion in Normal Subjects and Duodenal Ulcer Patients

Duodenal ulcer therapy with H2 antagonists initially aimed to control acid secretion throughout the 24-h period, but recently nighttime suppression has been advocated. The effect of single nighttime regimens of cimetidine 400 mg BID, cimetidine 800 mg HS, ranitidine 150 mg HS, and placebo on 24-h intragastric acidity, nocturnal acid output, and pepsin secretion were studied in four healthy volunteers and four patients with healed duodenal ulcer. A nonrandomized dose of cimetidine 1200 mg HS was also studied. For all four treatments, daytime (0730-2230 h) intragastric acidity was reduced by 4-30% in the normals and by 10-44% in the duodenal ulcer patients (NS), while 24-h intragastric acidity was reduced by 44-46% and 40-64%, respectively (p less than 0.05). Reduction in nocturnal acid output was 82-96% in normals and 91-99% in duodenal ulcer, respectively. Pepsin concentration was unaffected by treatment but pepsin concentration was significantly (p less than 0.05) lower in patients than in normals. Mean 24-h gastric acid secretion was reduced by a single nighttime treatment with an H2-receptor antagonist, while nocturnal acid secretion was virtually abolished. H2 antagonists given only at night deserve further clinical evaluation to determine the minimal effective dose and optimal duration of suppression to achieve ulcer healing.     

Nocturnal acid suppression with a new H2 receptor antagonist--nizatidine

To determine the potential efficacy of bedtime doses of the new furan H2 receptor antagonist nizatidine in the suppression of nocturnal acid secretion, this randomized, crossover, single-blind study was performed in 10 healthy male subjects. The actions of a single bedtime (21:00 hour) dose of the H2 receptor antagonists nizatidine (150 mg and 300 mg), ranitidine (300 mg) and cimetidine (800 mg), as well as placebo on nocturnal gastric acid and volume secretion (01:00 to 07:00 hours, and on overall 24 hour H+ ion concentration were studied. Compared with placebo, night-time (23:00 to 07:00 hours) H+ ion concentration was reduced by 70, 79, 95, and 76% (p less than 0.05-p less than 0.01). Nocturnal acid secretion, too, was significantly lower for the H2 blockers than for placebo (p less than 0.05-p less than 0.01). A significant reduction in night-time gastric volume secretion was observed in the hourly intervals from 04:00 to 07:00 hours and in total volume in the whole 6 hours period (p less than 0.05-p less than 0.01). Nizatidine 300 mg nocte, ranitidine and cimetidine significantly decreased H+ concentration for only 1 hour (08:00 to 09:00 hours, p less than 0.05-p less than 0.01) during the subsequent daytime period (08:00 to 13:00 hours). Since no significant pharmacodynamic differences between nizatidine 300 mg nocte, cimetidine 800 mg nocte and ranitidine 300 mg nocte were observed, it may be concluded that at the doses employed, these three H2-blockers will all be similarly effective in the acute therapy of peptic ulcer disease.     

Suppression of nocturnal acid secretion with famotidine accelerates gastric ulcer healing

Although nocturnal acid secretion has been emphasized in the pathophysiology and treatment of duodenal ulcer, its importance in gastric ulcer disease has been questioned. To explore this area, this multicenter U.S. trial compared the effect of a once-daily nighttime dose of H2-receptor antagonist with placebo on the healing of gastric ulcer and relief of associated symptoms. One hundred fifty-seven patients with endoscopically verified benign gastric ulcers were randomized in a double-blind fashion to either famotidine (40 mg at bedtime) or placebo. Antacid tablets were allowed as needed. The healing rates for famotidine were 45%, 66%, and 78% at weeks 4, 6, and 8, respectively. In comparison, placebo healing rates were 39%, 44%, and 64%. These differences were statistically significant in favor of famotidine at weeks 6 (p less than or equal to 0.01) and 8 (p less than or equal to 0.05), as well as in a life-table analysis (p less than or equal to 0.05). Nocturnal famotidine was also significantly better than placebo with respect to time to complete relief of pain and to the percentage of patients with complete relief of pain. No concomitant factor (including ulcer size, ulcer location, smoking history, or regular alcohol use) affected healing rates in this study. Famotidine was well-tolerated and no serious clinical or laboratory adverse effects were judged to be related to this dosing regimen of famotidine. In conclusion, suppression of nocturnal acid secretion with famotidine (40 mg at bedtime) was more effective than placebo in promoting the healing of acute benign gastric ulcer and its associated symptoms. The results of this study suggest that suppression of nocturnal acid secretion alone is as effective as "around the clock" acid suppression in the healing of benign gastric ulcer.     

睡前服用法替莫丁和奥美拉唑对十二指肠溃疡患者日间和夜间酸突破影响的对照研究

目的比较十二指肠溃疡患者晨服奥美拉唑,睡前加服法莫替丁和加服奥美拉唑后日间酸突破（DAB）和夜间酸突破（NAB）的情况.方法将20例十二指肠溃疡患者随机分成两组,日间服用奥美拉唑20 mg后,一组睡前加服奥美拉唑20 mg,一组睡前加服法莫替丁40 mg,疗程1周.治疗前后行夜间胃酸pH监测.结果治疗后奥美拉唑组夜间pH＜4的中位时间百分比减少62.4%,法莫替丁组减少83.95%,两组之间比较P＜0.05.奥美拉唑组NAB发生率为70%,法莫替丁组NAB发生率为30%,两组之间比较P＜0.001.两组日间pH＜4的中位时间百分比、DAB的发生率差异无显著性（P＞0.05）.结论睡前服用法莫替丁比睡前服用奥美拉唑对夜间胃酸分泌和酸突破的控制更为有效.     

Acid control with esomeprazole and lansoprazole: a comparative dose-response study

OBJECTIVE: To determine the level of acid control and the dose-response relationships achieved with esomeprazole and lansoprazole. These data are relevant in helping clinicians to decide on whether to increase a proton-pump inhibitor dose, or whether to switch to an alterative drug for increased acid control. MATERIAL AND METHODS: In an open-label, single-centre, randomized, six-way crossover study, 40 healthy subjects received esomeprazole 20, 40 and 80 mg, and lansoprazole 15, 30 and 60 mg once daily for 5 days. The mean time with intragastric pH >4 and mean 24-h median intragastric pH on day 5 were analyzed using a mixed-model ANOVA. Post-hoc analyses were completed for 0-12-h (daytime) and 12-24-h (night-time) post-dose intervals. RESULTS: Increasing the dose of esomeprazole from 20 mg to 40 mg resulted in significantly improved acid control over 0-12, 12-24 and 0-24 h post-dose (p<0.001), but no significant improvement in acid control for either period was seen when further increasing the dose to 80 mg. Increasing the dose of lansoprazole from 15 mg to 30 mg or from 30 mg to 60 mg significantly improved acid control over 0-12 and 0-24 h (p<0.01) but not over 12-24 h. With the exception of the esomeprazole 20 mg versus lansoprazole 30 mg comparisons, and the esomeprazole 20 mg versus lansoprazole 15 mg during 12-24 h post-dose comparison, esomeprazole provided significantly greater acid control than lansoprazole at each dose level over 0-12, 12-24 and 0-24 h (p<0.05). Mean 24-h median intragastric pH was higher following esomeprazole dosing compared with lansoprazole at each dose level. CONCLUSIONS: For low-, standard- and double-dose comparisons, esomeprazole achieved greater elevation of gastric pH and better acid control in more subjects than lansoprazole. Use of esomeprazole may therefore reduce the need for dose adaptations or drug switching.     

Persistent acid reflux and symptoms in patients with Barrett's oesophagus on proton-pump inhibitor therapy

OBJECTIVES: To assess both acid gastro-oesophageal reflux (GOR) suppression in patients with Barrett's oesophagus on proton-pump inhibitors (PPI) and the predictive value of symptoms.DESIGN A prospective study of patients with Barrett's epithelium (> 3 cm, containing specialized intestinal metaplasia).PATIENTS AND METHODS: Forty-five patients with Barrett's epithelium were recruited. Therapy was adjusted to omeprazole 20 mg twice daily. Oesophageal manometry and 24 h pH studies were performed on treatment. Heartburn score was calculated before and after PPI dose adjustment. In patients with persisting acid reflux, omeprazole dose was increased to 20 mg three times daily and pH studies repeated. Adequacy of GOR suppression, assessed by pH monitoring, was related to heartburn score (0-3). RESULTS: Twenty of the 45 patients were symptomatic (mean score 1.9) on pre-study treatment (mainly omeprazole < 20 mg once daily); on omeprazole 20 mg twice daily, only six patients remained symptomatic (mean score 1.6). Ten patients (22%) had persisting GOR on omeprazole 20 mg twice daily (median % total time with pH < 4 was 8%). Abnormal nocturnal reflux was found in nine and abnormal daytime reflux in only four patients. Heartburn persisted in three of these 10 patients (30%). Those remaining symptomatic had more daytime acid reflux than the asymptomatic patients with persistent reflux (median percentage daytime at pH < 4 was 13.6% vs 0.6%, respectively; P < 0.01). By increasing the omeprazole dose to 20 mg three times daily, only three of the 10 had persistent acid reflux. CONCLUSIONS: Persistent acid reflux on PPI therapy is common in patients with Barrett's oesophagus. Although nocturnal acid reflux is the most common finding, symptoms tended to occur in those with abnormal daytime reflux. Symptom resolution does not guarantee acid reflux control.     

Reduction of gastric acid secretion by 10 mg and 30 mg omeprazole once daily

The reduction in gastric acid secretion by 10 mg and 30 mg omeprazole was studied in 12 patients with ulcer disease in a randomized, double-blind, two-way balanced crossover study. A standardized pentagastrin test was performed before the study and 24 h after each treatment period of 6 days. Treatment was followed by a washout period of 7 days. Omeprazole, 30 mg/day, significantly reduced basal acid output (BAO) by 90% and pentagastrin-stimulated acid output (PAO) by 45% (p less than 0.01), whereas BAO and PAO were not significantly reduced by omeprazole, 10 mg/day.     

Analysis of the acidity index and integrated intragastric acidity in 645 patients presenting with gastroesophageal reflux disease symptoms

OBJECTIVE: In a recent study of patients receiving proton-pump inhibitor (PPI) therapy, a new parameter, the acidity index, was described as being less complicated to calculate and of comparable accuracy (r = 0.93) to integrated intragastric acidity (IA) in assessing intragastric pH control. The aim of this study was to correlate AI with IA using a large database of ambulatory 24-h pH-metry studies in untreated patients presenting with gastroesophageal reflux disease (GERD) symptoms. MATERIAL AND METHODS: We retrospectively analyzed 645 studies obtained from 1995 to 2001. Daytime (0800 h-2200 h), night-time (2200 h-0800 h) and 24-h IA and AI were calculated according to age, gender and the presence or absence of GERD, and correlations between these parameters were assessed using linear regression with F-statistic values, p-values and Akaike's Information Criterion values. GERD was defined as total esophageal pH time <4.0, 5 cm above the lower esophageal sphincter, for > or =4.2% of the day. IA and AI were calculated as follows: IA (mmol x h/l) = summation operator(acid in mmol/l at time "t" + acid in mmol/l at time "t - 1")/2 x ("t"-"t - 1"); AI = (%time pH < 4-%time pH < 3) x 1+(%time pH < 3-%time pH < 2) x 10+(%time pH < 2-%time pH < 1) x 100 + (%time pH < 1-%time pH < 0.8) x 1000. RESULTS: Overall, the mean 24-h IA value was 882.0+/-820.0 mmol x h/l (daytime 392.0+/-400.0, night-time 490.0+/-486.0). The mean 24-h AI value was 102.0+/-87.0 (daytime 86.0+/-80.0, night-time 120.0+/-114.0, p < 0.001). The mean 24-h IA value was 1057.0+/-829.4 mmol x h/l (daytime 459.8+/-406.0, night-time 597.2+/-500.4, p < 0.001) in GERD patients and 713.0+/-775.0 mmol x h/l (daytime 326.0+/-383.0, night-time 387.0+/-448.5) in non-GERD patients (p < 0.001). The mean 24-h AI value was 122.1+/-88.1 (daytime 101.4+/-82.5, night-time 145.3+/-120.7) in GERD patients and 83.0+/-81.0 (daytime 71.0+/-73.9, night-time 96.4+/-102.6) in non-GERD patients (p < 0.001). Our statistical modeling demonstrated that the correlation between the acidity index and IA becomes progressively poorer with increasing values of acidity. CONCLUSIONS: We conclude that gastric acid production assessed by both IA and AI is higher during evening hours in comparison with daytime hours and the difference between night-time and daytime values is statistically significant. In addition, gastric acid production assessed by both IA and AI is significantly higher in GERD patients than non-GERD patients. This difference is primarily due to differences in nocturnal acid production. The AI correlates poorly with measured IA, especially at higher levels of gastric acidity. Therefore, AI is not an acceptable surrogate for IA in assessing gastric acid production.