Alkaline intra-oesophageal pH and gastro-oesophageal reflux in patients with peptic oesophagitis

Simultaneous 22-h measurements of intra-oesophageal and intragastric pH were made in 22 patients with symptoms of gastro-oesophageal reflux (7 with peptic oesophagitis, 8 with peptic oesophageal stricture, and 7 with peptic oesophagitis and previous partial gastrectomy) to determine whether alkaline intra-oesophageal pH is a consequence of alkaline gastro-oesophageal reflux. In the three groups of patients intra-oesophageal pH was greater than 7 for 16.9 +/- 4.8%, 27.5 +/- 7.6%, and 21.0 +/- 7.7%, respectively, of total recording time (p = NS). Intragastric pH greater than 7 was recorded only in the patients with partial gastrectomy (10.3 +/- 5.3% of recording time; p less than 0.01 in comparison with the other groups). Elevations of intra-oesophageal pH to greater than 7 never occurred during episodes of alkalinization of intragastric pH. These results suggest that refluxed fluids are unlikely to be the cause of alkaline intra-oesophageal pH in patients with peptic oesophagitis.     

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。     

The diagnosis and treatment of peptic oesophagitis

An account is given of the treatment of peptic oesophagitis, in which the importance of repairing a hernia which is producing peptic ulceration is emphasized. Mobilization of the oesophagus muct be carried out as far up as is necessary for the hernia to reduce without tension.

When there is a firm stricture which will not respond to treatment, associated with shortening of the oesophagus, resection and interposing a loop of jejunum is the operation of choice which in this series has been performed without mortality.

     

奥美拉唑镁肠溶片与奥美拉唑胶囊治疗消化性溃疡的临床随机对照研究

目的　验证奥美拉唑镁肠溶片与奥美拉唑胶囊治疗消化性溃疡的生物等效性及评价其不良反应。方法　采用随机对照和开放试验的方法治疗经胃镜检查证实的消化性溃疡共 171例 ,其中奥美拉唑镁肠溶片组 (试验组 ) 68例 ,胃溃疡 2 1例 ,十二指肠溃疡 47例 ;奥美拉唑胶囊组 (对照组 ) 67例 ,其中胃溃疡 2 1例 ,十二指肠溃疡 46例 ;开放试验组 3 6例 ,其中十二指肠溃疡 2 9例 ,胃溃疡 7例。结果　试验组中胃溃疡的愈合率和总有效率分别为 80 9%和 10 0 %十二指肠溃疡的愈合率和总有效率分别为87 2 %和 97 8% ;对照组中胃溃疡的愈合率和总有效率为 85 7%和 95 2 % ,十二指肠溃疡的愈合率和总有效率为 84 7%和 97 8% ;开放试验组中胃溃疡的愈合率和总有效率均为 10 0 0 %十二指肠溃疡的愈合率和总有效率分别为 86 2 %和 10 0 % ;试验组中疼痛消失率及其他消化道症状的消失率在胃溃疡为 95 2 %和 89 0 %在十二指肠溃疡则为 97 8%和 98 3 % ;对照组中疼痛及其他消化道症状的消失率在胃溃疡为 95 2 %和 92 7% ,在十二指肠溃疡为 97 8%和 98 7%。两组在愈合率、总有效率、疼痛消失率和其他消化道症状消失率方面相比均无显著差别 (P >O 0 5 )。两组在治疗过程中均未见明显的不良反应。结论　奥美拉唑镁肠溶片与奥     

Characterization of the inflammatory infiltrate in peptic oesophagitis

BACKGROUND: The diagnosis of oesophagitis is mainly based on histology, but interpretation of endoscopic biopsies is often difficult. We performed immunohistochemical studies on oesophageal biopsies to see if better characterization of the inflammatory cell infiltrate would improve the accuracy of the histologic diagnosis of gastro-oesophageal reflux disease. METHODS: The study groups consisted of 40 consecutive children (mean age +/- SD: 79.6 +/- 5l.9 months; 20 boys) with gastro-oesophageal reflux disease and 7 symptomatic children (mean age +/- SD: 52.6 +/- 37.0 months; 3 boys) without gastro-oesophageal reflux disease. All patients underwent upper gastrointestinal endoscopy with oesophageal biopsies. The diagnosis of gastro-oesophageal reflux disease was established by conventional endoscopic and histologic criteria. In each mucosal biopsy specimen, the number of intraepithelial CD3+, CD25+ (IL2 receptor+), ICAM+, HLA-DR+ and mucosal mast cells were determined. RESULTS: Conventional histology was in close agreement with endoscopic findings (p<0.001) and reflected the clinical score even more than endoscopic findings. Conventional histology significantly correlated with each inflammatory immunohistochemical marker (<0.05 for each), but the markers were not predictive of symptom severity. Immunohistochemical markers were always abnormal in the gastro-oesophageal reflux disease patients, even in the mildest cases of oesophagitis. CONCLUSIONS: Although there is a good correlation between symptoms and histology, in a subset of patients, immunohistochemical studies appear useful in supporting the histological diagnosis of gastro-oesophageal reflux disease.     

Treatment of childhood peptic oesophagitis with famotidine or alginate-antacid

Both antacids and H2 receptor antagonists have a potential role in treating peptic oesophagitis associated with acid reflux. The aim of this study is to assess the efficacy and tolerability of famotidine and alginate-antacid in children with endoscopically documented peptic oesophagitis. We compared clinical, endoscopic and histological response to alginate-antacid (1 tablet to be chewed 30 min after each meal and at bed time) or famotidine (1 mg/kg before supper at 7 pm) in 49 children (mean age 9 years, 34 males). Twenty-four of them were randomly allocated to alginate-antacid treatment (group A), twenty-five to famotidine (group B). Both treatments were protracted for six months and endoscopy was then repeated. Symptoms disappeared in 43.4% and improved in 47.8% of children of group A and disappeared in 91.6% of those of group B (p less than .05). Mean time for symptom disappearance was 17 weeks for group A and 5 weeks for group B (p less than .01). After six months, at endoscopy oesophagitis was healed in 43.4% in group A and in 41.6% of group B, the difference between the two groups was not significant, however the improvement of endoscopic grades induced by famotidine was significantly better (p less than .05). Histology showed a healed peptic oesophagitis in 52.2% of the children in group A and in 70.8% of group B (p less than .001). No toxicity was observed with either treatment. We conclude that famotidine is superior to alginate-antacid in treating peptic oesophagitis associated with acid reflux, since it induces a better symptomatic response and a greater improvement of endoscopic lesions.     

Relation between oesophageal acid exposure and healing of oesophagitis with omeprazole in patients with severe reflux oesophagitis.

BACKGROUND/AIMS--Reducing oesophageal acid exposure by suppressing acid secretion with omeprazole is highly effective in healing reflux oesophagitis. Some patients with severe oesophagitis, fail to heal and whether this results from inadequate acid suppression or other factors is unclear. The aim of this study, was to investigate the relation between oesophageal acid exposure and healing in patients with severe reflux oesophagitis treated with omeprazole. METHODS--Sixty one patients with grade 3 or 4 ulcerative oesophagitis were treated for eight weeks with omeprazole 20 mg every morning. Those patients unhealed at eight weeks were treated with 40 mg every morning for a further eight weeks. Endoscopy and 24 hour oesophageal pH monitoring were performed before treatment and at the end of each treatment phase while receiving treatment. RESULTS--Thirty per cent of patients failed to heal with the 20 mg dose. Unhealed patients had greater total 24 hour oesophageal acid exposure before treatment, and while receiving treatment also had greater acid exposure and a smaller reduction in acid exposure than did patients who healed. Forty seven per cent of the unhealed patients also failed to heal with the 40 mg dose. These patients had similar levels of acid exposure before treatment to those who healed, but had greater acid exposure while receiving treatment, particularly at night when supine. CONCLUSIONS--Patients with severe ulcerative oesophagitis who are refractory to omeprazole have greater oesophageal acid exposure while receiving treatment than responding patients. This is due to a reduced responsiveness to acid suppression, and is likely to be an important factor underlying the failure of the oesophagitis to heal.     

Nosocomial pneumonia and the role of gastric pH. A meta-analysis.

PURPOSE: To examine the differential effect of drugs used for stress ulcer prophylaxis on nosocomial pneumonia in critically ill patients. DATA IDENTIFICATION: Computerized bibliographic search of published and unpublished research. STUDY SELECTION: Independent review of 48 randomized controlled trials of prophylaxis identified eight relevant studies. DATA ABSTRACTION: The population, intervention, and outcomes were evaluated by duplicate independent review. RESULTS: The incidence of pneumonia was lower in critically ill patients receiving antacids and/or histamine-2-receptor antagonists as compared with patients receiving no stress ulcer prophylaxis (common odds ratio 0.42, 95 percent CI 0.17 to 1.11). When stress ulcer prophylactic therapy was titrated to achieve a gastric pH of 3.5 or greater, there was a trend favoring a decreased incidence of pneumonia (0.66, 95 percent CI 0.24 to 1.78). In trials comparing sucralfate with pH-altering drugs, the common odds ratio of 0.55 (0.28 to 1.06) suggests a 45 percent risk reduction with the use of sucralfate. CONCLUSION: Stress ulcer prophylaxis with drugs which raise gastric pH does not increase the incidence of pneumonia in comparison to placebo or control therapy. The use of sucralfate is associated with a lower incidence of nosocomial pneumonia in comparison to agents which raise gastric pH. However, methodologic deficiencies, small sample sizes, and the failure to examine the effects of antacids and histamine-2-receptor antagonists separately make a large prospective randomized trial necessary to confirm or refute these findings.     

The effects of omeprazole on intragastric pH, intestinal motility, and gastric emptying rate.

BACKGROUND: The present study was designed to investigate whether omeprazole changes the characteristics and thereby the functions ascribed to fasting intestinal motility, postprandial motility, postprandial pH, and gastric emptying. METHODS: Ten healthy subjects were investigated. The studies were performed after 10 days of treatment with 40 mg omeprazole daily/placebo. Duodenal pressures and intragastric pH were detected by strain-gauge transducers and a pH electrode attached to a miniature computer. The meal consisted of an omelette labelled with 99mTc-sulphur colloids followed by 150 ml water labelled with 111In-diethylenetriamine pentaacetic acid. RESULTS: The difference in fasting intragastric pH between the two series was highly significant. The profile from the placebo series showed a relationship between phase activity and pH. The pH increased from phase I (median, 1.3; 95% confidence interval (CI), 0.9-1.6) to a maximum at 25% (1.8 (0.9-2.1)) and 50% (1.6 (1.1-3.8)) of cycle duration and decreased thereafter until the end of the cycle. The profile from the omeprazole series showed significantly higher values during the entire cycle but no relationship between phase activity and pH. Pretreatment with omeprazole was followed by a delay in gastric emptying of liquid at 30 min (64% (49%-66%) (omeprazole series) versus 78% (67%-83%); P < 0.01) and solid at 180 min (71% (48%-86%) (omeprazole series) versus 96% (87%-100%); P < 0.01). There was no significant difference in duration of postprandial motility (305 min (157-350 min) (omeprazole) versus 259 min (129-403 min)). CONCLUSIONS: Omeprazole eliminates the temporal relationship between intragastric pH and characteristics of the migrating motor complex and induces a delay in gastric emptying of both liquid and solid. A non-significant increase in duration of postprandial motility may represent a type-II error.     

Selection of patients for successful maintenance treatment of esophagitis with low-dose omeprazole: use of 24-hour gastric pH monitoring

OBJECTIVE: Treating patients with erosive esophagitis and maintaining remission in a cost-effective fashion is a desirable goal in clinical practice. There are no established criteria to identify patients with healed esophagitis who will subsequently remain in remission with low-dose omeprazole therapy. We investigated whether 24-h esophageal-gastric pH monitoring could provide criteria to select patients for low-dose omeprazole maintenance therapy. METHODS: Seventy consecutive symptomatic outpatients with grade 2-3 reflux esophagitis were prospectively investigated. They were treated with 20 mg/day omeprazole for 2 months. Those with healed esophagitis were given alternate-evening 20-mg omeprazole maintenance therapy for 6 months. Clinical evaluation, endoscopy, and 24-h esophageal-gastric pH were done at the end of each treatment period. Results of pH studies of patients in remission were compared with those with endoscopically documented relapse of esophagitis. RESULTS: In 63/70 patient (intention-to-treat, 90%; 95% confidence interval [CI], 83-97%) esophagitis was healed at 2 months. During the 6-month maintenance period esophagitis remain healed in 28 (G1) (40%; 95% CI, 29-52%), but recurred in 32 patients (G2). During healing with omeprazole 20 mg/day the 24-h gastric pH was below 4 for <10% of the time in 96% of the patients, who subsequently remained in long-term remission with low-dose maintenance therapy (G1), but not in any patient with recurrence of esophagitis (G2). The 10% threshold value has a specificity of 1.00 and sensitivity of 0.96. CONCLUSIONS: The 24-h intragastric pH monitoring during 20 mg/day omeprazole therapy provides criteria by which to preselect patients with reflux esophagitis who will remain in remission with low-dose omeprazole therapy.     

A comparison of oral omeprazole and intravenous cimetidine in reducing complications of duodenal peptic ulcer

Background  

Gastrointestinal bleeding is a common problem and its most common etiology is peptic ulcer disease. Ulcer rebleeding is considered a perilous complication for patients. To reduce the rate of rebleeding and to fasten the improvement of patients' general conditions, most emergency departments in Iran use H2-blockers before endoscopic procedures (i.e. intravenous omeprazole is not available in Iran). The aim of this study was to compare therapeutic effects of oral omeprazole and intravenous cimetidine on reducing rebleeding rates, duration of hospitalization, and the need for blood transfusion in duodenal ulcer patients.     

Conventional dose of omeprazole alters gastric flora

Quantitative cultures were carried out on samples from gastric juice obtained from 12 ambulatory patients with esophagitis before and one month after omeprazole therapy. An increase in the number of patients in whom gastric juice was culture-positive, as well as an increment in the bacterial counts were noted. The spectrum of microorganisms isolated from gastric juice was identical to the normal flora of the oral cavity, mainly -hemolytic streptococci, corynebacteria, andCandida species. Thus, the counts of organisms within gastric contents are simply a reflection of swallowed oral, microflora that were able to survive due to the less acidic environment.     

Healing and relapse of severe peptic esophagitis after treatment with omeprazole

We have studied the response of erosive or ulcerative esophagitis to treatment with omeprazole and its subsequent relapse on cessation of therapy in 196 patients. In the first phase of the study omeprazole (20 or 40 mg daily) was compared with placebo in 64 patients. After 4 wk there was endoscopic healing in 81% (25 of 31) of omeprazole-treated patients and in only 6% (2 of 32) of placebo-treated patients. Endoscopic healing of esophagitis was accompanied by symptom relief and histologic healing of ulceration. In the second (dose finding) phase a further 132 patients were randomized to omeprazole (20 or 40 mg daily) and endoscopic healing was assessed. In patients with the mildest grade of ulcerative esophagitis (grade 2), healing occurred at 4 wk in 87% receiving 20 mg and in 97% receiving 40 mg. In patients with grade 3 esophagitis, 67% (20 mg) and 88% (40 mg) were healed. Less than half the patients with grade 4 esophagitis (Barrett's ulcers or confluent ulceration) healed with either 20 mg (48%) or 40 mg (44%). Regression analysis in the 164 omeprazole-treated patients showed no evidence that healing was influenced by factors other than severity of esophagitis at entry and omeprazole dose. In phase 3 of the study the rate of endoscopic relapse was determined in 107 endoscopically healed patients after stopping omeprazole. Erosive or ulcerative esophagitis recurred in 88 of 107 (82%) by 6 mo. Neither initial dose, grade of esophagitis, nor smoking was shown to influence relapse rate. Omeprazole is a highly effective treatment for peptic esophagitis. The 40-mg/day dosage produces endoscopic healing slightly more quickly than the 20-mg/day dosage, and the initial endoscopic gradings are of prognostic value. Relapse occurs rapidly when treatment is stopped.