兰索拉唑治疗十二指肠球部溃疡胃内24小时PH监测

为了观察兰索拉唑对胃酸分泌作用的影响，对６２例十二指肠溃疡（ＤＵ）患者，分别给予兰索拉唑和空白对照，监测服药后胃内２４小时（８ａｍ～８ａｍ时间窗）ｐＨ变化。结果显示：３０例患者服药后２４小时ｐＨ指标明显升高，较空白组相比差异有非常显著性（Ｐ＜０．０１）。兰索拉唑组服用后，ＰＨ＞４的总时间和平均ｐＨ、中位ｐＨ均明显高于对照组（Ｐ＜０．０１）。ｐＨ密度分布曲线显示：兰索拉唑组呈明显右倾单峰（ｐＨ６～８），在白天的抑酸作用较夜间强。     

Total 24-hour gastric acid secretion in patients with duodenal ulcer. Comparison with normal subjects and effects of cimetidine and parietal cell vagotomy

The purposes of these studies were as follows: (a) to compare gastric acid secretion throughout an entire 24-h period in 8 patients with duodenal ulcer disease and in 7 normal subjects, and (b) to determine in duodenal ulcer patients to what extent total, 24-h acid secretion was reduced by oral cimetidine (n = 7) or parietal cell vagotomy (n = 7). Basal, interprandial, and nocturnal acid secretion were measured by gastric aspiration, whereas acid secretion in response to breakfast, lunch, and dinner was measured by in vivo intragastric titration. Total, 24-h acid secretion averaged 408.3 +/- 61.7 mmol in duodenal ulcer patients and 208.3 +/- 18.5 mmol in normal subjects (p less than 0.02). Acid secretion was higher in duodenal ulcer patients than in normal subjects during both day (p less than 0.01) and night (p less than 0.05). Cimetidine (400 mg twice daily) significantly (p less than 0.001) reduced total, 24-h acid secretion in duodenal ulcer patients to 235.3 +/- 58.6 mmol, a rate that was not significantly different from 24-h acid secretion in normal subjects. On the other hand, total, 24-h acid secretion averaged only 86.7 +/- 20.7 mmol after parietal cell vagotomy, a rate that was significantly lower than 24-h acid secretion in normal subjects (p less than 0.001) and in duodenal ulcer patients receiving cimetidine (p less than 0.05). These studies indicate that patients with duodenal ulcer disease secrete excessive amounts of gastric acid during the day and night and throughout an entire 24-h period. A twice-daily 400-mg dose of cimetidine reduces 24-h acid secretion in duodenal ulcer patients to nearly normal rates, whereas parietal cell vagotomy reduces acid secretion to well below normal rates.     

Intravenous omeprazole: effect on 24-hour intragastric pH in duodenal ulcer patients

This study was aimed to identify an intravenous dosage regime of omeprazole which would sufficiently suppress acid secretion to maintain intragastric pH greater than 4 continuously. Thirteen duodenal ulcer patients in remission received omeprazole in daily intravenous doses ranging from 40 to 200 mg. Doses were successively increased as dictated by patient response. The intragastric pH data indicated that omeprazole given in twice or thrice daily regimes in total intravenous amounts of 200, 160 and 160 mg over a consecutive 3-day period markedly inhibited acid secretion and maintained intragastric pH greater than 4 with few and short-term exceptions.     

Cytotoxin and urease activities of Helicobacter pylori isolates from Japanese patients with atrophic gastritis or duodenal ulcer

The vacuolating cytotoxin and urease secreted by Helicobacter pylori are thought to be virulent factors. Because vacuolation is potentiated by the presence of ammonium ion, which is produced by urease in vitro, it is of interest to examine whether cytotoxin and urease work reciprocally in the development of atrophic gastritis or duodenal ulcer. In the present study, patients (all H. pyloripositive) were divided into four groups: mild atrophic gastritis (group 1; nine patients), severe atrophic gastritis (group 2; 36 patients), duodenal ulcer with mild atrophic gastritis (group 3; 19 patients) and duodenal ulcer with severe atrophic gastritis (group 4; 12 patients). Cytotoxin production and urease activity of H. pylori isolated from these patients were analysed. Cytotoxin production was observed in four of nine (44.4%), 28 of 36 (77.8%), 11 of 19 (57.9%) and eight of 12 (66.7%) isolates from groups 1, 2, 3 and 4, respectively. Cytotoxin-producing H. pylori isolates were found significantly more in patients with severe atrophy than in patients with mild atrophy (P= 0.048). The mean of relative activity of cytotoxin in H. pylori isolate was 1. 6. ± 2. 3, 7. 9. ± 7. 4, 5. 8. ± 6. 0 and 9. 0 ± 9. 1 in groups 1, 2, 3 and 4, respectively. Helicobacter pylori isolates from severe atrophy or duodenal ulcer patients in groups 2 or 4 possessed significantly higher activity than those from non-ulcer patients in group 1 (P= 0.017 and 0.030, respectively). The mean of urease activity was 8. 6 ± 4. 6, 10. 0 ± 5. 9, 10. 0 ± 8. 5 and 11. 2 ± 7. 7 IU/mg in groups 1, 2, 3 and 4, respectively. These differences indicated no statistical significance. In each H. pylori isolate, the production of cytotoxin and urease were independent, which indicated that there was no reciprocal effect between them in vivo. Thus, cytotoxin-producing H. pylori isolates were more prevalent in patients with severe atrophic gastritis and the cytotoxin activities of H. pylori isolates from the patients with severe atrophic gastritis or duodenal ulcer were much higher than those from the patients with mild atrophic gastritis, which suggested that vacuolating cytotoxin may be a disease-inducing factor.     

Chronic gastritis and gastroduodenal ulcer: a case control study on risk of coexisting duodenal or gastric ulcer in patients with gastritis.

Chronic (atrophic) gastritis (AG) is common in active duodenal (DU) and gastric ulcer (GU) disease. In this case control study in consecutive prospective outpatients (571 cases and 1074 controls) who had undergone diagnostic upper gastrointestinal endoscopy and routine biopsies from both antral and body mucosa, we calculated the risk of coexisting active DU and/or GU in different gastritis of the antrum or body and according to grade (superficial gastritis, mild, moderate or severe atrophic gastritis). The risk of coexisting active gastroduodenal ulcer (ulcer in duodenum and/or stomach), as well as the risk of DU or GU, was dependent upon the presence and grade of gastritis in antrum and body mucosa. The risk of coexisting ulcer, as expressed as an age adjusted relative risk (RR) and calculated as odds ratio of gastritis in cases and controls, was significantly increased in the presence of superficial antral and body gastritis (RR = 8.5 (7.0-20.0) in men; RR = 5.8 (3.3-10.2) in women), as compared with the risk of ulcer in subjects with histologically normal mucosa (RR = 1). The risk of ulcer, and the risk of GU in particular, increased further with increasing severity of antral gastritis. In such patients with moderate or severe atrophic antral gastritis the RR of coexisting ulcer even exceeded 20 in men and 10 in women (RR = 25.6 (9.0-72.7) in men; RR = 11.7 (5.9-23.0) in women). On the other hand, the RR of ulcer, and the RR of DU in particular, was below 1 in the presence of atrophic gastritis in the gastric body, irrespective of the grade of gastritis in the antrum. We conclude that the type and grade of gastritis strongly predicts the risk of coexisting peptic ulcer, and that the risk of coexisting DU or GU increases with an increase in grade of AG of the antrum but decreases with an increase in grade of AG of the gastric body.     

24-hour study of intragastric acidity in duodenal ulcer patients and normal subjects using continuous intraluminal pH-metry

The circadian pattern of intragastric acidity was assessed in 19 healthy subjects and 37 patients with active, endoscopically proven duodenal ulcer using 24-hr continuous intraluminal pH-metry. The median pH 24-hr profiles showed that ulcer patients had lower postprandial pH elevations and a smaller decline in acidity during the early morning hours when compared with controls. The after-lunch and -dinner area under the curve and maximum pH values were significantly higher in controls compared to ulcer patients. In the nighttime, the median pH values in controls were significantly higher during 9 pm to 12 pm (P=0.02), 12 pm to 4 am P=0.01), and 4 am to 8 am (P=0.0008) compared to the ulcer patients. We conclude that the 24-hr acidity is higher in ulcer patients compared to healthy subjects and that the differences are particularly evident in the postprandial and nocturnal periods.This work was supported in part by grant 86.02120.03 from CNR.     

24-hour study of gastric acidity in normal subjects and in cholecystectomized patients using continuous pH monitoring

The circadian pattern of gastric acidity was assessed in 53 normal subjects and in 33 patients with prior cholecystectomy using continuous pH monitoring. The 24-hour and nocturnal median pH values were significantly higher in cholecystectomized patients than in controls (p less than 0.03 and p less than 0.001, respectively). In the operated group there were higher median pHs also in the after-dinner (p less than 0.003) and after-lunch (p less than 0.01) periods, while no difference between the two populations was observed after breakfast. The percentage of 24-hour pH readings above 4.0 units was markedly higher (p approximately 0) in postcholecystectomy patients. We conclude that circadian gastric acidity is reduced in cholecystectomized patients with respect to healthy subjects, both in nocturnal and postprandial states. Episodes of duodenogastric reflux may be responsible for this, but impaired acid production related to advanced age (14 patients were more than 60 years old) or to fundic chronic atrophic gastritis (5 cases) may also account for the elevation of pH values in our postcholecystectomy patients.     

Somatostatin in gastric juice in normal subjects and patients with duodenal ulcer

Somatostatin in gastric juice was determined in normal subjects and patients with duodenal ulcer. Gel exclusion chromatography of gastric juice revealed that the main immunoreactivity existed at the position of somatostatin-14. A large amount of somatostatin was present in gastric juice, and the quantity increased following tetragastrin stimulation. Furthermore, there was a good inverse correlation between somatostatin concentration and acidity of gastric juice; however, there was no difference between normal subjects and patients with duodenal ulcer in the amount of somatostatin released into gastric juice.     

24-hour intragastric acidity and plasma gastrin after omeprazole treatment and after proximal gastric vagotomy in duodenal ulcer patients

The relationship between suppressed gastric acidity and the increase in plasma gastrin levels after pharmacological and surgical treatment of peptic ulcer disease were compared in this study. Eight patients with chronic duodenal ulcer and referred for proximal gastric vagotomy were studied. 24-hour intragastric acidity and plasma gastrin levels were investigated in the same patients on three consecutive occasions: preentry without any treatment; after 4 weeks of administration of 20 mg of omeprazole daily, and 4-6 months after proximal gastric vagotomy. Intragastric acidity was slightly more reduced by omeprazole (94%) than after proximal gastric vagotomy (78%), with no difference found during the day or night with either. Plasma gastrin levels increased slightly more after proximal gastric vagotomy [284% (median, 2120 pmol.h/L; range, 733-2831 pmol.h/L)] than after omeprazole administration [186% (median, 1586 pmol.h/L; range, 495-2573 pmol.h/L)]. There is strong evidence that the increased plasma gastrin concentration following omeprazole treatment is caused by the reduced intragastric acidity. The slight increase in plasma gastrin concentration following proximal gastric vagotomy despite a lesser reduction in intragastric acidity may be the result of additional effects on gastrin release by the vagotomy. Both treatments resulted in a modest increase in plasma levels of gastrin that were far below the gastrin levels observed in achlorhydric patients, e.g., patients with pernicious anemia.     

Campylobacter pyloric, chronic gastritis, gastric ulcer and duodenal ulcer

After the initial report of Marshall and Warren, several publications have also demonstrated the presence of pyloric campylobacter in an elevated percentage of cases of chronic gastritis and peptic ulcer. We present our experience studying 672 patients examined by esophagogastroduodenoscopy after referral to clinical because of upper gastrointestinal symptoms. We used an Olympus GIF-K2 panendoscope taking two biopsies from the gastric antrum. Specimens were stained with hematoxilin-eosin and silver. In our experience these methods have given us the best results in detecting this bacteria. Diagnosis of gastric and duodenal ulcer was made by endoscopic criteria and chronic gastritis diagnosed by histology. Chronic gastritis was categorized into active and inactive based in the invasion of polymorphonuclear into mucosa. We have also quantitated damage of the mucin producing cells as well as the degree of bacterial colonization. We have found pyloric campylobacter in 91.8% of patients suffering from chronic active gastritis, 72.7% of patients with diagnosis of gastric ulcer and 84.2% of cases of duodenal ulcer. Our results agree with the ones reported by other authors. We conclude that pyloric campylobacter is not an opportunist microorganism within the stomach because it produces inflammatory changes as well as damage of the mucin producing cells. Its presence may play some role in the etiology of gastritis and peptic ulcer disease.     

Inhibition of pentagastrin-stimulated gastric secretion by duodenal acidification or administration of fat in normal subjects and in patients with duodenal ulcer

The inhibitory effect of duodenal acidification and intraduodenal fat infusion on pentagastrin-stimulated gastric secretion in normal subjects and in patients with duodenal ulcer was studied. Intraduodenal infusion of acid resulted in inhibition of HCl secretion found to be significant only in ulcer patients. Pepsin output, although lower during the first 15 minutes of duodenal acidification, later increased. Intraduodenal infusion of olive oil resulted in significant inhibition of HCl and pepsin output in both groups of patients, which was maximal 45–60 minutes after the beginning of fat infusion. Gastric secretion was more readily inhibited in ulcer patients than in normal subjects; this difference was particularly evident in inhibition of pepsin secretion. In addition, decrease in concentration of HCl and pepsin was observed to be significant only in ulcer patients. Mechanisms by which duodenal acidification and fat inhibit gastric secretion are discussed. The results obtained suggest that secretin, which is probably responsible for inhibition after duodenal acidification, is not the inhibitor during inhibition by fat. The ulcer patients were found to have unimpaired mechanisms of inhibition by acid and fat.     

Influence of cure of Helicobacter pylori infection on gastric acidity and gastroesophageal reflux: study by 24-h pH monitoring in patients with gastric or duodenal ulcer

Background Whether or not the eradication of Helicobacter pylori is a risk factor for reflux esophagitis (RE) is a question at issue. To find an answer, it is necessary to clarify the influence of H. pylori eradication on the mechanism of RE.Methods The authors investigated the influence of H. pylori eradication on gastric acidity and gastroesophageal reflux in ten gastric ulcer (GU) patients and ten duodenal ulcer (DU) patients by 24-h simultaneous determination of pH in the stomach and esophagus.Results Though the results indicated enhanced gastric acidity in GU patients at night after H. pylori eradication, no such influence was observed in DU patients. No significant changes in gastroesophageal reflux occurred in GU or DU patients before and after H. pylori eradication. RE after H. pylori eradication occurred in only one patient, with GU. This patient had several risk factors for RE, such as obesity, male sex, and dietary habits to add to the increase in gastric acidity at night that occurred after H. pylori eradication. No increase in gastroesophageal reflux occurred in any DU patients or in the other GU patients that demonstrated enhanced gastric acidity at night after H. pylori eradication.Conclusions The cure of H. pylori infection does not, by itself, cause RE in patients who have few other risk factors for RE.     

Comparison of coffee intake and coffee-induced symptoms in patients with duodenal ulcer, nonulcer dyspepsia, and normal controls

Coffee and decaffeinated coffee stimulate acid secretion. In addition, many patients experience dyspepsia after coffee ingestion. Therefore, coffee is often prohibited by physicians in patients with peptic diseases. However, the association between peptic disease and symptoms remains unclear. This study compares coffee intake and the induction of symptoms by coffee in patients with duodenal ulcer disease, nonulcer dyspepsia, and normal controls. We have studied the coffee drinking habits of 58 duodenal ulcer patients, 55 nonulcer dyspepsia patients, and 55 normal controls. The use of coffee on a daily basis was not significantly different between duodenal ulcer patients (64%) and controls (56%), or between nonulcer dyspepsia patients (55%) and controls. There was also no difference between the three groups in the use of decaffeinated coffee, the number of cups per day, the method of preparation, the length of time of coffee use, or any change in coffee intake in the previous year. The intake of tea, caffeinated carbonated beverages, and aspirin or nonsteroidal anti-inflammatory drugs was also similar in the three groups. The duodenal ulcer patients were more likely to be cigarette smokers (45%) than either the controls (16%) or the nonulcer dyspepsia patients (24%). Daily alcohol intake was not significantly different in the three groups. The prevalence of coffee induction of dyspeptic symptoms was similar in duodenal ulcer patients (29%) and controls (22%), but was much more common in nonulcer dyspepsia patients (53%) than in controls (22%), p = 0.0036. In conclusion, there was no difference in coffee intake between patients with duodenal ulcer, nonulcer dyspepsia, or normal controls. However, patients with nonulcer dyspepsia, but not duodenal ulcer, were more likely to experience dyspeptic symptoms after coffee ingestion.