Antacid maintenance therapy in the prevention of duodenal ulcer relapse.

The effectiveness of antacid maintenance therapy in preventing duodenal ulcer (DU) relapse was investigated. Two hundred and fifty one asymptomatic patients with healed DU were stratified into smokers and non-smokers and randomised to receive for one year either placebo, or Maalox TC three tablets (81 mmol) at bedtime (hs), or Maalox TC three tablets in the morning plus three tablets at bedtime (bd) (162 mmol), or cimetidine 400 mg at bedtime. A double dummy technique was used to render the study double blind. In 176 patients evaluable for efficacy, the cumulative relapse at one year was: placebo 57%; Maalox TC hs 39%; Maalox TC bd 23%; cimetidine 25%. Maalox TC bd and cimetidine were equally effective and superior to placebo (p less than 0.01) and bedtime Maalox TC (p less than 0.04). The benefit of treatment was significant for the overall sample and for the subgroup of smokers. The results for the non-smokers also supported efficacy for these two treatments but, perhaps because of small sample sizes, these comparisons were not significant. All 251 patients were assessed for safety. Approximately half the patients in each treatment group had adverse events, leading to withdrawal in three, seven, 12, and four patients on placebo, Maalox hs, Maalox bd, and cimetidine respectively. Diarrhoea occurred in 12 patients in Maalox TC bd and eight in each other group. Serum magnesium concentrations were unchanged; aluminium concentrations were higher than baseline at six and 12 months in both antacid groups and at 12 months in the cimetidine group but the differences were not significant. Maalox TC three tablets bd are as effective as cimetidine 400 mg at bedtime in reducing DU relapse and both are superior to placebo.     

Histamine and duodenal ulcer: effect of omeprazole on gastric histamine in patients with duodenal ulcer.

Gastric mucosal concentrations of histamine and of its metabolic enzyme, histamine methyltransferase activity, were measured in patients with duodenal ulcer disease and patients with an apparently normal stomach and duodenum. Patients with duodenal ulcer had significantly less (p less than 0.05) mucosal histamine (median 204 nmol/g) than control subjects (median 252 nmol/g). There was no significant difference between the two groups in their histamine methyltransferase activity values. Omeprazole therapy did not significantly change mucosal histamine (+23%), histamine methyltransferase activity (+5%), histamine release before (+5%) or during (+7%) pentagastrin infusion. It significantly decreased acid secretion during pentagastrin stimulation (median -73%, p less than 0.001). Omeprazole, like cimetidine, does not stop histamine release during pentagastrin stimulation.     

A squamous metaplasia in a gastric ulcer scar of the antrum

An 81-year-old man presented with epigastric pain and weight loss for one month, He had a past history of pulmonary tuberculosis, 10 years ago, We performed a gastroscopy, which showed a linear depressed whitish gastric ulcer scar （0.8 cm in length） in the posterior wall of the prepyloric antrum, The result of biopsy was reported as squamous epithelium, Immunohistochemical staining using an antibody to high molecular weight cytokeratin （HMC） revealed positive staining in the squamous epithelium, Two years later, the lesion was followed up, The lesion remained at same site endoscopically, but no squamous epithelium could be seen microscopically,     

Effect of omeprazole and cimetidine on prepyloric gastric ulcer: double blind comparative trial.

We conducted a six week double blind randomised study of 176 patients with prepyloric gastric ulcer to determine whether the proton pump inhibitor, omeprazole 30 mg daily would accelerate healing and pain relief, as compared with cimetidine 1 g daily. At two, four, and six weeks after entry ulcers healed in a larger percentage of patients treated with omeprazole (54, 81, and 86%) than of those treated with cimetidine (39, 73, and 78%) ('intention to treat' cohort; p less than 0.05 at two weeks). A higher proportion of patients on omeprazole became free of pain during the first week of treatment (p less than 0.05). No major clinical or biochemical side effects were noted. Omeprazole is an efficient treatment for patients with prepyloric gastric ulcers.     

Randomised, double blind comparison of omeprazole and cimetidine in the treatment of symptomatic gastric ulcer.

In a randomised, double blind, parallel group study in patients with symptomatic gastric ulcer (94% greater than or equal to 5 mm diameter), 102 received omeprazole 20 mg om and 87 cimetidine 400 mg bd. After four weeks 73% and 58% (p less than 0.05) respectively had healed (eight weeks: 84% and 75%, ns). After four weeks, a greater proportion (81%) of omeprazole treated patients was symptom free than of those receiving cimetidine (60%; p less than 0.01). Over the first two weeks, patients receiving omeprazole had less day pain, less night pain and took fewer antacids than those receiving cimetidine (all p less than 0.05). The difference between omeprazole and cimetidine was not appreciably affected by age, smoking, size of the ulcer and trial centre. Tolerability was similar in the two treatment groups. In the treatment of symptomatic gastric ulcer, omeprazole relieves the symptoms more quickly than cimetidine and heals a greater proportion of ulcers within four weeks.     

Are twelve days of omeprazole, amoxicillin and clarithromycin better than six days for treating H. pylori infection in peptic ulcer and in non-ulcer dyspepsia?

BACKGROUND/AIMS: To evaluate whether omeprazole, amoxicillin and clarithromycin for 12 days is more effective for Helicobacter pylori eradication than the same regimen for only 6 days; and to verify whether these eradication regimens are more effective in peptic ulcer disease than in non-ulcer dyspepsia. METHODOLOGY: We studied 411 patients in whom a gastroscopy was carried out due to symptoms related to the upper gastrointestinal tract and who were diagnosed with duodenal ulcer (175 patients, 43%), gastric ulcer (42 patients, 10%), or non-ulcer dyspepsia (194 patients, 47%), and concomitant infection by H. pylori. At endoscopy, biopsies were obtained for rapid urease test, and a 13C-urea breath test was carried out. Urea breath test was repeated four weeks after completing eradication treatment with 1) omeprazole (20 mg b.i.d.), amoxicillin (1 g b.i.d.) and clarithromycin (500 mg b.i.d.) for six days (239 patients), or 2) the same regimen for 12 days (172 patients). RESULTS: H. pylori eradication was achieved in 73.6% (95% CI, 68-79%) of the patients treated during 6 days, and in 84.3% (79-90%) of those receiving 12 days of therapy (P < 0.01). The overall eradication rate with both regimens (6 plus 12 days), respectively in patients with duodenal ulcer, gastric ulcer and non-ulcer dyspepsia, was 84.6% (79-90%), 75.6% (61-86%), and 72.8% (67-79%) (P < 0.01 when comparing duodenal ulcer vs. non-ulcer dyspepsia). Twelve-day regimen was more effective than 6-day regimen only in non-ulcer dyspepsia (62% vs. 83%, P < 0.01), but not in duodenal or gastric ulcer. In the multivariate analysis the duration (6 vs. 12 days) of eradication therapy (odds ratio: 2.2; 1.3-3.7) and the type of disease (duodenal ulcer vs. non-ulcer dyspepsia; odds ratio: 2.3; 1.3-3.8) were the only variables which influenced on H. pylori eradication efficacy (chi 2 model, 17; P < 0.001). CONCLUSIONS: Efficacy with omeprazole-amoxicillin-clarithromycin regimen in patients with duodenal ulcer is higher than in those patients with non-ulcer dyspepsia. The increase of H. pylori eradication rate by 21% in our non-ulcer dyspepsia patients justifies the prolongation from 6 to 12 days of omeprazole-amoxicillin-clarithromycin therapy, whilst the increase of cure rates in duodenal or gastric ulcer patients with a 12-day therapy would not be cost-effective.     

Bronchoalveolar lavage is better than gastric lavage in the diagnosis of pulmonary tuberculosis

Bronchoalveolar lavage was performed in 62/63 patients with suspected pulmonary tuberculosis and gastric lavage in 60 of the 63. Mycobacteria could be cultured from 14 of the patients. Cultures on bronchoalveolar lavage were positive in 13 of them, while gastric lavage was positive in only 7. Our conclusion is that bronchoalveolar lavage should be performed instead of gastric lavage when pulmonary tuberculosis is suspected.     

奥美拉唑对十二指肠溃疡患者胃液表皮生长因子浓度的影响

目的 观察奥美拉唑（Ｏｍｅ）愈合十二指肠溃疡（Ｄｕ）对胃液表皮生长因子（ＥＧＦ）浓度的影响。方法 ５８例Ｈｐ阳性Ｄｕ患者随机分为三组：奥美拉唑（Ｏｍｅ）＋胶体铋剂（ＣＢＳ）＋羟氨苄青霉素（Ａｍｏ）组，雷尼替丁（Ｒａ）＋ＣＢＳ＋Ａｍｏ组和ＣＢＳ＋Ａｍｏ组，服药４周（Ｏｍｅ、Ｒａ和ＣＢＳ分别服４周，Ａｍｏ２周）。于治疗前、后分别测定空腹血清胃泌素和胃液ＥＧＦ浓度并与１２例Ｈｐ阴性健康对照组比较。结果：     

Effects of clarithromycin,omeprazole and leminoprazole on gastric ulcer healing in Helicobacter pylori-infected rats

Abstract We examined whether a single inoculation of Helicobacter pylori can colonize the stomachs of ulcerated rats and delay their healing and whether an antibiotic drug and acid pump inhibitors can enhance the ulcer healing in infected rats. Ulcers were produced by a submucosal injection of acetic acid solution into the gastric wall. Helicobacter pylori (ATCC-43504) was inoculated into rats with and without gastric ulcers. The animals were killed 2, 4, 6, 8 or 10 weeks after the inoculation and the ulcerated area and H. pylori viability were determined. Each test drug and their combination was administered for 1 or 2 weeks after H. pylori inoculation. Helicobacter pylori could not colonize the stomachs of normal rats, but could colonize stomachs with ulcers for 10 weeks at an incidence of >80%. Spontaneous healing of gastric ulcers was delayed by H. pylori infection during these 10 weeks. Daily treatment with clarithromycin significantly and dose-dependently delayed ulcer healing in infected rats. Both omeprazole and leminoprazole significantly enhanced ulcer healing and inhibited the clarithromycin-delayed ulcer healing. We conclude that: (i) H. pylori can colonize rat stomachs with ulcers and delay ulcer healing; (ii) clarithromycin delays ulcer healing in H. pylori-infected rats; and (iii) acid pump inhibitors inhibited the clarithromycin-delayed ulcer healing.     

Ultrastructural morphometry of gastric endocrine cells before and after omeprazole. A study in the oxyntic mucosa of duodenal ulcer patients

Long-term toxicological experiments with inhibitors of acid secretion were found to induce hyperplasia and eventually carcinoid tumors of the enterochromaffin-like cells of the oxyntic mucosa. To evaluate the effects of 6 months' treatment with omeprazole in humans, the oxyntic endocrine cells were morphometrically investigated at the ultrastructural level in five patients with active duodenal ulcer. No omeprazole-induced changes were found in the volume density of the total endocrine cell population and specific cell types (including the enterochromaffin-like cell) as well as in the other cytological parameters investigated (number of cell profiles per unit area, mean cross-sectional area of cell profiles, nuclear-cytoplasmic ratio, and density of cytoplasmic secretory granules). Both pretreatment and post-treatment values in our patients with duodenal ulcer significantly differed from those of a previous investigation of healthy volunteers with regard to the volume density of enterochromaffin-like cells and non-granulated cells, which increased, and of D cells, which markedly decreased. The latter result may provide a cellular basis for impairment in the paracrine release of fundic somatostatin in peptic ulcer disease. Finally, morphometric data on endocrine cell volume density provided by electron microscopy were found to correlate with those obtained in the same patients using light microscopy techniques (Grimelius silver impregnation and chromogranin A immunostaining). It is concluded that 6 months' treatment with pharmacological doses of omeprazole is devoid of appreciable trophic effect on endocrine cells of human oxyntic mucosa.     

Effect of omeprazole and sucralfate on prepyloric gastric ulcer. A double blind comparative trial and one year follow up.

This study compared healing rates, relief of symptoms, frequency of adverse events, and proportion of patients in remission after one year follow up in 104 patients with active prepyloric ulcer during treatment with 40 mg omeprazole once daily or 2 g sucralfate twice daily, using a randomised double blind controlled trial. Healing rates after two, four, and six weeks were (omeprazole/sucralfate) 49%/23%; 83%/59%; 90%/70% respectively. After two weeks, omeprazole was more efficient than sucralfate in relief of daytime and nocturnal epigastric pain, nausea, and heartburn. The proportion of patients in remission after one year follow up was significantly higher in the omeprazole group (p < 0.01). Of the healed patients ulcers recurred in 36% in the omeprazole group and in 46% in the sucralfate group. It is concluded that the ulcer healing rate was higher and symptom relief was more pronounced in the omeprazole group compared with the sucralfate group, and that more patients were still in remission after a one year follow up period.     

Trimipramine in the treatment of gastric ulcer.

Forty patients with endoscopically confirmed gastric ulcers, completed a double-blind study comparing trimipramine with placebo during 4 weeks' treatment. The daily dose of trimipramine was 50 mg given before bedtime. No serious side-effects occurred. After four weeks' treatment 12 of the 20 patients receiving trimipramine had endoscopically completely healed ulcers, while in the placebo group only 4 of the 20 ulcers were healed (P = 0.025). With regard to the patients' complaints, a distinct and statistically significant improvement was also observed in the patients receiving trimipramine (P = 0.025). It is assumed that the previously shown antisecretory effect of the drug, together with the sedative and anti-depressive effect, make trimipramine a valuable drug in the treatment of peptic ulcer disease.     

Effects of low dose omeprazole on gastric secretion and plasma gastrin in patients with healed duodenal ulcer

The effects of seven days' treatment with omeprazole 5 and 10 mg daily on 24 hours gastric secretion and plasma gastrin concentrations were studied in a randomised double-blinded placebo-controlled study of six male patients with healed duodenal ulcer. Omeprazole 5 mg daily reduced mean daytime and nocturnal intragastric acidity by 31.4 and 40.1%, respectively. Omeprazole 10 mg per day produced very similar reductions of 33.6 and 42.0%, respectively. Total nocturnal acid output was reduced by 63.9% and 63.2%, respectively, by omeprazole 5 and 10 mg daily. There was a large degree of inter-subject variability in response to these low doses of omeprazole. Consequently, neither dose showed a statistically significant antisecretory effect when compared with placebo. Neither dose of omeprazole significantly affected fasting levels of gastrin, but omeprazole 10 mg daily produced a significant (P less than 0.05) increase in the integrated gastrin response to a meal. The lack of consistent antisecretory effect to low dose omeprazole is in accord with previous studies. This suggests that doses of 20 mg per day or greater are required to produce a consistent effect on acid secretion.     

Effects of omeprazole and famotidine on fibroblast growth factor-2 during artificial gastric ulcer healing in humans

BACKGROUND AND AIMS: Endoscopic mucosal resection is a widely accepted technique for the treatment of early gastric cancers, while large ulcers induced by the treatment should be treated promptly. This study aimed to compare the effects of omeprazole and famotidine on ulcer healing and fibroblast growth factor-2 levels in gastric ulcers induced by endoscopic mucosal resection. METHODS: Sixteen patients indicated for endoscopic mucosal resection were enrolled. They were treated by using either omeprazole (n = 8) or famotidine (n = 8) after endoscopic mucosal resection. Endoscopy was performed on days 4, 7 and 28 during each treatment period. Levels of fibroblast growth factor-2 in biopsy specimens were measured by using an enzyme-linked immunosorbent assay at the time of and after endoscopic mucosal resection. Histological variables were also assessed. RESULTS: Ulcer healing rates under endoscopy were not different between the two treatment groups. In both groups, levels of fibroblast growth factor-2 slightly increased on day 4, but the values were not different at any time point. There were no differences in histological variables on days 4 and 7, but fibromuscular hyperplasia was significantly greater in the omeprazole group than in the famotidine group on day 28 (P < 0.05). CONCLUSIONS: Omeprazole and famotidine have an equivalent value for the treatment of ulcers induced by endoscopic mucosal resection. While omeprazole had a more potent effect on fibromuscular hyperplasia than did famotidine, such a difference does not seem to be explained by fibroblast growth factor-2.