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At least 19 recordsLinked to original sources
PubMed1992

Ulcer recurrence following duodenal ulcer healing with omeprazole, ranitidine, or placebo: a double-blind, multicenter, 6-month study. The Omeprazole Duodenal Ulcer Study Group.

The present study determined whether the rate of relapse of duodenal ulcer was reduced after ulcer healing with omeprazole compared with ranitidine or placebo. It was made up of a double-blind, randomized, controlled multiple-center trial set within the United States. Patients were candidates if their duodenal or pyloric channel ulcer successfully healed in one of two large multicenter U.S. trials; one compared omeprazole, 20 mg once daily, before breakfast with ranitidine, 150 mg twice daily, and the other compared the same dose of omeprazole with placebo. Two hundred forty (73.8%) of the 325 patients with complete ulcer healing within 4 weeks of starting therapy who were eligible to enter the follow-up study were enrolled. There was no intervention. Endoscopic assessment of ulcer status was performed at 2, 4, and 6 months and whenever patients had symptoms thought to represent return of an ulcer. The lifetable relapse rates for duodenal ulcer according to initial ulcer therapy with omeprazole, ranitidine, or placebo were 76.7% [95% confidence interval (CI), 64%-89.3%], 59.8% (95% CI, 47.8-71.7%), and 50.4% (95% CI, 15.7%-85.2%), respectively. These rates were not statistically significantly different. Seventeen percent of recurrent ulcers occurred at a site different from that of the original ulcer. It is concluded that despite the more rapid rate of duodenal ulcer healing with omeprazole therapy, the rate of ulcer relapse appears similar and independent of whether ulcer healing was accelerated with omeprazole or ranitidine.

Adult↗
PubMed1991

[Gastric functional exploration. Comparison between secretory results in 72 non-ulcer dyspeptic patients and 289 non-operated duodenal ulcer patients. Predictive criteria for the efficacy of fundus vagotomy in duodenal ulcer].

Basal and pentagastrin- or insulin- stimulated secretion was studied in 72 non ulcer dyspectic patients (NUD), in 289 non operated duodenal ulcer patients (DU), and in 30 DU, before and after highly selective vagotomy (HSV). Acidity, proteolytic activity, choline indicating the presence of duodenogastric refluxed material and sialic acid bound to mucus glycoprotein, marker of mucus erosion, were measured. Basal and pentagastrin-stimulated acid and pepsin secretions in NUD were significantly reduced with regard to those in DU. Sialic acid content was weak in basal secretion and markedly increased in response to pentagastrin reaching the values observed in DU. DU basal secretions of acid and of pepsin were modulated according to the stimulating secretory mechanism. Mucus glycoprotein erosion was related to pepsin mucolytic activity and/or to the presence in gastric juice of refluxed material. In DU the increase of peptic mucolysis corresponded to a biological signal of the ulcer attack when no duodenogastric reflux was identified. High values pepsin output in basal secretion and in response to insulin and of basal sialic acid content combined with a pepsin/acid basal output ratio higher than 80 were biological arguments anticipating the efficacy of HSV in DU. Multiparametric analysis of gastric secretion allows to evaluate the ratio between aggressive factors and mucosal defense corresponding to an equilibrium in NUD and to greater aggressivity in DU whose intensity is related to the course of disease.

Adult↗
PubMed1991

Maintenance therapy with sucralfate in duodenal ulcer: genuine prevention or accelerated healing of ulcer recurrence?

We sought to compare the efficacy of sucralfate to placebo for the prevention of duodenal ulcer recurrence and to determine that the efficacy of sucralfate was due to a true reduction in ulcer prevalence and not due to secondary effects such as analgesic activity or accelerated healing. This was a double-blind, randomized, placebo-controlled, parallel groups, multicenter clinical study with 254 patients. All patients had a past history of at least two duodenal ulcers with at least one ulcer diagnosed by endoscopic examination 3 months or less before the start of the study. Complete ulcer healing without erosions was required to enter the study. Sucralfate or placebo were dosed as a 1-g tablet twice a day for 4 months, or until ulcer recurrence. Endoscopic examinations once a month and when symptoms developed determined the presence or absence of duodenal ulcers. If a patient developed an ulcer between monthly scheduled visits, the patient was dosed with a 1-g sucralfate tablet twice a day until the next scheduled visit. Statistical analyses of the results determined the efficacy of sucralfate compared with placebo for preventing duodenal ulcer recurrence. Comparisons of therapeutic agents for preventing duodenal ulcers have usually been made by testing for statistical differences in the cumulative rates for all ulcers developed during a follow-up period, regardless of the time of detection. Statistical experts at the United States Food and Drug Administration (FDA) and on the FDA Advisory Panel expressed doubts about clinical study results based on this type of analysis. They suggested three possible mechanisms for reducing the number of observed ulcers: (a) analgesic effects, (b) accelerated healing, and (c) true ulcer prevention. Traditional ulcer analysis could miss recurring ulcers due to an analgesic effect or accelerated healing. Point-prevalence analysis could miss recurring ulcers due to accelerated healing between endoscopic examinations. Maximum ulcer analyses, a novel statistical method, eliminated analgesic effects by regularly scheduled endoscopies and accelerated healing of recurring ulcers by frequent endoscopies and an open-label phase. Maximum ulcer analysis reflects true ulcer recurrence and prevention. Sucralfate was significantly superior to placebo in reducing ulcer prevalence by all analyses. Significance (p less than 0.05) was found at months 3 and 4 for all analyses. All months were significant in the traditional analysis, months 2-4 in point-prevalence analysis, and months 3-4 in the maximal ulcer prevalence analysis. Sucralfate was shown to be effective for the prevention of duodenal ulcer recurrence by a true reduction in new ulcer development.

Double-Blind Method↗
PubMed1986

Elevated serum pepsinogen I and II levels differ as risk factors for duodenal ulcer and gastric ulcer.

We investigated the possibility that serum pepsinogen I (PG I) and pepsinogen II (PG II) levels might differ as risk factors for duodenal ulcer and gastric ulcer. From 1967 to 1970, serum was obtained from 7498 Japanese men in Hawaii, and the cohort was followed up to 1981 for the development of peptic ulcer disease. Pepsinogen I and PG II levels in stored serum were significantly higher in the subjects who developed duodenal ulcer (n = 43) or gastric ulcer (n = 115) than in 212 control subjects. The linear trend in risk of each type of ulcer was highly significant for both PG I and PG II. An elevated serum PG I level (greater than or equal to 130 micrograms/L), however, was associated with about a threefold higher odds ratio for duodenal ulcer than for gastric ulcer (8.37 vs. 2.83), whereas an elevated PG II level (greater than or equal to 30 micrograms/L) was associated with about a threefold higher odds ratio for gastric ulcer than for duodenal ulcer (18.21 vs. 6.49). In contrast, the PG I/PG II ratio was significantly lower in the gastric ulcer than in the control and duodenal ulcer cases, and showed a significant linear trend in risk only for gastric ulcer. In addition, a PG I/PG II ratio of less than 4.0, which has been shown previously to be indicative of chronic gastritis, was associated with an almost 10-fold higher odds ratio for gastric ulcer than for duodenal ulcer (7.35 vs. 0.79). The results indicate that an elevated serum PG I level is a major risk factor for duodenal ulcer, whereas an elevated serum PG II level and a low PG I/PG II ratio are major risk factors for gastric ulcer.

Adult↗
PubMed1986

Effects of cimetidine on the healing and recurrence of duodenal ulcers and gastric ulcers.

The effects of cimetidine on the healing and recurrence of duodenal ulcers and gastric ulcers were compared. The extent of the acid secreting areas was examined by the endoscopic Congo red methylene blue test. Using the extent of acid secreting areas gastric ulcers were classified into ulcers with and without extensive acid secreting areas. Duodenal ulcers were all associated with extensive acid secreting areas. The gastric acid outputs in the basal state and after maximal stimulation with gastrin were highest in duodenal ulcers, and lowest in gastric ulcers without extensive acid secreting areas. Cimetidine treatment significantly promoted the healing of duodenal ulcers and gastric ulcers with extensive acid secreting areas when compared with placebo, but not of the gastric ulcers without extensive acid secreting areas. Cimetidine also significantly diminished the recurrence of duodenal ulcers, but not gastric ulcers with and without extensive acid secreting areas. These findings indicate that in Japan cimetidine promotes the healing of duodenal and gastric ulcers associated with high gastric acid production and prevents recurrence of duodenal ulcers, but has little or no influence on the healing and recurrence of gastric ulcers associated with low acid secretion.

Cimetidine↗
PubMed1992

Herpes simplex virus types 1 and 2 and cytomegalovirus in peptic ulcer disease and non-ulcer dyspepsia.

The prevalence and the serum levels of IgG antibody to Herpes simplex virus type 1 or 2 (HSV1, HSV2) and to cytomegalovirus (CMV) were studied by ELISA in patients with active peptic ulcer -- duodenal and gastric -- and non-ulcer dyspepsia. Two hundred and forty-two consecutive patients with endoscopically confirmed active peptide ulcer -- 170 duodenal ulcers, 72 gastric ulcers -- and 95 consecutive patients who fulfilled the criteria for the diagnosis of non-ulcer dyspepsia were included in the study. The patients, aged 17-80 years, were well matched for age and sex. Antibody to cytomegalovirus was found in 83% of duodenal ulcer, 85% of gastric ulcer and 75% of non-ulcer dyspepsia patients; differences were not significant. The prevalence of HSV1 antibody was significantly higher in patients with duodenal ulcer than in those with non-ulcer dyspepsia (p < 0.025); the prevalence of HSV2 antibody was significantly higher in patients with duodenal or gastric ulcer, than in those with non-ulcer dyspepsia (p < 0.05, p < 0.01, respectively); however, antibody levels (mean optical density) to the viruses studied were similar for all groups of patients. These results provide some evidence that HSV might be implicated in the pathogenesis of peptic ulcer disease.

Adolescent↗
PubMed1992

[Comparative pathologic study on the peri-ulcer mucosal lesion around benign and malignant gastric ulcer].

3441 peri-ulcerous mucosal lesions around benign and malignant gastric ulcers (1479 benign gastric ulcers, 421 cancerous degeneration of benign ulcers and 1541 ulcerative carcinomas) were studied comparatively. It was found that the ulcer of cancerous degeneration of benign ulcer was small and the epithelial regeneration at the ulcer's edge and fusion of the muscularis mucosa with the muscularis propria were very common. The cancerous tissue, extending down to the submucosa, was found at the margin but not at the base of the ulcer. Lymph node metastasis was rare. Therefore, the cancerous degeneration of ulcer was most likely an early carcinoma. These findings conform well with Hauser's criteria. Chronic atrophic gastritis intestinal metaplasia (IIb and type II), moderate and severe dysplasia were more commonly observed in cancerous degeneration of ulcers than in benign peptic ulcers or ulcerative carcinoma. These results suggest that multiple biopsies should be taken from the edge of chronic ulcers.

Adenocarcinoma↗
PubMed1992

[Endoscopic studies on refractory gastric ulcers, especially, linear ulcers, treated with proton pump inhibitor].

Seven patients with refractory gastric ulcers against H2-blocker therapy, were treated with omeprazole, and the endoscopic findings serially followed. Round ulcers improved steadily with treatment in two cases. However, healing of the ulcers was not complete and very small pin-point ulcers remained. Therefore, a prostaglandin E1 analogue was added at the 14 and 16th week of omeprazole therapy. The ulcers healed completely, two weeks later. In five cases with linear ulcers, one case discontinued the taking of omeprazole. The linear ulcers in the other four cases healed completely within 4 to 11 weeks. Endoscopically, some parts of the linear ulcers were initially scarred and the ulcers were divided into several short ulcers. The ulcers separated there after and healed respectively. These findings suggest that the healing process of linear ulcers may represent the reversed course of the developing process of linear ulcers. The results indicate that omeprazole is highly effective for the treatment of refractory gastric ulcers.

Adenosine Triphosphatases↗
PubMed1985

Effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one, a new anti-ulcer agent, on experimental acute and chronic ulcers.

The effects of 5-acetylspiro[benzofuran-2(3H),1'-cyclopropan]-3-one (AG 629), a newly synthesized compound, on various experimentally induced ulcers were investigated. Oral or intraduodenal administration of AG 629 in a dose range of 25-100 mg/kg inhibited water-immersion stress ulcer, exertion ulcer, Shay ulcer, indometacin- and acetylsalicylic acid (ASA)-induced gastric ulcer, and indomethacin-induced small intestinal ulcer in rats, histamine-induced gastric ulcer in guinea pigs, and ASA-induced gastric ulcer in dogs, though it was not effective against cysteamine-induced duodenal ulcer in rats. AG 629 in doses of 6.3-25 mg/kg p.o. twice a day significantly promoted the healing of acetic acid- or thermal-cortisone-induced gastric ulcers and acetic acid-induced duodenal ulcers in rats. AG 629 (25-100 mg/kg i.d.) inhibited the secretion of gastric acid and pepsin in pylorus-ligated rats and the acid secretion stimulated by distension of the rat stomach with air, whereas this compound did not affect acid secretion stimulated by histamine, pentagastrin, carbachol or 2-deoxy-D-glucose. This study shows that AG 629 has both prophylactic and curative effects on various ulcers. The anti-ulcer effect of this agent seems to be mediated primarily by increasing mucosal resistance and secondarily by an antisecretory activity.

Acetates↗