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PubMed1982

Gastric acid secretion and fasting serum gastrin in patients with duodenal ulcer, prepyloric ulcer or gastric ulcer.

In order to evaluate whether prepyloric ulcer (PPU) could be classified as an intermediate ulcer type between duodenal ulcer (DU) and gastric ulcer (GU), fasting serum gastrin as well as basal and pentagastrin-stimulated acid secretion were studied. The fasting serum gastrin values in the three groups were not significantly different. Patients with PPU and DU showed a higher basal acid output compared to GU patients. The basal acid output in DU patients increased in the last two periods before stimulation, and in the last basal period it was significantly higher compared to PPU patients. Patients with GU showed the lowest basal and stimulated acid output. However, the higher stimulated acid output in DU patients was insignificantly different from that of PPU patients. The results indicate that basal and stimulated gastric acid secretion values in PPU patients are closer to those of DU patients than of GU patients. Furthermore, it is concluded that PPU is a homogeneous ulcer type without secretory overlap with the GU group.

Adult↗
PubMed1994

[Ulcer surgery and anti-ulcer agents. Changes in surgical activities and sale of anti-ulcer agents in Nord-Trøndelag 1975-89].

During recent decades the number of operations for peptic ulcer has decreased significantly. The incidence of operations for peptic ulcer or related complications during the period 1975-89 in persons older than 15 years was investigated in the Nord-Trøndelag region of Norway, with a population of approximately 100,000. The number of elective surgical procedures decreased by 72% from 1975 to 1989. The greatest reduction was found for duodenal ulcers. The incidence of acute operations decreased by 35%. The main reason was fewer surgical interventions in patients with haemorrhage, since the number of operations for perforation remained almost constant during the period of 15 years. The reduction in surgical treatment can be explained mainly by the introduction of new H2-antagonists in the seventies, leading to more successful pharmacological treatment of peptic ulcer.

Adult↗
PubMed1998

Pressure ulcer research: pressure ulcer treatment. A monograph from the National Pressure Ulcer Advisory Panel.

The AHCPR guideline on Treatment of Pressure Ulcers was released in December 1994. This guideline was based on the best available scientific evidence published between 1966 and May 1, 1993. Over 45,000 abstracts were reviewed in the literature analysis. Yet only 63.2% of the guideline recommendations were based on research of any type, and only 4.5% of the recommendations were supported by two or more randomized clinical trials. A more recent literature review (covering articles on pressure ulcers listed in the MEDLINE database between May 1, 1993, and December 1, 1996), revealed minimal advances in the scientific body of knowledge on pressure ulcer treatment. Advances have been made in the knowledge of electrical therapy and growth factors, and efforts are under way to enhance tools for monitoring healing. In an era of limited research funding, we need to carefully target our research efforts to maximize the advancement of our knowledge of pressure ulcer treatment. It is the hope of the NPUAP that this monograph will guide the research needed to ensure the most efficient utilization of funds to improve patient outcomes.

Evidence-Based Medicine↗
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↗
PubMed2000

Prevention of chronic NSAID induced upper gastrointestinal toxicity.

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are important agents in the management of arthritic and inflammatory conditions, and are among the most frequently prescribed medications in North America and Europe. However, there is overwhelming evidence linking these agents to a variety of gastrointestinal (GI) toxicities. OBJECTIVES: To review the effectiveness of common interventions for the prevention of NSAID induced upper GI toxicity. SEARCH STRATEGY: A literature search was conducted, according to the Cochrane methodology for identification of randomized controlled trials in electronic databases, including MEDLINE from 1966 to January 2000, Current Contents for 6 months prior to January 2000, Embase to Febuary 1999, and a search of the Cochrane Controlled Trials Register from 1973 to 1999. Recent conference proceedings were reviewed and content experts and companies were contacted. SELECTION CRITERIA: Randomized controlled clinical trials (RCTs) of prostaglandin analogues (PA), H2-receptor antagonists (H2RA) or proton pump inhibitors (PPI) for the prevention of chronic NSAID induced upper GI toxicity were included. DATA COLLECTION AND ANALYSIS: Two independent reviewers extracted data regarding population characteristics, study design, methodological quality and number of patients with endoscopic ulcers, ulcer complications, symptoms, overall drop-outs, drop outs due to symptoms. Dichotomous data was pooled using Revman V3.1. Heterogeneity was evaluated using a chi square test. MAIN RESULTS: Thirty-three RCTs met the inclusion criteria. All doses of misoprostol significantly reduced the risk of endoscopic ulcers. Misoprostol 800 ug/day was superior to 400 ug/day for the prevention of endoscopic gastric ulcers (RR=0.18, and RR=0. 38 respectively, p=0.0055). A dose response relationship was not seen with duodenal ulcers. Misoprostol caused diarrhea at all doses, although significantly more at 800ug/day than 400ug/day (p=0.0012). Misoprostol was the only prophylactic agent documented to reduce ulcer complications. Standard doses of H2RAs were effective at reducing the risk of endoscopic duodenal (RR=0.24; 95% CI: 0.10-0. 57) but not gastric ulcers(RR=0.73; 95% CI:0.50-1.09). Both double dose H2RAs and PPIs were effective at reducing the risk of endoscopic duodenal and gastric ulcers (RR=0.44; 95% CI:0.26-0.74 and RR=0.37;95% CI;0.27-0.51 respectively for gastric ulcer), and were better tolerated than misoprostol. REVIEWER'S CONCLUSIONS: Misoprostol, PPIs, and double dose H2RAs are effective at preventing chronic NSAID related endoscopic gastric and duodenal ulcers. Lower doses of misoprostol are less effective and are still associated with diarrhea. Only Misoprostol 800ug/day has been directly shown to reduce the risk of ulcer complications.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2001

[Anorectal ulcers--etiology, diagnosis, therapy (simple rectal ulcer, radiogenic ulcer, CED].

Ulcers of the anorectal region are very variable in etiology and morphology. Often differential diagnosis is even possible by (excisional-)biopsy. As they are symptoms of any kind of disease, therapy has to be derived from this disease. Therefore surgery often only plays an additional part besides clearing the diagnosis, although the surgeon is mostly the first consultant, so being responsible for ongoing therapy. Some special diseases, their problems and therapeutical options, are described in detail.

Anal Canal↗
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↗
PubMed2005

An overview of acetic acid ulcer models--the history and state of the art of peptic ulcer research.

Four types of experimental chronic ulcer models, named acetic acid ulcer models, have been developed to examine the healing process of peptic ulcers, screen anti-ulcer drugs, and better evaluate the adverse effects of various anti-inflammatory drugs on the gastrointestinal mucosa. The model easily and reliably produces round, deep ulcers in the stomach and duodenum, allowing acetic acid ulcer production in mice, rats, Mongolian gerbils, guinea pigs, cats, dogs, miniature pigs, and monkeys. These ulcer models highly resemble human ulcers in terms of both pathological features and healing process. The models have been established over the past 35 years and are now used throughout the world by basic and clinical scientists. One of the characteristic features of acetic acid ulcers in rats is the spontaneous relapse of healed ulcers >100 d after ulceration, an endoscopically confirmed phenomenon. Indomethacin significantly delays the healing of acetic acid ulcers, probably by reducing endogenous prostaglandins and inhibiting angiogenesis in ulcerated tissue. Helicobacter pylori significantly delays healing of acetic acid ulcers and causes relapse of healed ulcers at a high incidence in Mongolian gerbils. Anti-secretory drugs (e.g. omeprazole), prostaglandin analogs, mucosal defense agents (e.g. sucralfate), and various growth factors all significantly enhance healing of acetic acid ulcers. Gene therapy with epidermal growth factor and vascular endothelial growth factor applied to the base of acetic acid ulcers in rats is effective in enhancing ulcer healing. Since an inhibitor of nitric oxide syntase prevents ulcer healing, nitric oxide might be involved in the mechanism underlying ulcer healing. We conclude that acetic acid ulcer models are quite useful for various studies related to peptic ulcers.

Acetic Acid↗
PubMed1981

Peptic ulcer in children: the predominance of gastric ulcers.

Thirty-two children with ulcer disease were seen over a four-year period. Twenty-seven children had a primary ulcer and five had an ulcer associated with an acute or chronic illness (secondary ulcer). Antral ulcer was diagnosed most commonly, followed by duodenal ulcer and gastric body ulcer. The ratio of gastric ulcer to duodenal ulcer was 17:11. Diagnosis of ulcer was accomplished by endoscopy in 97% of the patients and by radiography in 70% of those studied. Radiologic accuracy was obtained in 89% with duodenal ulcer but in only 50% of those with gastric ulcer. Children with primary gastric ulcer presented with no evidence of chronicity and 12% had persistence or recurrence of ulcer during follow-up. Eighty-two percent of the children with primary duodenal ulcer presented with chronic symptoms consisting of abdominal pain, nausea, vomiting or recurrent bleeding and 45% had persistence or recurrence of ulcer during follow-up. Children with secondary ulcer all presented with acute symptoms and none had persistence or recurrence. Twenty children were treated prospectively with cimetidine and 11 were treated with antacids. Repeat endoscopy was employed in 16 as a measure of healing. All children with isolated antral ulcer did well clinically, regardless of mode of therapy and of those studied by re-endoscopy all showed complete or substantial healing at six to eight weeks. Treatment of a small group of children with primary duodenal ulcer using cimetidine was initially efficacious, although recurrence of ulcer was noted after cessation of treatment in four of six children given cimetidine. In addition, cimetidine appears to offer no advantage compared to antacids in the treatment of uncomplicated antral ulcer in children.

Adolescent↗
PubMedDate not supplied

Usefulness of proton pump inhibitor (PPI) maintenance therapy for patients with H. pylori-negative recurrent peptic ulcer after eradication therapy for H. pylori: pathophysiological characteristics of H. pylori-negative recurrent ulcer scars and beyond acid suppression by PPI.

BACKGROUND/AIMS: Problems after Helicobacter pylori (Hp) eradication therapy include recurrence of Hp-negative peptic ulcers. We investigated the pathophysiological characteristics of Hp-negative recurrent ulcer scars, and performed proton pump inhibitor (PPI) maintenance therapy as a new therapy for prevention of recurrence in patients with Hp-negative recurrence after Hp eradication and investigated its usefulness. METHODOLOGY: The subjects were 21 patients with Hp-negative recurrent peptic ulcers after Hp eradication (gastric ulcer: 19, duodenal ulcer: 2) and 25 patients with non-recurrent ulcers (gastric ulcer: 20, duodenal ulcer: 5). The mucosa from the ulcer scar lesion was endoscopically obtained from patients, and HE staining, CD68 immunohistochemical staining, and investigation of the mucosal expression levels of TNF-alpha and IFN-gamma were performed by ELISA. Patients with recurrence after eradication were divided into two groups at the time of ulcer scar after the first treatment, and received maintenance therapy: the intermittent treatment group that received lansoprazole (LPZ), 30 mg/day, on two days on weekends (gastric ulcer: 9, duodenal ulcer: 1) and the ranitidine (RAN) 150 mg/day daily treatment group (gastric ulcer: 8, duodenal ulcer: 1). RESULTS: Infiltration of CD68-positive inflammatory cells was observed in the lamina propria mucosae over the epithelial layer in ulcer scars of the Hp-negative recurrent ulcer group compared with the non-recurrent ulcer group, and TNF-alpha and IFN-gamma significantly increased (27.22+/-6.23 pg/mg, 52.12+/-5.41 pg/mg vs. 4.23+/-2.14 pg/mg, 7.11+/-3.06 pg/mg, P<0.001). In the RAN maintenance therapy group, the ulcer recurred within 10 months in all patients, while the ulcer recurred in only one patient in the intermittent LPZ treatment group. CONCLUSIONS: These results suggested that the pathophysiological characteristic of Hp-negative recurrent ulcer scar lesions after eradication was infiltration of inflammatory cells, mainly monocytes/macrophages, in the lamina propria mucosae over the epithelial layer, and this may be a key factor in ulcer recurrence. Furthermore, intermittent PPI therapy using LPZ may be a useful maintenance therapy for prevention of recurrence in these cases.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1993

Prevalence of Helicobacter pylori infection in patients with peptic ulcer diseases and non-ulcer dyspepsia.

BACKGROUND: Helicobacter pylori is known to be a cause of active chronic gastritis and has been proposed as an etiologic factor in the development of peptic ulcer disease, but controversy continues regarding the pathogenic importance and mechanism. We examined the prevalence of H. pylori infection in patients with peptic ulcers and non-ulcer dyspepsia. METHOD: 749 patients (373 with duodenal ulcer, 303 with gastric ulcer, 73 with non-ulcer dyspepsia) were included. Endoscopic mucosal biopsies were done at antrum, duodenum, and, if present, ulcer margin. The specimens were tested by Gram staining, Giemsa staining, culture, urease testing for identification of H. pylori. Antibody to H. pylori was examined in 83 patient of these patients by ELISA, and the result was compared with the results of bacteriologic studies. RESULT: Prevalence of H. pylori in antral mucosa was higher in patients with duodenal ulcers (81.5%) than in patients with gastric ulcer and non-ulcer dyspepsia (56% and 52.8%) (P < 0.05). Also in the duodenal mucosa of non-ulcer sites, and the ulcer margin of patients with duodenal ulcers, the detection rates (12% and 40.7%) were higher than those in the duodenal mucosa of patients with gastric ulcer and non-ulcer dyspepsia (7% and 8%)(p < 0.005). Antibody to H. pylori was detected in all patients with duodenal and gastric ulcers and non-ulcer dyspepsia who were tested for antibody. In contrast, the detection rates of antibody in adult control and child control were 33.3% and 27%. Among patients with antibody to H. pylori, H. pylori was detected in 85.7% of patients with duodenal ulcer, 62.5% of patients with gastric ulcers and 22.2% of patients with non-ulcer dyspepsia (p < 0.05). CONCLUSION: These data suggest that H. pylori is a possible pathogen for duodenal ulcer by duodenal colonization probably via gastric metaplasia. Also the past or present infection of H. pylori in antral mucosa may play a role at least partially in generation of upper gastrointestinal symptoms.

Adolescent↗