Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection with active gastritis is comparably common in non-steroidal anti-inflammatory drug (NSAID) users and controls. The prevalence of active acute gastritis and its severity relate to H. pylori infection and not to use or non-use of NSAIDs. In individual patients active gastritis may deteriorate during long-term NSAID therapy but is rare in aspirin users. Among NSAID users those with H. pylori gastritis appear to have more dyspeptic symptoms, repeated intolerance to different NSAIDs, and often a history of ulcer disease. For current ulcers, NSAID use, chemical gastritis, and active gastritis due to H. pylori are independent risk factors. For gastric ulcer the risks are additive. For duodenal ulcer only H. pylori is a clearly defined risk factor: duodenal ulcers may not occur in H. pylori-negative NSAID users. In gastroduodenal mucosa NSAIDs may augment acute inflammation caused by H. pylori, and inflammation may exacerbate the biochemical injury to these tissues caused by NSAIDs.
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PMID:Helicobacter pylori infection and gastroduodenal injury by non-steroidal anti-inflammatory drugs. 177 31

Pathological sections of gastrectomized specimens of 74 patients with benign gastric ulcer and 79 with gastric cancer were reviewed. Intestinal metaplasia was found in 26 specimens with benign ulcer (35.1%) and in 43 with cancer (54.4%), a difference that is statistically significant. Further analysis of age groups showed that rate of occurrence of metaplasia in cancer patients older than 60 years was 70.3%, which was significantly higher than that of their younger counterparts (40.5%) and of patients with benign ulcer of either age group. A survey was also conducted by taking biopsies of mucosa of antrum and body of the stomach of 250 patients who underwent gastroscopic examinations. Acute and chronic gastritis was found in 22 and 156 patients, respectively. Intestinal metaplasia was found to be associated with acute gastritis in 2 (9.1%) and with chronic gastritis in 25 (16%) patients. In conclusion, intestinal metaplasia was associated with higher proportion than it was with benign gastric ulcer and gastritis among Thai patients.
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PMID:Occurrence of intestinal metaplasia of the stomach in Thai patients with gastritis, benign ulcer, and gastric cancer. 230 43

The purpose of this paper is to study the use of upper gastrointestinal (Gl) fiberoptic endoscopy in children. Two hundred consecutive patients referred to one of the authors were reviewed. The indications for performing upper gastrointestinal endoscopy in these 200 patients were: (1) recurrent abdominal pain (46.5%), (2) persistent vomiting (14.5%), (3) haematemesis (14.5%), (4) acute abdominal pain (13%) and (5) other indications such as foreign body removal, failure to thrive and unexplained chest pain (11.5%). The endoscopy was performed with the Olympus P3 or Olympus XP-10 gastroscopes. The sedation used was a combination of intravenous pethidine (2mg/kg) and diazepam (0.5 mg/kg). Among the patients with recurrent abdominal pain, upper Gl endoscopy showed duodenal ulcer in 7 patients (7.5%), duodenitis in 4 (4.3%), oesophagitis in 4 (4.3%) and gastric ulcer in 2 (2.2%). The rest of the patients were normal (81.7%). With regard to persistent vomiting, 37.9% of the patients showed gastroesophageal reflux and 6.9% had a hiatus hernia. Of 29 patients examined endoscopically for upper Gl bleeding, no focus of bleeding was identified in 27.6%. The remaining 72.4% were bleeding from acute gastric erosion (27.6%), oesophagitis (17.2%), oesophageal varices (13.8%), duodenal ulcer (10.3%) and Mallory-Weiss tear (3.5%). The Majority of the patients with acute abdominal pain were normal endoscopically (61.5%). The two common abnormal findings were acute gastritis (27.0%) and acute duodenitis (11.5%). No major complications were encountered during the procedure in these 200 patients. It was concluded that upper Gl endoscopy is useful for defining upper Gl mucosal pathology. The procedure can be performed safely in children under sedation.
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PMID:Upper gastrointestinal endoscopy in children. 237 74

Several studies have shown a striking association between the presence of Campylobacter pylori (C.p) in the gastric mucosa and histologically confirmed gastritis and ulcer disease. The microorganism has been found in up to 90% of patients with active chronic antral (type B) gastric ulcer, and in up to 70% of patients with duodenal ulcer. Voluntary ingestion of C.p. by two persons and two epidemic occurrences after apparent C.p. contamination of stomach probes, with demonstration of the bacterium in the mucosa, have shown that C.p. can induce acute gastritis; in one volunteer the acute gastritis progressed to the active chronic form. Eradication of C.p. by antibacterial treatment is associated with resolution of gastritis. Relapse of peptic ulcer is closely related to infection by C.p. The microorganism has important virulence factors allowing it to select an ecological niche below the mucus layer on the gastric mucosa. C.p. exhibits strong mucolytic activity through proteases which could damage the mucus barrier and therefore increase susceptibility to development of gastritis and peptic ulcers; however, the pathogenic impact of C.p. remains unknown. C.p. is diagnosed by histological or microbiological examination of gastric biopsy specimens or by serological techniques. Bismuth salts alone or in combination with antibiotics are effective against C.p., but the efficacy of antimicrobial treatment of gastritis and ulcer disease associated with C.p. has still to be proven by large double-blind placebo-controlled trials. The hitherto published findings do not allow definite evaluation of the pathogenetic significance of C.p. in gastritis and ulcer disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Campylobacter pylori: cause of gastritis and ulcer disease?]. 328 14

The authors describe cases urgently admitted for iatrogenic gastric lesions due to non-steroid antiinflammatory treatment during the past year. Nine patients were affected by peptic ulcer (bleeding in five cases), while in the remaining 11 an erosive acute gastritis could be observed. Among them, ten patients had been taking acetylsalicylic acid, one indomethacin and the others ketoprofen, indoprofen or similar drugs. In 11 patients, five presenting gastric ulcer and six affected by haemorrhagic gastric damage, an evident duodenogastric reflux was demonstrated. Fifteen patients were treated pharmacologically and complete healing of the lesions was obtained, while in five patients surgical treatment was necessary. The authors conclude by pointing out the high incidence (over 50%) and the pathogenetic role of duodenogastric reflux in gastric lesions appearing in patients treated with non-steroidal antiinflammatory drugs.
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PMID:Duodenogastric reflux and gastric damage from non-steroidal antiinflammatory drugs. 394 44

In the present study the release of somatostatin-like immunoreactivity (SLI) was evaluated in vitro from isolated rat antral and fundic mucosa and from biopsy specimens of human antral mucosa. Perifusion of antral mucosa with Earle's balanced salt solution showed a pH-dependent release of SLI. SLI release did not change in response to a reduction from pH 7 during the baseline period to pH 3, whereas a significant increase occurred when the pH was changed to 2.5 or 2, respectively. Fundic SLI release remained at baseline levels during the decrease of the pH value of the buffer solutions. Atropine at doses of 10(-6) to 10(-4) M did not alter acid-induced SLI release from the isolated antral mucosa, suggesting different mechanisms in vitro compared to the acid-induced SLI release in vivo. SLI release from human mucosa was 450 +/- 217 pg/min X mg wet weight in response to perifusion with the buffer pH 2 in 7 control subjects. No significant difference was observed in patients with duodenal ulcer or acute gastritis, whereas gastric ulcer patients had significantly lower values (66 +/- 44) compared to controls and duodenal ulcer patients. These data do not support the hypothesis that impaired somatostatin production and release might be a pathogenetic factor for gastric acid hypersecretion and development of duodenal ulcer.
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PMID:Somatostatin release from perifused rat and human gastric mucosa. 614 69

The gamma-glutamyl-transferase activity, the total glutathione content, the GSH-peroxidase activity, and the GSH S-transferase activity using an aryl substrate were estimated in the S9 fraction of gastric biopsy specimens taken from patients with normal stomach morphology (n = 24), acute gastritis (n = 15), chronic-atrophic gastritis (n = 10), gastric ulcer (n = 9), and carcinoma of the stomach (n = 12). The total glutathione content of normal gastric mucosal specimens was significantly higher than that of human liver biopsy specimens, whereas the GSH-peroxidase and the GSH S-aryltransferase activities were much lower than those found in the liver. Specimens of gastric ulcer had significantly lower enzyme activities of GSH-peroxidase and GSH-aryltransferase, whereas gastric cancer tissue had significantly lower concentrations of total glutathione. The intraindividual comparison of tumorous and non-tumorous tissue showed a consistent decrease of total glutathione as well as of GSH-aryltransferase activity in carcinomatous tissue.
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PMID:Glutathione and GSH-dependent enzymes in the human gastric mucosa. 670 2

Numerous studies implicated Helicobacter pylori as one causative agent producing gastritis and dyspepsia. Recent reports focus on another bacterium, Gastrospirillum hominis, as a possible pathogen producing gastritis. We report a 30-year-old researcher who became acutely ill with epigastric pain indicative of esophagitis or peptic ulcer disease. Gastritis and a gastric ulcer were observed endoscopically. Histological examination of the gastric mucosa revealed an acute gastritis and large spiral-shaped organisms. The spiral forms were present in large quantities in the gastric mucosa of experimental animals (cats) handled by the patient in his research. Electron microscopy confirmed that the organisms from the cat and patient were morphologically identical. The patient was successfully treated with bismuth subsalicylate. His symptoms resolved and the organisms were cleared from his stomach. This study provides evidence that another bacterium, a Gastrospirillum, may cause gastritis in man and may be transmitted from animal to man.
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PMID:Acute gastritis associated with spiral organisms from cats. 814 39

The article presents results of instrumental examinations of 152 patients in detection of causes of the appearance of false acute abdomen. Gastroduodenoscopy (90 observations) has established that its appearance is associated with acute gastroduodenitis (in 42% of the patients), acute gastritis (28%), erosive gastritis (27.4%), acute gastric ulcer (2.7%). The ultrasonic investigation (26 patients) of patients with pseudoabdominal syndrome is most effective in acute diseases of the kidneys, liver, pancreas. The article also presents data on the role of laparocentesis (25 cases) and laparoscopy (15) in the detection of causes of pseudosurgical pains in the abdomen.
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PMID:[The role of instrumental study methods in the diagnosis of "acute abdomen"]. 837 48

Rebamipide, a gastroprotective drug, is a compound selected from over 500 amino acid analogs of 2(1H)-quinolinone tested for gastroprotective action and for efficacy to heal experimental gastric ulcers. This drug stimulates prostaglandin generation in gastric mucosa and improves not only the speed but also the quality of ulcer healing. In addition, it protects the gastric mucosa against acute injury caused by various noxious and ulcerogenic factors. Based on these experimental results, rebamipide had been subsequently tested in several clinical trials and approved in Japan for therapeutic use in patients with gastric ulcers and patients with acute gastritis. The main purpose of developing this type of drug was to improve the quality of ulcer healing, especially in that antisecretory drugs lack this advantage. In a preliminary clinical study, rebamipide improved the quality of gastric ulcer healing and reduced future ulcer recurrence. A number of basic research studies have been performed to clarify the mechanisms of rebamipide's action. These studies demonstrated unique properties of rebamipide and convincingly showed that it increases gastric mucus glycoprotein components, stimulates migration and proliferation of wounded epithelial cell monolayers, increases expression of epidermal growth factor and its receptor in normal and ulcerated gastric mucosa, and scavenges active oxygen radicals. The drug also attenuates the activity of neutrophils and the production of inflammatory cytokines stimulated by NSAIDs and/or H. pylori. Therefore, rebamipide can contribute to the management of patients who are taking NSAIDs or are infected with H. pylori. The inhibition of immunoinflammatory responses by rebamipide in H. pylori-infected patients may prevent development of gastritis, peptic ulcer disease, its recurrence, and possibly gastric cancer. Moreover, rebamipide may enhance eradication of H. pylori-infection using standard eradication therapy. Further studies are needed to clarify these possible advantages of rebamipide.
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PMID:Rebamipide: overview of its mechanisms of action and efficacy in mucosal protection and ulcer healing. 975 20


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