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)

Endoscopic findings in a group of 169 aged patients are shown to be concentrated in the stomach, whereas pathologic findings in the duodenal bulb are less frequent. In comparison to a group of young patients gastric mucosal atrophy, gastric ulcer, carcinoma of the operated and unoperated stomach, polyps are predominant in the aged patients. Approximately one half of carcinomas were seen in patients operated by the Billroth II technique. On behalf of this fact it is necessary to review patients endoscopically from the fifteenth year after operation on with regularity in order to detect growth of carcinoma in the early stage.
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PMID:[Gastroscopic findings in aged patients (author's transl)]. 1 29

The clinical usefulness of lansoprazole in the healing of gastric and duodenal ulcers, the S2-stage shift rate (white scarring rate), and endoscopic healing rate with respect to degree of gastric mucosal atrophy were investigated. The subjects were 50 gastric ulcer and 37 duodenal ulcer patients. The endoscopic healing rate in patients with gastric ulcers after initial treatment with lansoprazole was 92% after 8 weeks. The S2-shift rate was 38% after 8 weeks. The 8-week healing rate in patients without atrophy was 100% and with atrophy was 92%, although the difference was not statistically significant. The S2-shift rate in patients without atrophy was 42% and in patients with atrophy was slightly lower, at 37%, although the difference was not statistically significant. The endoscopic healing rate in patients with duodenal ulcers was 93% after 6 weeks, and the S2-shift rate was 59%. It is firmly established that atrophic gastric mucosa shows a reduction in mucosal defense factors. However, lansoprazole achieved good endoscopic healing rates and S2-shift rates even in patients with gastric ulcers with atrophic background mucosa.
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PMID:Clinical evaluation of lansoprazole in the treatment of peptic ulcers: initial healing and prevention of relapse. Tohoku Peptic Ulcer Study Group. 759 42

Helicobacter pylori is a curvilinear motile gram-negative bacillus which is now recognized as the principal cause of type B gastritis, duodenal ulcer, gastric ulcer and MALT lymphoma. There is also a high degree of association between H. pylori gastritis and gastric carcinoma and non-Hodgkin's lymphoma of the stomach. H. pylori infection of the stomach is the most frequent chronic infection in the world. H. pylori is an extraordinary pathogen with virtually unrivaled versatility. The organism possesses the capacity to colonize and prosper in the hostile acidic gastric lumen, an environment in which other microorganisms cannot survive. H. pylori contains and expresses an assortment of proinflammatory biomolecules. H. pylori also stimulates host cells to release proinflammatory substances which participate in the initiation and perpetuation of inflammation and tissue injury. H. pylori elaborates a potent urease and a variety of other enzymes necessary for colonization and expression of the organism's pathogenicity. H. pylori is usually acquired in childhood, believed usually by fecal-oral transmission. The principal lesion induced by H. pylori is type B gastritis, which begins as acute inflammation involving the antrum. Type B gastritis then extends to the entire stomach with gradual progression to chronic gastritis and variable degrees of gastric mucosal atrophy. Much now is known but much more remains to be learned about H. pylori and the diseases which this extraordinary pathogen produces.
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PMID:Helicobacter pylori: the versatile pathogen. 890 15

Helicobacter pylori (H. pylori) colonizes the gastric mucosa of a half of the mankind. Duodenal ulcer is found in 15-25%, gastric ulcer in 13%, while gastric adenocarcinoma develops in 1% of all infected individuals. Pathogenesis of H. pylori infection is related to the virulence factors of the bacterium, environmental (dietary habits, hygiene, stress) and host factors (age, sex, blood type). Colonization of the gastric mucosa is related to the motility of the bacterium, presence of lipopolysaccharide (LPS) and various bacterial enzymes. Gastric mucosal injury is the result of H. pylori LPS, vacuolization cytotoxin (vacA), cytotoxin associated protein (cagA), heat shock proteins and factors responsible for neutrophil chemotaxis and activity. H. pylori colonizes the gastric mucosa and zones of ectopic gastric epithelium. H. pylori infection is transmitted via oral-oral, fecal-oral and iatrogenic way (during endoscopy). Higher prevalence of the infection is associated with lower socioeconomic level, lack of drinking water, and living in a community. Acute H. pylori gastritis is superficial pangastritis progressing into the chronic phase after 7-10 days. Gastric mucosal atrophy and intestinal metaplasia can develop during the course of H. pylori infection. Clearly defined factors that influence the outcome of H. pylori infection include bacterial strain, distribution of gastritis, acid secretion and gastric mucosal atrophy.
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PMID:[Pathogenesis of Helicobacter pylori infection--bacterium and host relationship]. 1579 58

Toll-like receptors (TLRs) play important roles in the signaling of many pathogen-related molecules and endogenous proteins associated with immune activation. -196 to -174del polymorphism affects the TLR2 gene and alters its promoter activity. We investigated the influence of TLR2 -196 to -174del polymorphism on the risk of gastro-duodenal diseases, on the severity of Helicobacter pylori-induced gastritis in a Japanese population. The study was performed on 309 patients with abdominal discomfort and 146 healthy controls. -196 to -174del polymorphism of TLR2 was investigated by allele-specific polymerase chain reaction method in all of the subjects. Gastritis scores of antral gastric mucosa were assessed according to the updated Sydney system in H. pylori-positive subjects (n = 156). Patients with abdominal discomfort was consisted of 80 gastric ulcers (25.9%), 38 duodenal ulcers (12.3%), five gastric + duodenal ulcers (1.6%), 105 patients with gastritis (34.0%) and 81 normal healthy stomachs (26.2%). We did not find any association between TLR2 polymorphism and risk of gastric ulcer, duodenal ulcer, gastric and duodenal ulcer and gastritis compared to healthy controls. However, the TLR2-196 to -174ins allele was associated with severity of intestinal metaplasia in more than 60 years of ages (P = 0.02). The same allele also increased the risks of developing more severe gastric mucosal atrophy and intestinal metaplasia in female subjects (P < 0.05, P = 0.07 respectively). No association was observed between TLR2 polymorphism and severity of neutrophil and mononuclear cell infiltration. Our data suggest that the TLR2-196 to -174ins allele was associated with more severe intestinal metaplasia in patients older than was correlated with severity of gastric mucosal atrophy and intestinal metaplasia in female subjects.
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PMID:Toll-like receptor 2 (TLR) -196 to 174del polymorphism in gastro-duodenal diseases in Japanese population. 1793 43