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)

Gastroendoscopic biopsy specimens from 366 patients were stained with HE, Warthin-Starrys or Giemsa and mucin histochemical methods. Positive rate of Helicobacter pylori (HP) was 73.8% in chronic gastritis. Positive rates of HP in gastric ulcer disease were 88.2%, 91.9%, and 11.1% at the near and distant mucosa of ulcer and in duodenitis, respectively. Positive rates of HP in duodenal ulcer disease were 81.5%, 24.6% and 7.2% at the pyloric-antral area and at the near and distant mucosa of duodenal ulcer, respectively. The number of HP in active inflammation was higher than that in inactive inflammation (P < 0.05). The HP almost lived in the neutral mucin. There was no statistical significant difference between near and distant mucosa of ulcer (P > 0.05). HP might play an important role in the pathogenesis of chronic gastritis, and it might aggravate the peptic ulcer disease.
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PMID:[A study on the pathogenicity of Helicobacter pylori in chronic gastritis and peptic ulcer disease]. 145 59

One hundred eighty-nine consecutive gastric biopsies showing colonization by Helicobacter pylori (HP) were studied. Epigastric pain and bleeding were the clinical presentations in 167 cases (88.4%). Major endoscopic findings were gastritis (n = 72, 38.1%) and ulceration (n = 101, 53.4%). Duodenal ulcer was associated with 32 (44.4%) and 29 (28.7%) cases of gastritis and gastric ulcer, respectively. Histologically, the HP-colonized gastric epithelium showed characteristic degenerative changes that were topographically related to the bacteria but unrelated to the inflammatory infiltrate. Disintegration and loss of apical mucus with formation of epithelial pits was seen in nearly all cases. Other changes included microerosion, conventional erosion, and frank ulceration. Only the disintegration of apical mucus, epithelial pit, and microerosion were specific for HP colonization. These conditions were absent in areas not colonized by HP and in 79 consecutive HP-negative gastric biopsies seen during the same study period. The epithelial degenerative changes in HP-colonized gastric mucosa are easy to recognize in routine hematoxylin-eosin-stained sections and they could serve as histologic guides to the localization of the bacteria. It is proposed that HP-colonized gastric mucosa is a distinct pathologic entity with a pathologic spectrum ranging from active chronic gastritis to erosion and frank ulcer. Damage to the mucin-containing portion of the gastric epithelial cells appears to be the basic cytopathologic effect of HP on the gastric mucosa. As effective specific treatment for HP infection is available, identification of HP colonization in gastric biopsies should be attempted in all cases of gastritis and gastric ulcer.
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PMID:Pathologic changes of gastric mucosa colonized by Helicobacter pylori. 142 63

The distribution of lysozyme in normal and pathological human gastric and colonic mucosa was studied by light and electron microscopic immunocytochemical techniques and compared with histological and histochemical features. Lysozyme was localized in pyloric glandular epithelial cells, mucous neck cells of fundic glands, Paneth cells and some crypt cells of the mature colonic mucosa. In addition, lysozyme was detected in a large spectrum of "immature" or "regenerative" epithelium: neck cells of the gastric regenerative zone, undifferentiated columnar cells of surface and hyperplastic interfoveolar crests of the stomach, regenerative cells in a healed gastric ulcer, some goblet cells in incomplete intestinal metaplasia, cells of the regenerative zone at the bottom of colonic crypts and, finally, fetal intestinal epithelium. Electron microscopically, we localized lysozyme in the central core of mucous granules in the pyloric gastric glandular epithelium and in the dense mucous granules in gastric mucous neck cells. Lysozyme was also detected in some immature mucin-producing cells of the gastric regenerative zone and in the rough endoplasmic reticulum of surface hyperplastic columnar gastric cells. At the electron microscopic level, a peculiar correlation between the immunopattern of lysozyme and the morphology of mucous granules has been postulated. All our data support and extend the view that the presence of lysozyme may be related to cell immaturity as well as to a regenerative state of the cell. Finally, the lysozyme distribution and its relation to mucosubstances in gastric and colonic carcinoma suggest that lysozyme should not be considered an exclusive marker of cells of gastric derivation.
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PMID:Lysozyme localization in normal and diseased human gastric and colonic mucosa. A correlative histochemical, immunohistochemical and immunoelectron microscopic investigation. 164 44

To elucidate the role of Helicobacter pylori infection in the pathogenesis of gastric ulcer, we investigated the intracellular mucin content by measuring the periodic acid-Schiff-Alcian blue (PAS-AB)-stained substances, by means of computer, in the biopsy sample of gastric mucosa from patients with and without H. pylori infection. In the antral mucosa the intracellular PAS-AB-stained mucin content was significantly smaller in patients with infection than in patients without infection, whereas in the oxyntic gland mucosa the intracellular mucin content showed no significant change between patients with and without infection. In an animal study we investigated the effect of ammonia, which might be produced by H. pylori in the presence of urea. The ammonia, administered orally, caused a greater decrease of intracellular PAS-AB-stained mucin content in the gastric antral mucosa than in the body mucosa, in a dose-dependent manner. The results suggested that H. pylori infection had a different effect on the gastric mucosal intracellular PAS-AB-stained mucin and lowered specifically the antral intracellular PAS-AB-stained mucin content, possibly due to generation of ammonia by H. pylori.
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PMID:Different effect of Helicobacter pylori on the human gastric antral and body mucosal intracellular mucin. 170 31

Within the past decade, there has been an explosion of investigative activity and publications about Helicobacter pylori (H. pylori). Its role in gastroduodenal disease is becoming greater with definite etiologic association in chronic type B gastritis and a probable role in duodenal ulcer, a probable role in gastric ulcer, and possibly a factor in the development of interstitial type gastric carcinoma. Epidemiologic studies have shown H. pylori to be worldwide in distribution with higher prevalence rates and earlier initial infection rates in developing countries compared with industrialized nations. Person-to-person transmission appears to occur via the fecal-oral route. Pathogenesis of H. pylori-associated diseases remains unclear. We are, however, gaining insights into the role that H. pylori extracellular products play in damage to mucin and gastric epithelial cells as well as other gastroduodenal physiologic processes. Antimicrobial treatment, when effective, produces remission of mucosal pathologic changes and reduces duodenal recurrence rates. A major as yet unsolved problem is that there is no completely effective treatment regimen that consistently eradicates H. pylori in infected patients. Concepts of pathogenesis and future directions of research are discussed.
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PMID:Helicobacter pylori: current perspectives. 194 Jan 86

The mucus barrier is a layer of water-insoluble gel adherent to the gastroduodenal epithelium. In man most previous studies have focused on luminal mucus or histological assessment of presecreted, intracellular mucus--neither of which can be directly correlated with the protective capacity of the adherent mucus barrier. We here describe direct observation of adherent mucus thickness in man, and changes in peptic ulceration. Adherent mucus gel on human antral mucosa is a continuous homogeneous layer of variable thickness, in the range 50-450 microns (median 180 microns), comprising 67% polymeric mucin. In gastric ulcer patients, adherent antral mucus is significantly increased in thickness (median 240 microns), but is very heterogeneous and structurally a substantially weaker gel, comprising only 35% polymeric mucin. Adherent antral mucus from duodenal ulcer patients is homogeneous, significantly thinner (median 110 microns), and structurally a weaker gel, comprising 50% polymeric mucin. The adherent mucus layer from patients with gastric carcinoma resembled that from subjects with gastric ulcer in that it was very heterogeneous, of significantly increased thickness (median 240 microns) and structurally a very weak gel (23% polymeric mucin). These results are discussed in the context of gastroduodenal mucosal protection against acid and pepsin in the gastric juice.
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PMID:The adherent gastric mucus gel barrier in man and changes in peptic ulceration. 220 Apr 18

Histochemically differentiated mucins have been studied in the mucosal lining of the esophagus and the stomach. Acid mucin was differentiated from neutral mucin by the alcian blue/PAS technique and sulphomucin by the high iron diamine/alcian blue technique. Neutral mucin secreted normally by the stomach mucosa was replaced by acid mucin in 17 of the 19 mucin secreting adenocarcinomas involving the lower third of the esophagus, and in 24 of the 28 mucin secreting gastric adenocarcinomas studied. The intestinal metaplasia (IM) seen in the gastric mucosa associated with adenocarcinoma, chronic gastric ulcer and chronic gastritis was classified according to the type of mucin secreted by the goblet cells. IM secreting sulphomucins was seen to be associated with gastric adenocarcinoma.
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PMID:Mucin histochemistry of the upper gastrointestinal tract. 270 46

Campylobacter pylori, a spiral-shaped bacterium, commonly colonizes the gastric epithelium where it induces chronic gastritis; this organism has also been implicated in the etiology of chronic peptic ulcer disease. Once introduced to the gastric mucosa or an area of gastric metaplasia, it tends to migrate to the vicinity of the epithelial tight junction where it probably utilizes host urea and other substances to sustain itself. Campylobacter pylori also produces a proteolytic enzyme that degrades mucin. As the mucous layer slowly degrades, noxious luminal contents such as acid and pepsin have an opportunity to diffuse closer to the epithelium. We hypothesize that C. pylori, which is sensitive to low-pH environments, eventually migrates away from the compromised area to an area where the mucous layer is still protective. The injured epithelial focus left behind either regenerates its mucous layer and heals, or ulcerates depending upon the balance between other aggressive and protective factors. This interaction between C. pylori and the mucous layer is then repeated at the organism's new location. This hypothesis is consistent with existing data regarding C. pylori. It explains how C. pylori can be present in most duodenal ulcer patients and many gastric ulcer patients, as well as in otherwise healthy individuals. It also explains why ulceration is localized rather than diffuse when it does occur.
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PMID:Campylobacter pylori, mucus, and peptic ulceration. A dynamic interaction. 279 27

After the initial report of Marshall and Warren, several publications have also demonstrated the presence of pyloric campylobacter in an elevated percentage of cases of chronic gastritis and peptic ulcer. We present our experience studying 672 patients examined by esophagogastroduodenoscopy after referral to clinical because of upper gastrointestinal symptoms. We used an Olympus GIF-K2 panendoscope taking two biopsies from the gastric antrum. Specimens were stained with hematoxilin-eosin and silver. In our experience these methods have given us the best results in detecting this bacteria. Diagnosis of gastric and duodenal ulcer was made by endoscopic criteria and chronic gastritis diagnosed by histology. Chronic gastritis was categorized into active and inactive based in the invasion of polymorphonuclear into mucosa. We have also quantitated damage of the mucin producing cells as well as the degree of bacterial colonization. We have found pyloric campylobacter in 91.8% of patients suffering from chronic active gastritis, 72.7% of patients with diagnosis of gastric ulcer and 84.2% of cases of duodenal ulcer. Our results agree with the ones reported by other authors. We conclude that pyloric campylobacter is not an opportunist microorganism within the stomach because it produces inflammatory changes as well as damage of the mucin producing cells. Its presence may play some role in the etiology of gastritis and peptic ulcer disease.
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PMID:[Campylobacter pyloric, chronic gastritis, gastric ulcer and duodenal ulcer]. 332 2

Ulcer formation after pylorus ligation was assessed in control, testosterone treated and castrated male rats after cimetidine treatment. The stomach was studied for incidence of ulcers and its contents analysed for pH, volume, total acidity, free acidity, pepsin and mucin activity. Testosterone and cimetidine when used alone protected from ulceration while when used in combination the degree of protection was decreased. Castration per se ead no effect on ulcer index but potentiated cimetidine induced gastric ulcer protection.
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PMID:Relevance of male hormonal status with antiulcer effect of cimetidine in pylorus ligated rats. 345 Jun 32


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