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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic gastritis is a common inflammatory disease. In a number of patients, the inflamed gastric mucosa shows a gradual tendency to become atrophic (atrophic gastritis). Gastritis tends to be lifelong, and spontaneous healing is rare. With very few exceptions (e.g. in patients with autoimmune chronic corpus gastritis), gastritis is associated with the presence of the bacterium Helicobacter pylori. Inflammation and atrophy of the gastric mucosa result in impairment of gastric secretory functions (e.g. secretion of gastric acid, pepsin and gastrin). Such impairment is dependent on the topographic type of gastritis; i.e. whether the inflammation and atrophy occur in the antrum (chronic antral gastritis), corpus (chronic corpus gastritis) or in both the antrum and corpus simultaneously (chronic pangastritis). Gastritis of different topographic types associates with different gastric diseases. In patients with H. pylori-related antral or pangastritis, peptic ulcer disease, and in particular duodenal ulcer, is common (with an incidence exceeding 20% after 10 years' follow-up), as compared with peptic ulcer disease, which is very rare in patients with a normal stomach. Gastric ulcer may sometimes occur in patients with a rather atrophic stomach, but both gastric and duodenal ulcers are extremely rare in patients in whom the gastritis accompanies severe atrophic changes in the corpus mucosa. Routine biopsies from the antrum and corpus, and interpretation of the results in the light of the data on gastritis and its atrophic sequelae, allow the gastroenterologist to predict the risk and likelihood of peptic ulcer disease in patients with gastritis.
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PMID:Natural history of gastritis and its relationship to peptic ulcer disease. 139 47

The effects of a weakly acidic polysaccharide fraction, GL-4, from the leaves of Panax ginseng C. A. Meyer on various experimental gastric ulcer models in mice and rats have been studied. Oral administration of GL-4 at doses of 50 to 200 mg/kg inhibited the formation of the gastric lesions induced by necrotizing agents such as HCl/ethanol and ethanol in a dose-dependent manner. This protective effect was observed not only upon oral but also upon subcutaneous administration of GL-4 (50-100 mg/kg). GL-4 also inhibited the formation of gastric ulcers which were induced by water immersion stress, indomethacin, or pylorus-ligation. The contents of prostaglandin E2 in the gastric juice from rats were not influenced by oral administration of GL-4. The protective action of GL-4 against HCl/ethanol-induced gastric lesions was not abolished by pretreatment with indomethacin. When GL-4 (100 mg/kg, p.o.) was administered into pylorus-ligated rats, both gastric acidity and pepsin activity in the gastric juice decreased significantly.
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PMID:Anti-ulcer activity and mode of action of the polysaccharide fraction from the leaves of Panax ginseng. 147 Jun 67

We have recently reported that basic fibroblast growth factor (bFGF) acts in the brain to inhibit the secretion of gastric acid and pepsin, two major aggressive factors in the pathogenesis of gastric ulcer formation. In the present study, we determined whether or not bFGF has an anti-ulcer action via the central nervous system, using male Wistar rats. The intracisternal injection of bFGF dose-dependently (0.1-1.0 microgram(s)/rat) inhibited the severity of gastric ulcers induced by water-immersion restraint stress or central thyrotropin-releasing hormone. The same doses of peripherally injected bFGF failed to protect the gastric mucosa from these ulcerogenic procedures. These results suggest for the first time that bFGF has a mucosal protective effect through a mechanism involving the central nervous system. It is speculated that this anti-ulcer action of bFGF is, at least in part, dependent upon its gastric antisecretory effect.
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PMID:Central basic fibroblast growth factor inhibits gastric ulcer formation in rats. 190 25

Hydrogen clearance was used to assess blood flow in fundal and antral gastric mucosa as well as in the lobule of the auricle in 127 patients with ulcer (99 duodenal and 28 gastric ulcer cases), 34 patients with gastric, duodenal, pancreatic and biliary ++non-ulcer lesions against 20 healthy subjects. The findings underwent analysis in relation to the disease form and phase, baseline characteristics of the mucosa (morphological, functional and bacteriological) and changes in them in response to pentagastrin (6 micrograms/kg), alupent (0.0075 mg/kg), clofelin (0.0015 mg/kg) administration. For ulcer involving the body of the stomach and sutured perforated duodenal ulcer, fundal and antral mucosa blood flow showed a decrease by 1/3, the lowest values presenting in the active disease phase. Diminution in gastric mucosa blood flow correlated with gravity of its gastritic lesion and was not directly related to its Campylobacter contamination. Pentagastrin stimulated blood flow in fundic mucosa and led to its 30% increase whereas the flow intensity remained unaffected in the antral mucosa and skin (lobule of the auricle). Acid production in response to pentagastrin introduction rose 3.5-fold, pepsin 2.1-fold. Alupent and clofelin do not affect blood flow causing a 30-50% increase and decrease in acid and pepsin production, respectively. Separate neurohumoral regulation of gastric mucosa blood flow and secretory activity of the latter permits differential correction of each of the impaired functions.
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PMID:[Characteristics of blood flow in the gastric mucosa in relation to its structure and function in patients with peptic ulcer]. 194 70

Despite extensive research, the etiology of peptic ulcer disease remains unclear. Given the multiple processes that control acid and pepsin secretion and defense and repair of the gastroduodenal mucosa, it is likely that the cause of ulceration differs between individuals. Acid and pepsin appear to be necessary but not sufficient ingredients in the ulcerative process. It is clear that the majority of gastric ulcers and a substantial number of duodenal ulcers do not have increased gastric acid secretion. Recent research has focused more on protection and repair of the stomach and duodenum. NSAIDs cause a significant number of gastric and duodenal ulcers; this is probably due to inhibition of prostaglandin production with loss of its protective effects. In the absence of NSAIDs and gastrinoma, it appears that most gastric ulcers and all duodenal ulcers occur in the setting of H. pylori infection. Evidence is mounting in support of H. pylori as a necessary ingredient in the ulcerative process, similar to acid and pepsin. It is not known whether the bacteria or the accompanying inflammation is the more important factor in the pathophysiology. Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity. These facts suggest the following process: increased peptic activity coupled with decreased duodenal buffering capacity may lead to increased mucosal injury and result in gastric metaplasia. In the presence of antral H. pylori, the gastric metaplasia can become colonized and inflamed. The inflammation or the infection itself then disrupts the process of mucosal defense or regeneration resulting in ulceration. A cycle of further injury and increased inflammation with loss of the framework for regeneration may then cause a chronic ulcer. Gastric ulcer often occurs with decreased acid-peptic activity, suggesting that mucosal defensive impairments are more important. The combination of inflammation, protective deficiencies, and moderate amounts of acid and pepsin may be enough to induce ulceration. Many questions remain in understanding the pathophysiology of peptic ulcer disease. The physiology and pathophysiology of mucosal regeneration and the mechanisms by which H. pylori and inflammation disrupt normal gastroduodenal function will be fruitful areas of future investigation.
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PMID:Peptic ulcer pathophysiology. 207 87

Clonidine 2 mg/kg ig inhibited the rat gastric ulcers induced by pyloric ligation, stress and indomethacin by 71%, 77% and 82%, respectively. Clonidine 2 mg/kg ig tended to accelerate the healing of gastric ulcer induced by acetic acid, and the healing rate was 61%. Clonidine decreased the secretion of gastric acid and pepsin, and increased the release of gastric barrier mucus. These actions may contribute to its protective effect against ulceration.
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PMID:[Effects of clonidine on experimental stomach ulcer in rats]. 213 Jun 4

Zinc sulfadiazine (ZnSD) 50, 100, 200 mg/kg ig inhibited the formation of gastric ulcer induced by indomethacin, stress and pyloric ligation in rats respectively and showed dose-dependently. ZnSD 200 mg/kg ig accelerated the healing of gastric ulcer induced by acetic acid. ZnSD 25 mg/kg ig was effective in preventing ethanol-induced damage of rat gastric mucosa. The amount of gastric mucus glycoprotein in gastric tissues was increased by ZnSD. In general, ZnSD did not influence the volume of gastric juice and pepsin output, but ZnSD 200 mg/kg ig decreased gastric acidity. In vitro, ZnSD also influenced the neutralization of acid. It is suggested that antiulcer action of ZnSD may be related to its preservation of the gastric mucosal barrier and neutralization of acid.
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PMID:[Anti-gastric ulcer activity of zinc sulfadiazine in rats]. 213 Jun 5

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

In the present paper, effects of scopolia drugs (scopolamine, anisodine, anisodamine) on experimental gastric mucosal lesion models in rats were investigated. Scopolia drugs were found to be effective anti-ulcer agents in three experimental gastric ulcer models (i.e. cold-restraint stress induced ulcer, indomethacin induced ulcer and acetic acid induced chronic ulcer) in rats in a dose dependent manner. Biochemical analysis of gastric juice and blood showed that scopolia drugs could inhibit gastric acid secretion and pepsin activity, increase gastric barrier mucus and concentration of serum gastrin, suggesting that these actions may contribute to its anti-ulcer effect.
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PMID:[Effect of scopolia drugs on the gastric mucosal lesion in rats]. 223 28

408 cases of chronic superficial gastritis diagnosed by fibergastroscopy and histology were treated with Wei-Nin granules (WNG), The symptomatic effective rate was 90.5%, while therapeutic effect proved by gastroscopy and histology was 81.9% and 72.8% respectively. These results compared with the control were statistically significant. In animal experiment, it is shown that WNG had an evident protective effect to the mucous membrane of rats and guinea pigs. These animals had suffered gastritis and gastric ulcer induced by drugs. The effect of WNG was similar to cimetidin. The pharmaceutical mechanism of WNG proved that it could inhibit the secretion of pepsin. The acute and chronic poisoning test was negative both in vitro and in vivo. WNG were nearly no any side effects in this study. Therefore it is a new type of herbs in treatment of chronic superficial gastritis and is different from H2-receptor inhibitor.
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PMID:[Clinical and experimental study of wei-nin granules in the treatment of chronic superficial gastritis]. 239 40


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