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

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

Helicobacter pylori infection has been associated with gastritis, duodenal ulcer, gastric ulcer, and the epidemic form of gastric carcinoma. Eradication of H. pylori infection has proven to be difficult. Recently, combinations of antimicrobial drugs have been shown to eradicate greater than 50% of infections; however, the results have proven variable, and the factors influencing effectiveness of therapy are unclear. In the present study, the effectiveness of a triple therapy for eradication of H. pylori infection was evaluated. Triple therapy consisted of 2 g tetracycline, 750 mg metronidazole, and five or eight tablets of bismuth subsalicylate daily in 93 patients (70 with duodenal ulcer, 17 with gastric ulcer, and 6 with simple H. pylori gastritis). Combinations of a sensitive urea breath test, serology, culture, and histology were used to confirm the presence of infection, eradication, or relapse. Eradication was defined as inability to show H. pylori greater than or equal to 1 month after ending therapy. The overall eradication rate was 87%. The factors evaluated for their effect on predicting eradication included age, gender, type of disease, duration of therapy, amount of bismuth subsalicylate [five or eight Pepto-Bismol tablets daily (Procter & Gamble, Cincinnati, OH)], and compliance with the prescribed medications. Stepwise regression showed that compliance was the most important factor predicting success; the success rate was 96% for patients who took greater than 60% of the prescribed medications and 69% for patients who took less. For those taking greater than 60% of the prescribed therapy, the eradication rates were similar (a) for patients receiving therapy for 14 days or when tetracycline and bismuth subsalicylate were taken for an additional 14 days; (b) for patients with duodenal ulcer, gastric ulcer, and simple H. pylori gastritis; and (c) whether five or eight bismuth subsalicylate tablets were taken. It is concluded that triple therapy is effective for eradication of H. pylori and that future studies need to take compliance into account for comparisons between regimens.
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PMID:Factors influencing the eradication of Helicobacter pylori with triple therapy. 173 20

Helicobacter pylori is a microaerophilic, Gram-negative, spiral rod, the role of which in different gastric diseases has been investigated worldwide since the beginning of the 1980s. H. pylori has been shown to be the causative agent in active chronic gastritis, and it is regularly found in patients endoscopied for duodenal ulcer. The bacterium is also frequently isolated from persons with gastric ulcer, gastric carcinoma and non-ulcer dyspepsia. Apart from cultivation of the bacterium, other diagnostic procedures include various staining methods and urease tests of gastric biopsy samples. The application of non-invasive diagnostic methods, serology and urea breath tests, is rapidly increasing. H. pylori is susceptible to several antimicrobials in vitro, but eradication of the bacterium from the gastric mucosa is not always achieved. The best results until now have been obtained with the combined use of bismuth salts and two antibiotics. In active chronic gastritis and duodenal ulcer patients, eradication of the bacteria has resulted in healing of the disease with permanent decrease of circulating antibodies and negative urease tests. H. pylori has been found worldwide and the infection shows an age-dependent increase. Man, apparently, is the reservoir of the bacterium, but the exact mechanisms of interhuman transmission are still not defined.
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PMID:Helicobacter pylori and associated gastroduodenal diseases. Review article. 185 43

Ammonia, released in the gastric mucosa by the action of Helicobacter pylori urease on transuded plasma urea, curtails the biosynthesis of mucus and/or causes the mucus to be disassembled at the mucosal surface. These changes facilitate colonisation by H pylori and may promote gastric ulcer formation.
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PMID:Hypothesis: Helicobacter pylori, urease, mucus, and gastric ulcer. 196 87

We examined the morphological changes in gastric mucosa and the generation of ammonia after exposure of the rat stomach to urea in the presence of urease, in attempts to investigate a pathophysiological role of urea, urease, and ammonia system in gastric ulcer diseases. Exposure of the stomach for 20 min to 2 ml urea (0.025-0.2%) together with urease (100 IU) induced histological damages in a concentration-related manner. Either urea or urease alone did not induce any histological change in the mucosa. Instillation of urea into the stomach generated ammonia in the presence of urease; the amount of ammonia was increased depending on the concentration of urea, and was closely associated with the severity of histological damage. The exposure of the stomach to ammonia (NH4OH: 0.01-0.1%) also produced histological damages in the gastric mucosa in a concentration-related manner. The characteristics of injury induced by 0.5-1.0% ammonia were stasis of microcirculation, disruption of the surface epithelial cells, and necrosis of the mucosa. These results demonstrated that ammonia generated from the hydrolysis of urea by urease in the stomach causes damages in the gastric mucosa.
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PMID:Generation of ammonia and mucosal lesion formation following hydrolysis of urea by urease in the rat stomach. 221 35

Campylobacter pylori has been associated with gastro-duodenal inflammatory disease. Ninety-five adults with dyspepsia were examined for the presence of C. pylori in the gastric antrum and near gastric or duodenal ulcers (when present) by means of culture, Gram and acridine orange stains, and urease activity of biopsies. C. pylori was identified from 51 out of 67 patients with chronic gastritis, from 9 out of 9 patients with duodenal ulcer, and from 8 out of 10 patients with gastric ulcer. Acridine orange stain revealed the highest number of positive cases, followed by culture, Gram stain and urease test. The latter showed a 100% specificity when carried out with a selective urea broth containing colistin, trimethoprim, vancomycin and amphotericin B. It has to be considered a further diagnostic tool which enables clinicians and microbiologists to diagnose the etiology of a dyspeptic syndrome even at the patient's bedside.
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PMID:[Comparison of methods for the identification of Campylobacter pylori in gastric biopsies of patients with dyspepsia]. 245 24

Campylobacter pylori has been cultured from 85-90% of antral biopsies of patients of gastritis, duodenal ulcer and gastric ulcer at different centres in the world. It has been now firmly implicated in the aetiology of active gastritis as well as suspected to cause repeated recurrences of peptic ulcers. However, the organism is very fastidious and is difficult to grow by standard culture methods as a result of which low positivity is often obtained even in well equipped centres. The rapid biopsy urease test for the diagnosis of C pylori infection, in which the biopsy is directly cultured in a solid medium containing urea, is a very simple test. A change in colour indicates the growth of the organism. This test is 100% specific and 98% sensitive. We performed this test in 100 patients; 93 of gastritis, 6 of DU and 1 of GU during a three month period. 87 of 93 cases of gastritis (90%) and all 6 cases of DU (100%) were positive. The single case of gastric ulcer was negative. Treatment of C pylori positive cases showed that they responded poorly to 4 weeks therapy with tinidazole; 33% were cured after 2 weeks of 1.5 g amoxycillin daily, but all responded when the therapy was continued for 4 weeks.
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PMID:Rapid diagnostic test of Campylobacter pylori infection in patients of gastritis, duodenal ulcer and gastric ulcer. A study of 100 cases. 261 35

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

Campylobacter pylori infection has been associated with duodenal ulcer, gastric ulcer, and non-ulcer dyspepsia. Although in vitro studies have shown that C. pylori is susceptible to most commonly used antibiotics, predictions from in vitro sensitivity studies have not led to a safe and generally effective therapy; C. pylori has proved to be very difficult to eradicate in vivo. We used the urea breath test to assess the susceptibility of C. pylori in vivo to various drugs. C. pylori was susceptible to bismuth subsalicylate, bismuth subnitrate, and furazolidone. C. pylori was not susceptible (i.e., urease activity remained despite administration of the drug) to the following drugs: 1) antiulcer agents (cimetidine, ranitidine, famotidine, omeprazole, misoprostol, sucralfate, liquid antacids); 2) NSAIDs (aspirin, indomethacin, ibuprofen, naproxen, tolmetin); 3) antibiotics (oral penicillin V, trimethoprim-sulfamethoxazole, dicloxacillin); 4) salts (lithium, ferrous sulfate, gold); 5) miscellaneous (acetaminophen, phenytoin, hydrochlorothiazide, propranolol, metoprolol, metoclopramide, ursodeoxycholic acid). Oral antimicrobials can be administered directly onto the site of infection, so that a very low oral dose will provide many multiples of the in vitro minimal inhibitory concentration. Furazolidone suspension (7 mg) was administered seven times daily (daily dose 49 mg) to three individuals infected by C. pylori during suppression of gastric acid secretion with famotidine (40 mg bid). After 4 days, all subjects had significant reductions in urease activity (two to normal and one to a borderline value). This response suggested that very low-dose therapy may be useful either alone or combined with bismuth. Conclusive establishment of an etiologic (or major contributory) relationship of C. pylori to ulcer disease will require a safe and reliable method to eradicate the organism from the stomach and duodenum.
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PMID:In vivo susceptibility of Campylobacter pylori. 291 80

Campylobacter pylori has been associated with gastritis, duodenal ulcer, gastric ulcer, and nonulcer dyspepsia. Evidence that C. pylori may be the causative agent or at least a major contributory factor in peptic ulcer disease has generated intense interest in the development of reliable methods for detecting C. pylori infections. We have developed a specific and sensitive enzyme-linked immunosorbent assay (ELISA) that detects serum immunoglobulin G antibodies directed against high molecular weight cell-associated proteins (HM-CAP) of C. pylori. In a blinded fashion we tested sera from 300 individuals and found that all of 147 HM-CAP ELISA-negative individuals were also negative for C. pylori, as documented by a negative urea breath test; also, 151 of 153 C. pylori-positive (by urea breath test) individuals were HM-CAP ELISA-positive. Campylobacter pylori was cultured from the two ELISA-negative but infected patients and these isolates did possess HM-CAP antigens, showing that these two individuals had failed to seroconvert. Thus, the specificity and positive predictive value of the HM-CAP ELISA were each 100%; the sensitivity of the assay was 98.7%, and the negative predictive value was 98.6%. The HM-CAP ELISA and the urea breath test both proved valuable for detecting C. pylori infection, the urea breath test being a more direct method whereas the ELISA is less expensive and easier to perform. Furthermore, the results of a serologic test such as the HM-CAP ELISA would not be influenced by recent ingestion of bismuth compounds or antimicrobial therapy, which might suppress C. pylori and cause a transient false-negative result in the urea breath test.
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PMID:A sensitive and specific serologic test for detection of Campylobacter pylori infection. 277 37


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