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)

The Mongolian gerbil model for Helicobacter pylori infection is an animal model that mimics human disease. We examined the serum immune response to H. pylori infection in gerbils by enzyme-linked immunosorbent assay (ELISA) and Western blotting, both with whole-cell (H. pylori) extracts. A total of 66 7-week-old specific-pathogen-free male gerbils were inoculated orogastrically with H. pylori strain ATCC 43504. Sera were collected 1, 2, 4, 8, 12, 26, 38, and 52 weeks after H. pylori inoculation. Sixty-nine noninfected gerbils and their sera were used as controls. The specificity of the ELISA was 95.7%. The frequency of seropositivity increased over time: 2 of 10 (20%), 7 of 10 (70%), and 7 of 7 (100%) samples of sera from inoculated gerbils were positive for H. pylori at 2, 4, and 8 weeks postinoculation, respectively. Western blot assays showed that the primary immunoglobulin G (IgG) response against low-molecular-mass (25-, 30-, and 20-kDa) proteins appeared after a lag period of 2 to 8 weeks after inoculation. Antibodies against 160-, 150-, 110-, 120-, 80-, 66-, and 63-kDa proteins were observed 12 weeks after inoculation. The early reactive 30-kDa protein was identified as a urease alpha subunit by N-terminal amino acid sequencing. After 26 weeks, two groups of animals could be distinguished: one group developed ulcers (n = 5), and the other developed hyperplastic polyps without ulcers (n = 19). Gerbils in the gastric ulcer group showed significantly higher serum anti-H. pylori IgG levels than did gerbils in the hyperplastic group (P = 0.001) as measured by ELISA. Furthermore, a higher proportion of animals developed antibodies to H. pylori proteins of 26, 25, and 20 kDa in the ulcer group than those animals with hyperplastic polyps (75 to 100% versus 17 to 50%) in Western blot assays. These results highlight the importance of the immune response of the host in the development of H. pylori-related gastric lesions.
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PMID:Serum immunoglobulin G immune response to Helicobacter pylori antigens in Mongolian gerbils. 1128 42

The results of the in vitro metronidazole resistance on Helicobacter pylori (H. pylori) eradication have been inconclusive. Metronidazole resistance varies among different geographical locations and a previous study from Thailand reported an in vitro metronidazole resistance of H. pylori of 51 per cent. This study was designed to investigate further the effect of the in vitro metronidazole resistance on the outcome of eradication of H. pylori in the Thai population. Fifty two patients with active gastric ulcer (GU) and duodenal ulcer (DU) who had positive culture for H. pylori were studied. All of these patients had positive rapid urease test (CLO test, Delta West, Australia) using gastric biopsy specimens from the antrum and body taken at the time of initial upper endoscopy. In vitro antimicrobial susceptibility test was performed using Epsilometer test (AB Biodisk, Solna, Sweden). All patients received a one-week triple regimen consisting of omeprazole 20 mg twice daily, clarithromycin 500 mg twice daily, metronidazole 500 mg twice daily. Patients with GU continued with another five weeks of omeprazole 20 mg twice daily and patients with DU received another three weeks of omeprazole 20 mg twice daily. Upper endoscopy was repeated at four weeks after the end of the treatment. Three antral and two body biopsy specimens were obtained for identification of H. pylori using CLO test, histology (modified Giemsa stain) and culture. All of these tests had to be negative to confirm a successful eradication. Metronidazole-resistant (MR) strains with MIC > or = 32 mg/l were identified in 27 of the 52 patients (51.92%), whereas, metronidazole-susceptible (MS) strains were isolated from 25 patients (48.08%). Five patients were lost to follow-up and one patient had drug allergy. Successful eradication as defined by negative CLO test, histology and culture was attained in 17/23 (73.91%) patients (GU = 6, DU = 16, GU and DU = 1) with MR strains. 20 out of 23 (86.96%) patients (GU = 9, DU = 12 GU and DU = 2) who had MS strains. The difference was not statistically significant in both groups (P > 0.05). The ulcer healing was, however, highly achieved in both groups (MS = 95.65%, MR = 91.30%, P > 0.05). In vitro metronidazole resistance was high in this population group although this does not predict the outcome of eradication in patients with GU and DU.
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PMID:Eradication rates of Helicobacter pylori between metronidazole-sensitive and metronidazole-resistant strains with metronidazole containing regimen in Thai patients with peptic ulcer disease. 1152 78

Gastroscopy is the preferred method of diagnosis of upper gastrointestinal (UGI) disorders which often present with dyspepsia. Since the discovery of helicobacter pylori (H. pylori) as an important aetiological agent in gastroduodenal disease, investigation for this organism during UGI endoscopy has become a standard clinical practice. We have studied a large number of Nigerian patients with dyspeptic symptoms referred for endoscopy for the spectrum of gastroduodenal diseases and the incidence of H. pylori infection. Detection of H. pylori was done on gastric muscosal biopsies either by the Campylobacter-Like Organism (CLO)-urease test or by histropathology. A total of 834 patients were studied out of which 268 were investigated for H. pylori. A hundred and ninety-five patients (73%) were positive for H. pylori and the peak age was in the fourth decade. Duodenal ulcer (DU) was the most common endoscopic finding (38.7%). The incidence of H. pylori infection was 76% among patients with DU, gastritis, gastroduodenitis and gastric outlet obstruction. However, all the anterior and pyloric channel Duus tested for H. pylori were positive gastric ulcer (GU) was diagnosed in only 4.7% of patients but 82% of them tested for H. pylori were positive. H. pylori was significantly associated with GU occurring with gastritis. Gastric carcinoma was diagnosed in 52 patients (6.2%) and 50% of those tested for H. pylori were positive. This study shows that H. pylori plays an important role in the aetiopathogenesis of peptic ulcer disease among Nigerian patients and that the diagnosis of anterior and pyloric channel Duus or gastroesophageal polyp disease may be an indicator of massive H. pylori infection.
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PMID:Upper gastrointestinal findings and incidence of Helicobacter pylori infection among Nigerian patients with dyspepsia. 1176 14

The discovery of Helicobacter pylori (H. pylori) has revolutionised the pathophysiological and clinical approach to gastric and duodenal ulcer. Since the first paper identifying H. pylori was published only 19-20 years ago, it has been found out that this bacterium causes probably the commonest human infection. Like other revolutions in history, the original directions of the H. pylori story have changed in response to conflicting ideologies, observation, and practices. It is known that once H. pylori is acquired, colonisation continues for life unless the organism is eliminated by antimicrobial treatment or by the usually late-in-life development of the atrophic gastritis. If any recent achievement in the world of medicine is to be called revolutionary, then it is the discovery of the role of this spiral bacterium in the etiopathogenesis of gastritis, gastric ulcer, duodenal ulcer, gastric adenocarcinomas and gastric mucosa-associated lymphoid type (MALT) B-cell lymphomas. Essentially everyone who carries the organism in the gastric mucous layer has evidence of tissue reaction (termed chronic active gastritis), but most colonised persons remain asymptomatic for life. In the absence of treatment, the presence of H. pylori can be determined with a high degree of confidence by endoscopy (with culture, histologic examination, or urease testing of gastric biopsy specimens), by serologic testing, or by urea breath tests. After successful treatment, specific antibody levels decrease so slowly that serologic testing cannot be used to document success for at least 6 months. In most patients, elimination of H. pylori changes the natural history of peptic ulcer disease and of gastric MALT lymphomas. It is now recommended that these patients have to be treated to eliminate H. pylori because the benefits seem to substantially outweigh the risks and costs. Currently, enthusiasts, drug companies, and the lay press are putting pressure on physicians to eliminate H. pylori from all patients, symptomatic or not, in whom it is detected. There is little evidence that this is appropriate, and management will continue to change as new knowledge emerges and socioeconomic environments change in ways that are relevant to H. pylori and clinical medicine.
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PMID:[Is the only good Helicobacter a dead Helicobacter?]. 1205 16

The aim of the study was to demonstrate the sensitivity, specificity and accuracy of gastric juice urease test and brushing-urease test compared to the biopsy-urease test for Helicobacter pylori (H. pylori) detection. For each patient, two milliliters of gastric juice was collected and one milliliter in the supernatant was tested for rapid urease reactions. One gastric mucus brushing and two biopsies were taken from the body and the antrum. The brushing specimens were tested for rapid urease reaction by shaking the brush into the urea broth. The gold standards for diagnosing of H. pylori are positive H. pylori upon specimen culture or positive identification of H. pylori from polymerase chain reaction (PCR) assay using primer for vac A gene. Forty patients were enrolled in the study including ten patients with gastric ulcer, six patients with duodenal ulcer and twenty four patients with non-ulcer dyspepsia. Brushing-urease test and biopsy-urease test were not different sensitivity (87.50% vs 93.20%), specificity (100% vs 100%) and accuracy (90.25% vs 95.50%). The gastric juice urease test had a sensitivity of 65.25 per cent, specificity of 100 per cent and accuracy of 75 per cent for detecting of H. pylori infection. In conclusion, gastric juice urease test had low sensitivity in the diagnosis of H. pylori infection. Brushing-urease test is as accurate as biopsy-urease test in detecting H. pylori infection. However, the brushing method had lower gastric tissue injury than the biopsy and so should be used for detecting H. pylori infection in patients with coagulopathy.
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PMID:Gastric juice urease test and brushing urease test for Helicobacter pylori detection. 1218 55

Gastric Helicobacter pylori (H. pylon) plays an important role in the pathogenesis of duodenal ulcer (DU), although not all H. pylori infected persons will develop disease. Duodenal H. pylori was supposed to be one of the factors related with DU. The aim of this study was to investigate whether H. pylori in the duodenum of patients with DU plays a critical role in the pathogenesis of DU regarding the gastric H. pylori status. Furthermore, it was to determine the prevalence of duodenal H. pylori infection in Thailand. Ninety three patients were included in the study. They underwent gastroscopic evaluation for dyspeptic symptoms and none of them had previous H. pylori eradication therapy. An upper gastrointestinal endoscopy was performed and two specimens were collected each form the antrum, midcorpus and duodenal bulb in order to diagnose H. pylori infection. The gold standard for H. pylori detection is a positive specimen culture or polymerase chain reaction (PCR) assay for the vac A gene or positive urease test plus H. pylori seen in the pathology. Ninety three dyspeptic patients (43 males and 50 females; mean age 48.2 years; range 22 to 79 years) were included in the study. Duodenal H. pylori was detected in 31/93 (33.33%) patients which included 15 (48.38%) patients with duodenal ulcer, 2 (6.45%) patients with gastric ulcer and 14 (45.16%) patients with NUD. Five of thirty one (16.21%) patients with duodenal H. pylori infection had negative gastric H. pylori. These five patients included 1 with DU, 1 with DU and 3 with NUD. Duodenal H. pylori was associated with DU dependent of the presence of gastric H. pylori (p<0.05) and there was no association between duodenal H. pylori with negative gastric H. pylori and duodenal ulcer (p>0.05). Duodenal H. pylori is associated with duodenal ulcer dependent on the presence of gastric H. pylori. These results suggest that transmission of gastric H. pylori to the duodenum was prerequisited for the formation of DU.
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PMID:Duodenal Helicobacter pylori associated duodenal ulcer depend on gastric Helicobacter pylori status. 1218 59

Since Marshall's discovery before 20 years, Helicobacter pylori (H. pylori) infection is reportedly to be associated with a variety of clinical outcomes including peptic ulcer disease and gastric cancer. The first step of the H. pylori colonization might be its adhesion to the surface epithelial cells, which evokes gastric inflammatory events initiated by neutrophil recruitment from the microcirculation. Mongolian gerbil is one of the suitable animal models for H. pylori infection, which exerts gastric ulcer and cancer with its bacterial infection. In H. pylori-colonized gerbils, extensive levels of microvascular leukocyte adhesion and migration into the parenchymal side and significant levels of inflammatory cell infiltration are encountered. Bacterial urease not only neutralizes gastric luminal acid, but also plays as an adhesion factor to the surface epithelium. Recently, such an adhesion to the epithelium is reported to be important for bacterial type IV secretory system, which intermediates Cag A injection into the epithelial cells. Then, multiple chemokine and cytokine networks are activated and mucosal inflammatory lesion formation would be completed. In the long-term colonization of H. pylori, gastric mucosal cell turnover would be modified due to persistent inflammation and then such deregulation of cell turnover might link to the precancerous lesion formation.
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PMID:Gastric mucosal response to Helicobacter pylori. 1252 36

Gastric Helicobacter pylori (Hp) infection in Mongolian gerbils is an established experimental model of gastric carcinogenesis resulting from the long-term Hp infection but functional aspects accompanying this Hp-induced progression from gastritis to the cancer, especially changes in gastric acid secretion, gastric blood flow (GBF) and gastrin-somatostatin link have been little studied. It is unclear whether Hp eradication therapy alters the functional and the histopathological changes in this animal model of Hp-infection. We examined the effects of intragastric (i.g.) inoculation of Mongolian gerbils with Hp strain (cagA+ vacA+, 5 x 10(6) CFU/ml) that had been isolated from a patient with gastric ulcer as compared to those induced by vehicle (saline) in gerbils with or without gastric fistula (GF) at 1.2, 4, 6, 9, 12 and 30 wks upon gastric inoculation with this bacteria. An attempt was made to evaluate the influence of anti-Hp triple therapy with omeprazole, amoxicillin and tinidazol on gastric Hp-infection and Hp-induced functional impairment of the gastric mucosa. Gastric mucosal biopsy specimens were taken for the assessment of the morphological changes and the presence of Hp infection using rapid urease test (CLO-test) and the density of Hp-colonization were assessed by counting of the number of bacterial colonies per plate. Gastric blood flow (GBF) was measured by H2-gas clearance technique and the venous blood and the gastric content were collected for the measurement of plasma gastrin levels and the gastric luminal somatostatin level by radioimmunoassay (RIA). The Hp in gastric mucosa was detected in all animals by culture and rapid urease test at various periods upon Hp inoculation. Basal gastric acid in non-infected conscious gerbils with GF reached the level of about 28 +/- 4 micromol/h and this was reduced by over 50% immediately upon the Hp-inoculation and persisted for time intervals tested up to 30 wk. Early lesions were seen 4 wks after the Hp-inoculation and consisted of chronic gastritis with thickened gastric mucosal foldings and elongated interfoveolar ridges. Edema and congestion as well as significant mucosal inflammatory infiltration with lymphoid infiltrate in lamina propria of the mucosa occurred in all infected gerbils. Adenomatous hyperplasia with cellular atypia was observed at 12 wk upon Hp-inoculation together with increased mitotic activity and numerous apoptotic bodies formation, while lamina propria was reduced leaving dilated atypical gastric gland situated "back-to-back". This glandular atypia failed to show lamina propria or submucosa infiltration corresponding to gastric intraepithelial neoplasia. The GBF in Hp-infected gerbils was significantly lower, and a 6-7 fold increase in plasma gastrin levels combined with a significant fall in gastric luminal somatostatin contents observed at all tested periods as compared to vehicle-controls and these effects were counteracted by anti-Hp triple therapy. We conclude that: 1). Hp-infection in Mongolian gerbils in early stages before adenocarcinoma formation results in the development of typical functional and pathological changes such as suppression of gastric secretion and impairment of both, gastric mucosal microcirculation and gastrin-somatostatin link, and 2). this deleterious influence of Hp on gastric morphology and gastric functions is greatly attenuated in gerbils treated with Hp-eradication therapy.
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PMID:Triple eradication therapy counteracts functional impairment associated with Helicobacter pylori infection in Mongolian gerbils. 1267 17

An antibody precipitating urease was found in 171 out of 180 human sera. Data obtained on limited material (50 cases) suggest that the anti-urease titre is appreciably higher in the serum of patients suffering from gastric ulcer. This is a pointer towards a possible antigen-antibody mechanism in the genesis of chronic gastric ulceration.
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PMID:AN ANTIBODY PRECIPITATING UREASE AND ITS POSSIBLE RELATION TO GASTRIC ULCER. 1408 40

The purpose of the study was to examine particular features of the clinical course of stomach ulcer (SU) and duodenal ulcer (DU) in conjunction with bronchial asthma (BA) in elder patients. We examined 59 patients with BA in conjunction with SU and DU at the age of 69-89 (46 males and 13 females). All patients underwent esophagogastroduodenoscopy (EGDS) and H. pylori examination of tissue samplings from the mucous coat of the stomach and duodenum (urease test). BA was diagnosed based on the clinical picture, examination of the external respiration function, reversibility of bronchial obstruction of not less than 20% after the pharmacological test or anti-inflammatory treatment.
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PMID:[Features of peptic ulcer with concomitant bronchial asthma in the elderly]. 1465 32


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