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 mechanism by which Helicobacter pylori (Hp) predisposes to duodenal and gastric ulcers remains still unclear. It is possible that Hp infection impaires gastric secretion. Evaluation of gastric acid and mucus secretion before and after Hp eradication would let to estimate the influence of Hp infection on gastric secretion. To evaluate the effect of Hp infection on gastric acid and gastric mucous secretion before and one year after Hp eradication. We examined 28 Hp positive peptic ulcer disease patients (10-gastric ulcer GU, 18-duodenal ulcer DU) before and one year after antibacterial treatment. Gastric acid output was examined basely (BAO) and in response to pentagastrin (6 micrograms/kg) (MAO) using Kay's standard method. Some components of gastric mucus as fucose, galactose, hexosamines and sialic acid were measured using calorimetric methods basaly and after pentagastrin stimulation. Plasma gastrin concentration was measured in 20 patients (6-GU, 14-DU) by radioimmunoassay before and one year after eradication. Hp status was determined by rapid urease test (CLO) and histology (Giemsa stain). One year after Hp successful eradication gastric acid secretion was significantly reduced-BAO: 3,31 vs 1,474 mmol/h; MAO: 19,63 vs 14,85 mmol/h, p < 0.05. Plasma gastrin concentration decreased significantly from 9,783 to 6,017 pmol/I, p < 0.05. In patients with ineffective eradication we did not observe any significant changes in gastric acid secretion. An evident, but not statistically significant, decrease of sialic acid output in eradicated patients was noted. The study has shown the significant influence of Hp infection on gastric acid secretion. Those results support the hypothesis that increased gastric acid secretion may be one of the pathogenic mechanism of Hp infection inducing mucosal damage.
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PMID:Helicobacter pylori infection and gastric secretion in duodenal and gastric ulcer patients--the effect of eradication after one year. 937 18

There are no studies of changes in immunoglobulin G (IgG) titers to Helicobacter pylori, serum pepsinogen, and gastrin in patients with H. pylori-positive gastric ulcers. We investigated the effect of therapy for H. pylori-positive gastric ulcer on IgG titers to H. pylori, serum pepsinogen I and II, and gastrin. Thirty-six patients with H. pylori-positive gastric ulcer were treated with lansorazole and antibiotics for 2 weeks. Serum pepsinogen I and II concentrations, serum gastrin, and IgG titers to H. pylori were measured before treatment and then at 4 and 12 weeks after stopping the treatment. The presence or eradication of H. pylori was determined using the rapid urease test and by histologic H. pylori staining. For 19 patients in whom H. pylori had been successfully eradicated, the pepsinogen I/II ratio increased, pepsinogen II levels decreased, and the anti-H. pylori IgG decreased compared with the results from before therapy and with those from 4 and 12 weeks after therapy. Gastrin levels decreased compared with pretreatment results and those from 4 weeks after the end of treatment. In 17 patients in whom the therapy failed to eradicate H. pylori infection, there were no sequential significant changes in the pepsinogen I/II ratio or in the levels of pepsinogen I, pepsinogen II, anti-H. pylori IgG, and gastrin. A decrease in the serum levels of the IgG antibody to H. pylori and gastrin and also an increase in the pepsinogen I/II ratio could be used as predictors for the eradication of H. pylori infection in gastric ulcer.
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PMID:Changes in serum pepsinogen, gastrin, and immunoglobulin G antibody titers in helicobacter pylori-positive gastric ulcer after eradication of infection. 941 11

Intestinal metaplasia (IM) appears to be an important stage in the pathogenesis of intestinal type of gastric cancer. The purpose of the study was to evaluate how H. pylori eradication modifies IM in gastric antrum. 35 patients (19 M + 16 F) with peptic ulcer (28 duodenal ulcer +7 gastric ulcer) and antral IM with accompanying H. pylori infection proven by urease test and histological examination were followed-up after healing an ulcer achieved by 14 days treatment with 40 mg/d omeprazole and 2 g/d amoxicillin. Endoscopy examination was done every 4 months during 2 years after eradication. At least two antral biopsies were taken during each endoscopy. H. pylori eradication was achieved in 23 patients (66%). No reinfection was observed during the time of observation. The medium grade of intestinal metaplasia after eradication of H. pylori declined from 1.76 to 0.57 over the period of follow-up (p < 0.01). The difference became statistically significant from the 12 months after eradication. No significant change was seen in the group of non-eradicators (1.83 at the beginning of observation and 1.91 at the end point). Statistical difference between eradicators and non-eradicators was stated from the 12th month after eradication. Total regression of intestinal metaplasia was observed in 30% cases after one year and 61% cases after two years after H. pylori eradication. The cure of H. pylori infection significantly reduces the presence of antral IM. Regression of IM appears to be a long-term process taking many months after H. pylori eradication.
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PMID:Helicobacter pylori eradication and antral intestinal metaplasia--two years follow-up study. 944 62

To determine the mechanisms of gastric mucosal injury associated with Helicobacter pylori infection, we investigated the contents of cytokines and inflammatory cell infiltration in the gastric mucosa. Ninety-six patients with dyspepsia were studied (58 gastric ulcer, 38 nonulcer dyspepsia). Of the 96 patients, 63 were infected with H. pylori as determined by microscopic examination with HE staining, culture of H. pylori, or the rapid urease test. Endoscopic biopsy specimens were obtained from both the antrum and the body to examine interleukin (IL)-8, IL-6, IL-1 beta, and tumor necrosis factor-alpha contents in the gastric mucosa by enzyme-linked immunosorbent assay. Inflammatory cell infiltration was assessed according to the Sydney system. IL-8 content was enhanced in both the antral and body mucosa of the H. pylori-positive patients compared with the H. pylori-negative patients. Furthermore, IL-8 content correlated well with the infiltration of both mononuclear cells and polymorphonuclear cells. These results suggest that IL-8 plays important roles in the pathogenesis of gastric mucosal injury associated with H. pylori infection.
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PMID:Increased cytokine production by gastric mucosa in patients with Helicobacter pylori infection. 947 50

To evaluate if the infection with strains of cytotoxin-associated gene A (CagA)-positive Helicobacter pylori is associated with either peptic ulcer and gastric atrophy or intestinal metaplasia in the elderly, we studied 71 H. pylori-positive patients older than 62 years old (34 men, 37 women; mean age, 77.5 years; range, 62-89 years) affected with gastric ulcer (GU) (n = 10), duodenal ulcer (DU) n = 22), or chronic gastritis (CG) (n = 39). H. pylori infection was documented by means of gastric histology, rapid urease test, and polymerase chain reaction (PCR) assay performed on gastric biopsies using two sets of primers: one for the ureC gene specific for H. pylori, and the second specific for the CagA gene. H. pylori-CagA positivity was significantly more common in patients with GU (9 of 10, 90%) than with DU (11 of 22, 50%; p < 0.05) or CG (17 of 39, 43.5%; p = 0.01). Gastric atrophy and intestinal metaplasia were significantly more common in CagA-positive patients than in CagA-negative patients (gastric atrophy: 40.54% vs 11.76, p = 0.007; intestinal metaplasia: 40.54% vs 14.70%, p = 0.01). No difference in prevalence of gastric atrophy and intestinal metaplasia was found in patients divided according to pathology (GU, DU, or CG). Logistic regression demonstrated that gastric atrophy and intestinal metaplasia were independent factors significantly associated with CagA-positivity (gastric atrophy: odds ratio = 4.53, 95% confidence interval 1.25-16.4; intestinal metaplasia: odds ratio = 3.44, 95% confidence interval 1.01-11.7). Our findings help to confirm the hypothesis that an infection with CagA-positive H. pylori strains may be catalytic in inducing gastric changes which can evolve into malignancies.
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PMID:Cytotoxin-associated gene A-positive Helicobacter pylori infection in the elderly. Association with gastric atrophy and intestinal metaplasia. 949 57

The objective of this study was to evaluate the long-term efficacy of Helicobacter pylori (HP) eradication treatment in elderly patients with HP-associated peptic ulcer. A total of 56 subjects, 25 affected with gastric ulcer (GU, 9 males, 16 females, mean age 77.8 years, range 67-93) and 31 with duodenal ulcer (DU, 19 males, 12 females, mean age 76.5 years, range 65-87) were confirmed to be HP-positive by gastric histology and the rapid urease test. All patients were then consecutively treated with omeprazole for 4 weeks plus one or two antibiotics for 1 week as anti-HP treatment. Clinical checkups were then performed every 3 months for 1 year for the evaluation of symptoms and clinical recurrences. Endoscopy with gastric biopsies was repeated after 1, 3 and 12 months for the evaluation of ulcer healing, HP infection and chronic gastritis activity. Statistical analysis was performed by means of the Student t test for unpaired data, the Fisher exact test (two-tailed), and the McNemar chi 2 test. After 4 weeks of treatment, endoscopy confirmed healing of the ulcer in all patients, regardless of the treatment used to cure HP infection. Two months after the end of therapy, a total of 44 patients were HP-negative and 12 patients were still HP-positive. During the 1-year follow-up period 1/44 (2.2%) of the HP-eradicated patients and 5/12 (41.6%) of the still HP-positive patients suffered relapses (p = 0.001): the difference between the two groups remained statistically significant when patients were divided into the subgroups, GU (p = 0.01) and DU (p = 0.04). Two months after the end of therapy, there was still a significant reduction of symptoms both in HP-eradicated (p < 0.0000) and in HP-positive (p = 0.002) patients. After 1 year, however, there was a significantly decreased symptomatology only in HP-eradicated subjects (p < 0.0000) and not in patients still HP-positive. After both 2 months and 1 year of follow-up, chronic gastritis activity demonstrated a significant improvement only in HP-eradicated patients (p = 0.0000). In conclusion, the eradication of HP infection significantly improved the long-term clinical outcome of peptic ulcer disease in the elderly, reducing the recurrences of GU and DU, the patient's symptomatology and the histological signs of chronic gastritis activity. The cure of HP infection is, therefore, strongly recommended in elderly patients with HP-associated peptic ulcer disease.
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PMID:The long-term clinical outcome of elderly patients with Helicobacter pylori-associated peptic ulcer disease. 959 87

Given that chagasic patients in the indeterminate form of this disease, can have abnormal motility of the digestive tract and immunologic abnormalities, we decided to assess the frequency of peptic disease and Helicobacter pylori (Hp) infection in these individuals. Twenty-one individuals, 13 males and 8 females, mean age 37.6 +/- 11.1 years, were examined. Biopsies of the duodenum, antrum, lesser and greater gastric curvature and esophagus were performed. The endoscopic findings were of chronic gastritis in 20 (95.2%) patients, duodenal ulcer in 3 (14.3%), gastric and duodenal ulcer in 3 (14.3%), gastric ulcer alone in 1 (4.8%), esophagitis in 5 (23.8%), and duodenitis in 5 (23.8%). The diagnosis of infection by the Hp was done by the urease test and histologic examination. Hp infection was found in 20 (95.2%) individuals: in 20 out of them in the antrum, in 17 in the lesser curvature, and in 17 in the greater curvature. Hp was not found in the esophagus and duodenum. The only individual with no evidence of infection by Hp was also the only one with normal endoscopic and histologic examinations. The histologic examinations confirmed the diagnoses of gastric ulcer as peptic, chronic gastritis in 20 patients, duodenitis in 14, and esophagitis in 9. In this series the patients had a high frequency of peptic disease, which was closely associated with Hp infection.
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PMID:Peptic disease and Helicobacter pylori are highly prevalent in patients with the indeterminate form of Chagas' disease: report of 21 cases. 964 Jul 83

One hundred and twenty consecutive patients above 12 years of age with dyspepsia were studied from June 1993 to September 1994. They underwent upper gastrointestinal endoscopy to find the mucosal lesions which were associated with their dyspeptic symptoms. At endoscopy gastric mucosal biopsies were taken in order to identify Helicobacter pylori (H. pylori) using three different techniques: culture, histology and the rapid urease test. Normal looking mucosa was the commonest single endoscopic finding, accounting for 34.2%, followed by gastritis 31.7% and duodenal ulcer 29.2%. However, when duodenal ulcers and gastric ulcers were put together, then peptic ulcer was the most prevalent finding accounting for 38.4%. Peptic ulcer was the most prevalent pathological finding in both young (less than 50 years) and older patients (50 years and above). Duodenal ulcer was more prevalent than gastric ulcer in the younger age group with a ratio of 5.8:1, however, the ratio in the older age group was 1:1. Gastric cancer was only found in patients aged 50 years and above, accounting for 17.4% of dyspeptic symptoms in this age group. Females were found to have more normal endoscopic findings than males (59.6%, versus 17.8% respectively). The difference being statistically significant (p < 0.001). All our cases of peptic ulcer disease had evidence of H. pylori infection while dyspeptic patients with normal endoscopic mucosal findings had H. pylori in 80.5% of cases. The difference in prevalence of H. pylori in the two groups was statistically significant (p < 0.001). Surprisingly, evidence of H. pylori in gastric cancer cases was very low in this study, being found in only 25% of patients.
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PMID:Endoscopic findings and prevalence of Helicobacter pylori in Kenyan patients with dyspepsia. 964 Aug 29

C-X-C Chemokines play an important role for neutrophil extravasation through microvessels. Although the level of interleukin (IL)-8 is known to increase in the Helicobacter pylori-infected gastric mucosa, another C-X-C chemokine, GROalpha, has not been evaluated in the H. pylori-associated gastric mucosal injury. The present study was designed to investigate gastric contents of GROalpha in relation to those of IL-8 in the gastric mucosa of H. pylori-infected peptic ulcer patients. Thirty-eight patients with gastric ulcer and 41 with gastritis underwent endoscopy with informed consent and 49 were found to be H. pylori positive and 30 H. pylori negative. Biopsies from the gastric corpus were performed in each patient to examine the H. pylori colonization by bacterial culture, the rapid urease test and histological specimens as well as measurement of the contents of human GROalpha and IL-8. Helicobacter pylori infection was eradicated in 21 patients by triple therapy (lansoprazole 30 mg, amoxycillin 2.0 g, clarithromycin 600 mg; 2 weeks). The samples for GROalpha and IL-8 assay were homogenized in 0.02% aprotinin containing phosphate-buffered solution and the mucosal contents of GROalpha and IL-8 in the supernatants were quantified by sandwich enzyme immunoassay methods. The levels of GROalpha and IL-8 in H. pylori-positive gastric mucosa were significantly higher than those in the H. pylori-negative mucosa. There was a significant linear correlation between the levels of GROalpha and IL-8 (r = 0.798, P < 0.01). After the eradication of H. pylori by the triple therapy, the levels of GROalpha and IL-8 were significantly decreased. The GROalpha showed an increase in the H. pylori-positive gastric mucosa in a similar fashion as IL-8 contents, suggesting a pathogenetic role for GROalpha in H. pylori-associated gastric mucosal injury.
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PMID:Enhanced levels of C-X-C chemokine, human GROalpha, in Helicobacter pylori-associated gastric disease. 964 51

Helicobacter pylori is the most common bacterial pathogen world-wide and has been identified in all countries. As long-term infection with H. pylori could potentially lead to duodenal or gastric ulcer disease, asymptomatic chronic gastritis, chronic dyspepsia, or gastric malignancy, including both adenocarcinoma and B-cell lymphoma, a large number of different treatment regimens aimed at eradicating H. pylori has been evaluated and reported. Despite numerous H. pylori treatment studies the optimum regimen for its eradication remains unclear. A treatment regimen, which is effective, safe and inexpensive could be used widespread and reduce the risks of the long-term complications of infection. In this study we compared the efficacy, side effects and cost-effectiveness of 12 different therapy regimens for H. pylori eradication by using meta-analysis methodology. 486 patients (256 male, 230 female; mean age 40.8 years) with H. pylori associated duodenal ulcer (n = 140), gastritis (n = 254), gastroduodenitis (n = 92) were treated with 12 different therapy-regimens. Endoscopy was performed at baseline and 6 weeks after discontinuation of eradication therapy. H. pylori status was assessed by urease test and histology. The therapy with a H2-receptor antagonist is less effective than the triple therapies with omeprazole or lansoprazole. Bismuth-based triple therapies have a mean overall eradication rate of 68%, but are limited by frequent side effects causing poor drug compliance.
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PMID:[Meta-analysis of determining the pathogen eradicating efficacy of various therapeutic regimens in Helicobacter pylori infection]. 1002 50


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