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Gastritis Patients (gastritis + patient)
Selected AbstractsAssociation of peptic ulcer with increased expression of Lewis antigens, but not vacuolating cytotoxin activity or babA2 gene status, in Helicobacter pylori strains from ChinaJOURNAL OF DIGESTIVE DISEASES, Issue 1 2006Peng Yuan ZHENG OBJECTIVE: Controversies exist regarding the virulence factors, such as vacA, babA2 and Lewis blood group antigens, of Western and Asian strains of Helicobacter pylori. The aim of the present study was to determine the significance of these potential virulence factors in the Chinese population. METHODS: Seventy-two strains of H. pylori isolated from patients in Zhengzhou, China, including 43 cases of peptic ulcer (PU) and 29 cases of chronic gastritis, were determined. Vacuolating cytotoxin assay was performed by HeLa cells. The expression of Le blood group antigens (Lea, Leb, Lex and Ley) was performed by enzyme-linked immunosorbent assay (ELISA). babA2 gene was identified by polymerase chain reaction. Frequencies were compared using two-tailed Fisher's exact test. Cytotoxin activities were compared using Spearman's rank correction test. RESULTS: Vacuolating cytotoxin activity was detected in 61 of the 72 strains (84.7%), but there was no significant difference in vacuolating cytotoxin activity (83.7% vs 86.2%, P = 0.821) or titer (4.4 ± 3.8 vs 4.2 ± 4.1, P = 0.876) between the PU and gastritis strains. Significantly more PU strains expressed two or more Lewis antigens (Lex, Ley, Lea or Leb) than strains from the chronic gastritis patients (90.7% vs 65.5%, P = 0.029). Of the 43 strains from PU patients, 17 (39.5%) were positive for babA2, compared with 11 (38.5%) of the 29 strains from gastritis patients (P = 0.924). There was no significant difference in the vacuolating cytotoxin activity or titer between strains expressing two or more Lewis antigens and less than two antigens (84.5% vs 85.7%, P = 1.000; 4.4 ± 4.2 vs 4.3 ± 3.2, P = 0.965). Of the 72 H. pylori strains, 28 were babA2 positive, of which 24 were cytotoxic, compared with 37 of 44 babA2-negative strains (P = 1.000). CONCLUSION: The present study suggests that PU is associated with increased Lewis antigen expression, but not vacuolating cytotoxin production or the presence of babA2, in the H. pylori strains in the Chinese population. [source] Deregulation of E-cadherin,catenin complex in precancerous lesions of gastric adenocarcinomaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2003ANNIE ON-ON CHAN Abstract Background and Aim: Decrease in expression of the E-cadherin,catenin complex is an important element in gastric carcinogenesis. However, the expression of the complex in gastric precancerous lesions has not been well studied. The present study aimed to examine the serial change in expression of E-cadherin,catenin complex in the precancerous lesions of gastric cancer patients. Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved. Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for ,-catenin, ,-catenin and E-cadherin. The results were scored semiquantitatively by two independent pathologists using a validated scoring system. Results: A significant decrease in score was observed in 5% (1/22) of ,-catenin, 0% (0/22) of ,-catenin and 9% (2/22) of E-cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of ,-catenin, 67% (10/15) of ,-catenin and 57% (8/14) of E-cadherin in intestinal metaplasia patients. The scoring of ,-catenin, ,-catenin and E-cadherin correlated with each other. Forty-three percent of patients had concordant changes of scores along the gastritis,adenocarcinoma sequence. There was no association between Helicobacter pylori status and E-cadherin,catenin complex expression. Conclusion: Deregulation of the E-cadherin,catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications. © 2003 Blackwell Publishing Asia Pty Ltd [source] Gastritis OLGA-staging and gastric cancer risk: a twelve-year clinico-pathological follow-up studyALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 10 2010M. RUGGE Aliment Pharmacol Ther,31, 1104,1111 Summary Background, Intestinal-type gastric cancer (GC) still ranks among the high-incidence, highly lethal malignancies. Atrophic gastritis is the cancerization field in which GC develops. The current histological reporting formats for gastritis do not include any (atrophy-based) ranking of GC risk. Aim, To test the gastritis OLGA-staging (Operative Link for Gastritis Assessment) in prognosticating neoplastic progression. Methods, Ninety-three Italian patients were followed up for more than 12 years (range: 144,204 months). Clinical examinations, pepsinogen serology, endoscopy and histology (also assessing Helicobacter pylori status) were performed both at enrolment (T1) and at the end of the follow-up (T2). Results, All invasive or intra-epithelial gastric neoplasia were consistently associated with high-risk (III/IV) OLGA stages. There was a significant inverse correlation between the mean pepsinogen ratio and the OLGA stage (test for trend; P < 0.001). OLGA-staging at T1 predicted both the OLGA stage (Kaplan,Maier log-rank test, P = 0.001) and the neoplasia at T2 (Kaplan,Maier log-rank test, P = 0.001). Conclusions, This long-term follow-up study provides the first evidence that gastritis OLGA-staging conveys relevant information on the clinico-pathological outcome of gastritis and therefore for patient management. According to OLGA-staging and H. pylori- status, gastritis patients could be confidently stratified and managed according to their different cancer risks. [source] Systematic review: Heliocobacter pylori infection and impaired drug absorptionALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 4 2009E. LAHNER Summary Background, Impaired acid secretion may affect drug absorption and may be consequent to corporal Heliocobacter pylori- gastritis, which may affect the absorption of orally administered drugs. Aim, To focus on the evidence of impaired drug absorption associated with H. pylori infection. Methods, Data sources were the systematic search of MEDLINE/EMBASE/SCOPUS databases (1980,April 2008) for English articles using the keywords: drug malabsorption/absorption, stomach, Helicobacter pylori, gastritis, gastric acid, gastric pH, hypochlorhydria, gastric hypoacidity. Study selection was made from 2099 retrieved articles, five studies were identified. Data were extracted from selected papers, investigated drugs, study type, main features of subjects, study design, intervention type and results were extracted. Results, In all, five studies investigated impaired absorption of l -dopa, thyroxine and delavirdine in H. pylori infection. Eradication treatment led to 21,54% increase in l -dopa in Parkinon's disease. Thyroxine requirement was higher in hypochlorhydric goitre with H. pylori- gastritis and thyrotropin levels decreased by 94% after treatment. In H. pylori- and HIV-positive hypochlorhydric subjects, delavirdine absorption increased by 57% with orange juice administration and by 150% after eradication. Conclusions, A plausible mechanism of impaired drug absorption is decreased acid secretion in H. pylori -gastritis patients. Helicobacter pylori infection and hypochlorhydria should be considered in prescribing drugs the absorption of which is potentially affected by intragastric pH. [source] Occurrence and risk factors for benign epithelial gastric polyps in atrophic body gastritis on diagnosis and follow-upALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2005E. Di Giulio Summary Background :,Benign epithelial gastric polyps have been reported to be more common in atrophic body gastritis. The role of Helicobacter pylori infection in the induction of gastric atrophy is well-known. The development of hyperplastic polyps may be in relation to H. pylori infection. Aim :,To investigate occurrence of benign epithelial gastric polyps in atrophic body gastritis patients at diagnosis and follow-up, and the role of H. pylori and other risk factors for the development of benign epithelial gastric polyps. Methods :,A total of 259 consecutive atrophic body gastritis patients included in a follow-up programme, of whom 202 were followed up for median period of 4 years (range: 2,11). At baseline and follow-up gastroscopies, the presence of benign epithelial gastric polyps was evaluated. Biopsies for histology were obtained from all detected benign epithelial gastric polyps. Results :,Frequency of benign epithelial gastric polyps in atrophic body gastritis patients were 4.6% at baseline and 5.9% at follow-up. About 91.7% were hyperplastic polyps. H. pylori infection was detected in 79.2% atrophic body gastritis patients with benign epithelial gastric polyps, and in 70.8% without benign epithelial gastric polyps. Smoking was more frequent among patients with benign epithelial gastric polyps [42% vs. 20%, OR 2.8 (95% CI: 1.2,6.9)]. Conclusions :,Benign epithelial gastric polyps occur in about 5% of atrophic body gastritis patients, and the vast majority are hyperplastic polyps. Smoking habit, but not H. pylori infection, increases the risk for benign epithelial gastric polyps in atrophic body gastritis patients. [source] Anti-inflammatory and tissue-protectant drug effects: results from a randomized placebo-controlled trial of gastritis patients at high risk for gastric cancerALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2001L. A. Fischbach Background: The inflammatory process involving Helicobacter pylori- associated gastritis is thought to lead to epithelial damage and contribute to the development of gastric cancer. Evidence exists from animal and in vitro studies suggesting that tetracyclines have both anti-inflammatory and tissue-protectant effects unrelated to their antimicrobial activity. We attempted to modulate components of H. pylori's inflammatory process by: (i) eliminating the infection; (ii) using tetracycline to alter the host's reaction to the infection without reducing the bacterial load; and (iii) using calcium to counteract the effect of excessive dietary salt. Methods: We conducted a 16-week placebo-controlled clinical trial with 374 H. pylori- associated gastritis patients randomly assigned to one of five groups: (1) triple therapy consisting of metronidazole, amoxicillin and bismuth subsalicylate for 2 weeks, followed by bismuth alone for 14 weeks; (2) calcium carbonate; (3) triple therapy and calcium carbonate; (4) tetracycline; or (5) placebo. Results: Subjects in the tetracycline and triple therapy groups, but not the calcium carbonate only group, showed a reduction in inflammation and epithelial damage vs. those in the placebo group, independent of a change in H. pylori density and other factors. Our results also indicate that epithelial damage may be affected by mechanisms independent of H. pylori density or inflammation. Conclusion: The results are consistent with the hypothesis that tetracycline can decrease inflammation independent of a reduction in the bacterial load. More research is needed to investigate mechanisms leading to epithelial damage which are independent of H. pylori density and inflammation. [source] High-dose ecabet sodium improves the eradication rate of Helicobacter pylori in dual therapy with lansoprazole and amoxicillinALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 11 2000H. Kagaya The additive effect of ecabet sodium in combination with dual therapy on Helicobacter pylori eradication was evaluated. Methods: H. pylori -positive chronic gastritis patients were randomly assigned to one of the following three groups and medicated for 2 weeks. Group LA: dual therapy (lansoprazole 30 mg o.d. plus amoxicillin 750 mg b.d.). Group LA1E: dual therapy plus ecabet sodium (1 g b.d.). Group LA2E: dual therapy plus ecabet sodium (2 g b.d.). Patients were evaluated 4 weeks after the cessation of treatment by culture and 13C-urea breath test. Results: Seventy-one patients (mean age, 56.6 years; range, 26,79 years; 40 males, 31 females) were enrolled in this prospective, single-blind study, and 68 completed the protocol. The eradication rates per protocol patient were 43% in group LA, 62% in group LA1E, and 79% in group LA2E, and those on the intention-to-treat basis were 42% in group LA, 57% in group LA1E and 79% in group LA2E. The eradication rate in group LA2E was significantly higher than group LA (P=0.032 in per protocol, P=0.022 in intention-to-treat). Adverse effects were observed in 10 patients in this study. There were no severe adverse effects caused by ecabet sodium. Conclusion: High-dose ecabet sodium increases eradication rates of H. pylori in dual therapy with lansoprazole and amoxicillin. [source] Overexpression of caspase recruitment domain (CARD) membrane-associated guanylate kinase 1 (CARMA1) and CARD9 in primary gastric B-cell lymphomaCANCER, Issue 9 2005Shigeo Nakamura M.D. Abstract BACKGROUND Although caspase recruitment domain (CARD) membrane-associated guanylate kinase (MAGUK) protein 1 (CARMA1) and CARD9 play important roles in lymphocyte activation, the significance of CARMA1 and CARD9 in the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma remains to be elucidated. METHODS By using reverse transcription-polymerase chain reaction analysis, the expression levels of mRNA of CARMA1, CARD9, Bcl10, and the apoptosis inhibitor 2 (API2)-MALT1 chimeric transcript were determined in tissue specimens from 65 patients with primary gastric B-cell lymphoma (43 patients with low-grade MALT lymphoma, 16 patients with MALT lymphoma plus diffuse large B-cell lymphoma [DLBL], and 6 patients with DLBL without MALT lymphoma) and in tissue specimens from 18 patients with chronic gastritis. The expression levels of CARMA1 and BCL10 were examined immunohistochemically in 30 patients with lymphoma. RESULTS CARMA1 mRNA was detected in 55% of lymphoma patients but in only 17% of chronic gastritis patients. The positive rates for CARD9, Bcl10, and API2-MALT1 chimeric transcript in the lymphoma patients were 48%, 98%, and 8%, respectively, whereas the 3 molecules were not detected in any specimens from patients with chronic gastritis. The expression of CARMA1 and CARD9 was frequent in the Helicobacter pylori -negative patients (100% and 86%, respectively), in the API2-MALT1 chimeric transcript-positive patients (100% and 100%, respectively), and in the specimens from patients who did not respond to H. pylori eradication (76% and 71%, respectively). In addition, CARMA1 expression was positive more frequently in patients of DLBL without MALT lymphoma (100%) than in patients of MALT lymphoma (51%). CARMA1 protein expression was correlated significantly with the expression of CARMA1 mRNA and also with the expression of nuclear BCL10. CONCLUSIONS The overexpression of CARMA1 and CARD9 presumably is associated with the development or progression of gastric B-cell lymphoma, especially among patients who have disease in which the pathogenesis is not related to H. pylori. Cancer 2005. © 2005 American Cancer Society. [source] Study of p53 immunostaining in the gastric epithelium of cagA-positive and cagA-negative Helicobacter pylori gastritisCANCER, Issue 3 2002Ming Teh M.D. Abstract BACKGROUND p53 mutations are an early event in the multistep progression of gastric carcinoma. These mutations are often present in dysplastic and intestinal metaplastic gastric epithelium. However, the presence of immunohistochemically detectable p53 protein and p53 mutations in nondysplastic/nonmetaplastic gastric mucosa is more controversial. Recent reports have suggested that immunohistochemically detectable p53 protein may be present in the gastric epithelium of Helicobacter pylori gastritis. Furthermore, because cagA-positive H. pylori is associated with greater mucosal injury but decreased apoptosis, it would be interesting to determine if this phenotype is associated with greater immunostaining of p53, as the wild-type p53 gene helps to initiate apoptosis. METHODS One hundred thirty-five patients with H. pylori -associated gastritis were immunohistochemically stained for p53 and quantified for the extent and intensity of the staining using a semiquantitative method (0, nil staining; 6, extensive and strong staining). The cagA status of the organism was determined by Western blot. RESULTS Thirty-one patients (23%) showed strong p53 staining (, 4 of 6) in inflamed but otherwise normal gastric epithelium. In the 123 cagA-positive H. pylori gastritis patients, the average p53 staining score was 2.5 of 6. This is significantly higher than the corresponding score of 1.7 of 6 observed in the 12 patients with cagA-negative H. pylori gastritis (P = 0.04). CONCLUSIONS Our results indicate that p53 protein is immunohistochemically detectable even before gastric metaplastic/dysplastic change occurs. The results also suggest that cagA-positive H. pylori might be associated with greater p53 immunohistochemical staining. This would indicate that p53 immunohistochemical staining does not reliably differentiate between gastric dysplasia and reactive inflammatory atypia. If the p53 protein detected is a consequence of mutation, this would help to explain why cagA-positive H. pylori gastritis is associated with decreased apoptosis. Cancer 2002;95:499,505. © 2002 American Cancer Society. DOI 10.1002/cncr.10697 [source] | ||||||||||