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No associations of Helicobacter pylori infection and gastric atrophy with plasma total homocysteine in Japanese  [cached]
Simon Itou, Yasuyuki Goto, Takaaki Kondo, Kazuko Nishio, Sayo Kawai, Yoshiko Ishida, Mariko Naito, Nobuyuki Hamajima
International Journal of Medical Sciences , 2007,
Abstract: Recent studies have suggested that Helicobacter pylori (H. pylori) infection might be a risk factor for atherosclerosis. Since the bacterium has not been isolated from atherosclerotic lesions, a direct role in atherogenesis is not plausible. We examined associations of plasma total homocysteine (tHcy) and serum folate, independent risk factors for atherosclerosis, with H. pylori infection and subsequent gastric atrophy among 174 patients (78 males and 96 females) aged 20 to 73 years, who visited an H. pylori eradication clinic of Nagoya University from July 2004 to October 2005. Polymorphism genotyping was conducted for methylenetetrahydrofolate reductase (MTHFR) C677T and thymidylate synthase (TS) 28-bp tandem repeats by PCR with confronting two-pair primers and PCR, respectively. H. pylori infection and gastric atrophy were not significantly associated with hyperhomocysteinemia (tHcy ≥ 12 nmol/ml), when adjusted by sex, age, smoking, alcohol, and genotypes of MTHFR and TS. The adjusted odds ratio of gastric atrophy for low folate level (≤ 4mg/ml) was 0.21 (95% confidence interval = 0.05-0.78). The associations of tHcy with serum folate and MTHFR genotype were clearly observed in this dataset. The present study demonstrated that folate and MTHFR genotype were the deterministic factors of plasma tHcy, but not H. pylori infection and subsequent gastric atrophy, indicating that even if H. pylori infection influences the risk of atherosclerosis, the influence may not be through the elevation of homocysteine.
Relation Between Helicobacter Pylori, Inflammatory (neutrophil) Activity, Chronic Gastritis, Gastric Atrophy And Intestinal Metaplasia
MN Tanko, AN Manasseh, GO Echejoh, BM Mandong, AO Malu, EN Okeke, N Ladep, EI Agaba
Nigerian Journal of Clinical Practice , 2008,
Abstract: Background: To determine the relation of Helicobacter pylori infection with chronic inflammation, atrophy, activity level and intestinal metaplasia. Patients and Methods: A cross-sectional study of 100 consecutive patients with dyspepsia. These patients were fasted for 12 hours and gastroscopic biopsy specimens were obtained from their gastric mucosae. The specimens were histologically evaluated for H. pylori, inflammatory activity, chronic inflammation, gastric atrophy and intestinal metaplasia. Results: There were 50(50%) females and 50(50%) males. The average ages of women and men were 36.3±11.5 and 42.9±12.8 respectively. Helicobacter pylori was found in 79%. Neutrophil activity was observed in 83%. Inflammation was found in 95%, glandular atrophy in 38%, intestinal metaplasia in 28% of the cases. Incidental (early gastric) cancer was found in 3%, dysplasia in 2% and reactive gastropathy in 7% of the cases. A statistically significant relationship was found between Helicobacter pylori colonization intensity and the degrees of neutrophil activity, chronic inflammation and intestinal metaplasia. Conclusion: We concluded that Helicobacter pylori infection results in neutrophil activation and chronic gastritis, and that it has a role in the development of intestinal metaplasia. The greater the intensity of Helicobacter pylori infection, the greater the degrees of neutrophil activation, chronic gastritis and intestinal metaplasia.
Helicobacter pylori-Induced Chronic Gastritis and Assessing Risks for Gastric Cancer  [PDF]
Gonzalo Carrasco,Alejandro H. Corvalan
Gastroenterology Research and Practice , 2013, DOI: 10.1155/2013/393015
Abstract: Chronic gastritis is an inflammation of the gastric mucosa and has multiple etiologies. Here we discuss the pathological alterations induced by Helicobacter pylori (HP) leading to chronic gastritis and the epigenetic bases underlying these changes. We review the histology of the normal gastric mucosa and overview the role of HP in the multistep cascade of GC. We attempt to define the role of the Operative Link for Gastritis Assessment (OLGA) staging system in assessing the risk of GC. The epigenetic bases of chronic gastritis, mainly DNA methylation, are presented through examples such as (i) the methylation of the promoter region of E-cadherin in HP-induced chronic gastritis and its reversion after HP eradication and (ii) the association of methylation of the promoter region of Reprimo, a p53-mediated cell cycle arrest gene, with aggressive HP strains in high risk areas for GC. In addition, we discuss the finding of RPRM as a circulating cell-free DNA, offering the opportunity for noninvasive risk assessment of GC. Finally, the integration of OLGA and tissue biomarkers, by systems pathology approach, suggests that severe atrophy has a greater risk for GC development if, in addition, overexpressed p73. This trial is registered with ClinicalTrials.gov NCT01774266. 1. Introduction Since 1870, both human and veterinary pathologists have described bacterial infections based on the observation of tiny curved bacteria within gastric mucosa [1, 2]. However, these organisms were dismissed as irrelevant contaminants. In 1947, when gastroscopy was first being used, Schindler deemed gastritis as “one of the most debated diseases of the human body” and predicted that its significance would be discussed “for some time to come” [3]. Schindler himself claimed that the “bacteriological etiology of chronic gastritis has not been convincingly proved in a single case” [3]. In 1984, Marshall and Warren proposed that chronic “idiopathic” gastritis had a bacterial cause, that is, Helicobacter pylori [4]. Their hypothesis was met with great skepticism. However, within a few years, the association between H. pylori gastritis, peptic ulcer, and gastric cancer came to be acknowledged and ultimately accepted [4]. For the purpose of this paper, we will focus mainly on the cascade of events produced by Helicobacter pylori infection leading to chronic changes in the gastric mucosa and the risk assessment for the development of gastric cancer. In addition, we will explore the epigenetic bases that underlie the changes of chronic gastritis. 2. Normal Gastric Histology In order to
Gastric Atrophy, Intestinal Metaplasia in Helicobacter pylori Gastritis: Prevalence and Predictors Factors  [PDF]
S. Adadi, B. Bennani, M. Elabkari, A. Ibrahimi, S. Alaoui, M. Elkhadir, T. Harmouch, M. Mahmoud, C. Nejjari, D. Benajah
Journal of Biosciences and Medicines (JBM) , 2016, DOI: 10.4236/jbm.2016.410005
Abstract: Gastric atrophy and intestinal metaplasia represent the most important premalignant lesions in gastric carcinogenesis. The severity of gastric mucosal inflammation depends on the bacterium Helicobacter pylori (HP), on the host and on environmental factors. The aim of our study is to determine the prevalence and factors associated with Gastric atrophy and intestinal metaplasia in patients infected with Helicobacter pylori. Methods: This is a prospective study over a period of 4 years (May 2009 - January 2015) conducted in the service of Hepatology and Gastroenterology in hospital university Hassan II of Fez in collaboration with microbiology and molecular biology laboratory and epidemiology service of Faculty of Medicine and Pharmacy Fes. We included in our study all patients aged over 15 years, having ulcerative dyspepsia, peptic ulcer disease, gastritis or esophagitis. Results: During the study period, 1190 patients were included of which 70% had HP infection (N = 833). The average age was 48.21 years [16 - 99 years], sex ratio M/F was 1, 11. 60% of patients were older than 45 years. Chronic smoking was found in 12% of patients. Gastric atrophy was observed in 84% (N = 699) of patients infected with HP. Gastric atrophy was localized in 70% in the antrum and 30% in the fundus and 24% in both. The activity of gastritis (p = 0.0001) and the density of the HP (p = 0.005) were factors associated with atrophy. Intestinal metaplasia was observed in 13.5% of patients (N = 112). The density of HP (p = 0.037) and severe atrophy (p = 0.001) were factors associated with metaplasia. Other factors studied: age, sex, smoking, CagA+ genotype were not associated with either gastric atrophy or intestinal metaplasia. Conclusion: In our study, the prevalence of atrophic gastritis and intestinal metaplasia in patients infected with Helicobacter pylori was 84% and 13.5% respectively, which was a high prevalence. The activity of gastritis, and density of HP were factors associated with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.
Functional Analysis of an Acid Adaptive DNA Adenine Methyltransferase from Helicobacter pylori 26695  [PDF]
Arun Banerjee,Desirazu N. Rao
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0016810
Abstract: HP0593 DNA-(N6-adenine)-methyltransferase (HP0593 MTase) is a member of a Type III restriction-modification system in Helicobacter pylori strain 26695. HP0593 MTase has been cloned, overexpressed and purified heterologously in Escherichia coli. The recognition sequence of the purified MTase was determined as 5′-GCAG-3′and the site of methylation was found to be adenine. The activity of HP0593 MTase was found to be optimal at pH 5.5. This is a unique property in context of natural adaptation of H. pylori in its acidic niche. Dot-blot assay using antibodies that react specifically with DNA containing m6A modification confirmed that HP0593 MTase is an adenine-specific MTase. HP0593 MTase occurred as both monomer and dimer in solution as determined by gel-filtration chromatography and chemical-crosslinking studies. The nonlinear dependence of methylation activity on enzyme concentration indicated that more than one molecule of enzyme was required for its activity. Analysis of initial velocity with AdoMet as a substrate showed that two molecules of AdoMet bind to HP0593 MTase, which is the first example in case of Type III MTases. Interestingly, metal ion cofactors such as Co2+, Mn2+, and also Mg2+ stimulated the HP0593 MTase activity. Preincubation and isotope partitioning analyses clearly indicated that HP0593 MTase-DNA complex is catalytically competent, and suggested that DNA binds to the MTase first followed by AdoMet. HP0593 MTase shows a distributive mechanism of methylation on DNA having more than one recognition site. Considering the occurrence of GCAG sequence in the potential promoter regions of physiologically important genes in H. pylori, our results provide impetus for exploring the role of this DNA MTase in the cellular processes of H. pylori.
Gastric Mucosal Atrophy Might Be Associated with the Efficacy of First-Line Therapy Using Vonoprazan for Helicobacter pylori  [PDF]
Mika Miura, Masahiko Ohtaka, Mitsuhiko Hanawa, Naoki Shimura, Yoshioki Yoda, Sho Suzuki
Open Journal of Gastroenterology (OJGas) , 2017, DOI: 10.4236/ojgas.2017.79026
Abstract: Aim: To investigate the factors related to the effect of eradication therapy with vonoprazan for Helicobacter pylori (H. pylori). Methods: We retrospectively reviewed medical records of H. pylori-positive patients who received first-line (40 mg vonoprazan/60 mg lansoprazole or 20 mg rabeprazole, 1500 mg amoxicillin, 400 mg clarithromycin, all 2/day for 7 days) (n = 4118). H. pylori eradication was assessed by the 13C-urea breath test with success defined as a result of < 2.5‰. Using propensity score matching, successful eradication rates were compared between two groups: those receiving vonoprazan and those receiving a proton pump inhibitor. Related factors and adverse events were investigated. Results: Successful first-line eradication rates according to ITT analysis and PP analysis, respectively, were 79.8% and 91.4% for VPZ therapy. Eradication rates using propensity matched patients (n = 1053) who received first-line vonoprazan therapy were higher than in those using proton pump inhibitor (PPI) therapy (92.1% vs. 79.7% in per-protocol analysis, p < 0.0001). Multivariate analysis confirmed that gastric mucosal atrophy was associated with treatment success. Conclusions: Low-dose clarithromycin triple therapy for first-line H. pylori eradication therapy using vonoprazan was more effective than standard triple therapy with proton pump inhibitor. Gastric mucosal atrophy was associated with treatment success.
Mucosal patterns of Helicobacter pylori-related gastritis without atrophy in the gastric corpus using standard endoscopy  [cached]
Sheng-Lei Yan, Shwu-Tzy Wu, Chien-Hua Chen, Yeh-Huang Hung, Tsung-Hsun Yang, Vun-Siew Pang, Yung-Hsiang Yeh
World Journal of Gastroenterology , 2010,
Abstract: AIM: To identify the mucosal patterns of Helicobacter pylori (H. pylori)-related gastritis in the gastric corpus using standard endoscopy and to evaluate their reproducibility.METHODS: A total of 112 consecutive patients underwent upper gastrointestinal endoscopy. The endoscopists classified the endoscopic findings into 4 patterns. In the second part of the study, 90 images were shown to 3 endoscopists in order to evaluate the inter-observer and intra-observer variability in image assessment.RESULTS: The mucosal patterns of the gastric body were categorized into 4 types. Type 1 pattern was defined as cleft-like appearance, type 2 as regular arrangement of red dots, type 3 pattern as the mosaic mucosal pattern and type 4 pattern as the mosaic pattern with a focal area of hyperemia. Type 1 and type 2 mucosal patterns were statistically significant in predicting H. pylori-negative status as compared with other mucosal types (χ2 = 12.79 and 61.25 respectively, P < 0.01). Type 3 and type 4 mucosal patterns were statistically significant in predicting a H. pylori-positive status as compared with other mucosal types (χ2 = 21.22 and 11.02 respectively, P < 0.01). Furthermore, the sensitivity, specificity, positive and negative predictive values of type 3 plus type 4 patterns for predicting H. pylori-positive gastric mucosa were 100%, 86%, 94%, and 100%, respectively. The mean κ values for inter- and intra-observer agreement in assessing the various endoscopic patterns were 0.808 (95% CI, 0.678-0.938) and 0.826 (95% CI, 0.727-0.925) respectively.CONCLUSION: Our study suggests that mucosal patterns in H. pylori-infected gastric mucosa without atrophy can be reliably identified using standard endoscopy in the gastric corpus.
Additional corpus biopsy enhances the detection of Helicobacter pylori infection in a background of gastritis with atrophy  [cached]
Lan Hung-Chieh,Chen Tseng-Shing,Li Anna Fen-Yau,Chang Full-Young
BMC Gastroenterology , 2012, DOI: 10.1186/1471-230x-12-182
Abstract: Background The best sites for biopsy-based tests to evaluate H. pylori infection in gastritis with atrophy are not well known. This study aimed to evaluate the site and sensitivity of biopsy-based tests in terms of degree of gastritis with atrophy. Methods One hundred and sixty-four (164) uninvestigated dyspepsia patients were enrolled. Biopsy-based tests (i.e., culture, histology Giemsa stain and rapid urease test) and non-invasive tests (anti-H. pylori IgG) were performed. The gold standard of H. pylori infection was defined according to previous criteria. The sensitivity, specificity, positive predictive rate and negative predictive rate of biopsy-based tests at the gastric antrum and body were calculated in terms of degree of gastritis with atrophy. Results The prevalence rate of H. pylori infection in the 164 patients was 63.4%. Gastritis with atrophy was significantly higher at the antrum than at the body (76% vs. 31%; p<0.001). The sensitivity of biopsy-based test decreased when the degree of gastritis with atrophy increased regardless of biopsy site (for normal, mild, moderate, and severe gastritis with atrophy, the sensitivity of histology Giemsa stain was 100%, 100%, 88%, and 66%, respectively, and 100%, 97%, 91%, and 66%, respectively, for rapid urease test). In moderate to severe antrum or body gastritis with atrophy, additional corpus biopsy resulted in increased sensitivity to 16.67% compare to single antrum biopsy. Conclusions In moderate to severe gastritis with atrophy, biopsy-based test should include the corpus for avoiding false negative results.
Association of polymorphism of PTPN 11 encoding SHP-2 with gastric atrophy but not gastric cancer in Helicobacter pylori seropositive Chinese population
Jing Jiang, Zhi-Fang Jia, Fei Kong, Mei-Shan Jin, Yin-Ping Wang, Suyan Tian, Jian Suo, Xueyuan Cao
BMC Gastroenterology , 2012, DOI: 10.1186/1471-230x-12-89
Abstract: The subjects comprised 414 patients with gastric cancer, 109 individuals with gastric atrophy and 923 healthy controls. Blood was collected from October 2008 to October 2010. Five htSNPs rs2301756, rs12423190, rs12229892, rs7958372 and rs4767860 from the PTPN11 gene were selected and genotyped by Taqman assay. Serum Ig G antibodies to H. pylori were detected by ELISA. Gastric atrophy was screened by the levels of serum pepsinogenIandII, and confirmed by endoscopy and histopatholgical examinations. Odds ratio (ORs) and 95% confidence intervals (CIs) were calculated by a multivariate logistic regression.Among H. pylori seropositive subjects, age and gender-adjusted OR of gastric atrophy was 2.47 (95%CI 1.13-4.55, P?=?0.02) for CC genotype compared with CT/TT genotypes, suggesting a recessive model of genetic risk for rs12423190. The prevalence of H. pylori seropositivity were significantly higher in groups of gastric cancer and gastric atrophy compared to the control group (70.3% vs. 75.2% vs. 49.7%, P <0.001). However, the distributions of genotypes and haplotypes in patients with gastric cancer were not significantly different from healthy controls.Our study provides the first evidence that rs12423190 polymorphism of the PTPN11 gene is significantly associated with an increased risk of gastric atrophy in H. pylori infected Chinese Han population, suggesting that rs12423190 polymorphism could be used as a useful marker of genetic susceptibility to gastric atrophy among H. pylori infected subjects. The biological roles of this polymorphism require a further investigation.
The Efect of Helicobacter Pylori Eradication on Atrophic Gastritis and Intestinal metaplasia  [PDF]
Güldem Kilciler,Zulfikar Polat,Ahmet Uygun,Murat Kantarc?o?lu
Journal of Clinical and Analytical Medicine , 2011, DOI: 10.4328
Abstract: Aim: The aim of this prospective study was to evaluate whether helicobacter pylori eradication could improve gastric atropy or intestinal metaplasia. Material and Method: Forty-two pylori infected patients were evaluated for the status of atrophic gastritis and intestinal metaplasia. Two biopsy specimens from antrum and two biopsy specimens from corpus were taken before and 6 months after the helicobacter pylori eradication therapy. Helicobacter pylori status was determined by C-urea breath test 2 and 6 months after for helicobacter pylori eradication. Severity of gastric atrophy and intestinal metaplasia was classified as mild, moderate or severe according to the updated Sydney classification. Results: The scoring of gastric atrophy was found significantly decreased in helicobacter pylori eradicated group after 6 months, while no significant change was found in H. pylori non-eradicated group. Intestinal metaplasia wasn’t recorded as improved in neither helicobacter pylori eradicated group nor helicobacter pylori noneradicated group. Conclusion; It can be suggested that reversal of atrophy and intestinal metaplasia may occur even after several years, so the positive effect of eradication therapy might have been even better with a longer follow-up period. The results reported here are those obtained during the 6 months period.
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