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Andrea Varro - One of the best experts on this subject based on the ideXlab platform.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
PLOS Pathogens, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
bioRxiv, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Objective: Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. Design: 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Results: Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phosphate 1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Conclusion: Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
Bryony N Parsons - One of the best experts on this subject based on the ideXlab platform.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
PLOS Pathogens, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
bioRxiv, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Objective: Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. Design: 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Results: Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phosphate 1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Conclusion: Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
Robert M. Genta - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter-negative Gastritis: A distinct entity unrelated to Helicobacter pylori infection
Alimentary Pharmacology & Therapeutics, 2014Co-Authors: Robert M. Genta, Amnon SonnenbergAbstract:SummaryBackground Helicobacter-negative Gastritis is diagnosed when no organisms are detected in a gastric mucosa with typical features of Helicobacter Gastritis (Hp-Gastritis). If Helicobacter-negative Gastritis consisted mostly of ‘missed’ Helicobacter infections, its prevalence should represent a constant percentage of these infections in a population, and their clinico-epidemiological features would overlap. Aim To compare the epidemiologic patterns of Hp-positive and Hp-negative Gastritis. Methods From a pathology database, we extracted demographic, clinical and histopathological data from patients with gastric biopsies (1.2008–12.2013). We allocated patients to high (≥12%) and low (≤6%) H. pylori prevalence regions defined by ZIP code-based data. The prevalence of H. pylori-positive and -negative Gastritis by sex, age and state were expressed as a per cent of the total study population stratified accordingly. Results Of 895 323 patients, 10.6% had Hp-Gastritis and 1.5% Helicobacter-negative Gastritis. Hp-Gastritis, but not Helicobacter-negative Gastritis, was more common in males than females (OR 1.17, 95% CI: 1.16–1.19). While Hp-Gastritis was more prevalent in high than in low-prevalence areas (OR 3.65, 95% CI: 3.57–3.74), Helicobacter-negative Gastritis was only minimally affected by the underlying H. pylori prevalence (1.7% vs. 1.5%). The age-specific prevalence of Hp-Gastritis peaked in the 4th to 5th decades; Helicobacter-negative Gastritis exhibited a low and relatively flat pattern. The geographic distribution of H. pylori-positive and -negative Gastritis showed no significant correlation. Intestinal metaplasia was found in 13.0% of patients with Hp-Gastritis and in 6.1% of those with Helicobacter-negative Gastritis (OR 0.43, 95% CI: 0.40–0.47). Conclusion These data suggest that Helicobacter-negative Gastritis is, in the vast majority of cases, a nosologically and epidemiologically distinct entity that deserves further investigation.
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Autoimmune atrophic Gastritis—pathogenesis, pathology and management
Nature Reviews Gastroenterology & Hepatology, 2013Co-Authors: William L. Neumann, Massimo Rugge, Elizabeth Coss, Robert M. GentaAbstract:Atrophic Gastritis can be associated with long-standing Helicobacter pylori infection (multifocal atrophic Gastritis) and with an autoimmune process that progressively destroys the oxyntic mucosa (autoimmune atrophic Gastritis) Both types of atrophic Gastritis are underdiagnosed, in part because of inadequate biopsy sampling Autoimmune atrophic Gastritis progresses from a mild chronic inflammation of the gastric corpus to an advanced stage associated with a severe form of vitamin B_12 deficiency anaemia known as pernicious anaemia Traditionally, autoimmune atrophic Gastritis has been viewed as a disease affecting predominantly elderly women of Northern European descent, but growing evidence suggests that there might be no racial specificity The diagnosis of autoimmune Gastritis rests on the demonstration of its characteristic histopathological features and the demonstration of autoantibodies against intrinsic factor and parietal cells Management of the early stages of autoimmune atrophic Gastritis is focused on the prevention of vitamin B_12, folate and iron deficiencies Autoimmune Gastritis is a chronic progressive inflammatory condition that results in the replacement of the parietal cell mass by atrophic and metaplastic mucosa. This Review summarizes the epidemiology, pathogenesis and pathological aspects of autoimmune atrophic Gastritis. The authors also provide practical advice for the diagnosis and management of patients with this disease. Autoimmune Gastritis is a chronic progressive inflammatory condition that results in the replacement of the parietal cell mass by atrophic and metaplastic mucosa. A complex interaction of autoantibodies against the parietal cell proton pump and sensitized T cells progressively destroy the parietal cells, inducing hypochlorhydria and then achlorhydria, while autoantibodies against the intrinsic factor impair the absorption of vitamin B_12. The resulting cobalamin deficiency manifests with megaloblastic anaemia and neurological and systemic signs and symptoms collectively known as pernicious anaemia. Previously believed to be predominantly a disease of elderly women of Northern European ancestry, autoimmune Gastritis has now been recognized in all populations and ethnic groups, but because of the complexity of the diagnosis no reliable prevalence data are available. For similar reasons, as well as the frequent and often unknown overlap with Helicobacter pylori infection, the risk of gastric cancer has not been adequately assessed in these patients. This Review summarizes the epidemiology, pathogenesis and pathological aspects of autoimmune metaplastic atrophic Gastritis. We also provide practical advice for the diagnosis and management of patients with this disease.
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OLGA staging for Gastritis: a tutorial
Digestive and Liver Disease, 2008Co-Authors: Massimo Rugge, Robert M. Genta, Francesco Di Mario, David Y. Graham, Pelayo Correa, Emad M. El-omar, Roberto Fiocca, Karel Geboes, Takanori Hattori, Peter MalfertheinerAbstract:Atrophic Gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for (intestinal-type) gastric cancer development and the extent/topography of the atrophic changes significantly correlates with the degree of cancer risk. The current format for histology reporting in cases of Gastritis fails to establish an immediate link between Gastritis phenotype and risk of malignancy. The histology report consequently does not give clinical practitioners and gastroenterologists an explicit message of use in orienting an individual patient's clinical management. Building on current knowledge of the biology of Gastritis and incorporating experience gained worldwide by applying the Sydney System for more than 15 years, an international group of pathologists (Operative Link for Gastritis Assessment) has proposed a system for reporting Gastritis in terms of stage (the OLGA staging system). Gastritis staging arranges the histological phenotypes of Gastritis along a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). This tutorial aims to provide unequivocal information on how to consistently apply the OLGA staging system in routine diagnostic histology practice.
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a genetic basis for atrophy dominant non responsiveness and helicobacter induced Gastritis in f1 hybrid mice
Gut, 1999Co-Authors: Philip Sutton, Jeremy S Wilson, A Savinainen, Robert M. Genta, Dana Torrey, J PappoAbstract:BACKGROUND—The importance of host factors in helicobacter induced Gastritis has been shown in animal models. Infection of most mouse strains with Helicobacter felis results in a functional atrophic Gastritis, while other strains remain Gastritis free. AIMS—To investigate these host factors further by using genetic crosses of responder and non-responder mice. METHODS—F1 hybrids of the non-responder CBA/Ca strain and three strains of mice known to develop H felis induced Gastritis were infected for three months with H felis. Gastritis was assessed by histopathology and serum antibody responses by ELISA. RESULTS—Infection of CBA/Ca mice and F1 hybrids induced little or no Gastritis. Analyses of the antibody responses in these mice revealed virtually undetectable anti-helicobacter antibody levels despite colonisation with high numbers of H felis. In contrast, infection of H felis responsive strains induced Gastritis and a significant humoral immune response. CONCLUSIONS—The non-responsiveness of CBA/Ca mice to H felis infection is dominantly inherited. The lack of Gastritis in CBA mice and their offspring is probably due to active suppression of the immune response normally mounted against H felis. Investigation of these mechanisms will provide important insights relevant to induction of gastric atrophy and cancer in humans. Keywords: helicobacter; non-responsiveness; Gastritis; F1 hybrid; CBA
Yoichi Saitoh - One of the best experts on this subject based on the ideXlab platform.
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Helicobacter pylori may cause “reflux” Gastritis after gastrectomy
Journal of Gastrointestinal Surgery, 1997Co-Authors: Yoshi Nagahata, Yasutomo Azumi, Noribisa Numata, Masafumi Yano, Teruyuki Akimoto, Yoichi SaitohAbstract:Patients with “reflux” Gastritis after gastrectomy suffer from a variety of symptoms, and this type of Gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in Gastritis, the association between H. pylori and reflux Gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic Gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of Gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic Gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of “nonreflux” Gastritis after gastrectomy.
Carrie A Duckworth - One of the best experts on this subject based on the ideXlab platform.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
PLOS Pathogens, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phospahte1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
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comparison of the human gastric microbiota in hypochlorhydric states arising as a result of helicobacter pylori induced atrophic Gastritis autoimmune atrophic Gastritis and proton pump inhibitor use
bioRxiv, 2017Co-Authors: Bryony N Parsons, Umer Zeeshan Ijaz, Rosalinda Damore, Michael D Burkitt, Richard Eccles, Luca Lenzi, Carrie A Duckworth, Andrew R Moore, Laszlo Tiszlavicz, Andrea VarroAbstract:Objective: Several conditions associated with reduced gastric acid secretion confer an altered risk of developing a gastric malignancy. Helicobacter pylori-induced atrophic Gastritis predisposes to gastric adenocarcinoma, autoimmune atrophic Gastritis is a precursor of type I gastric neuroendocrine tumours, whereas proton pump inhibitor (PPI) use does not affect stomach cancer risk. We hypothesised that each of these conditions was associated with specific alterations in the gastric microbiota and that this influenced subsequent tumour risk. Design: 95 patients (in groups representing normal stomach, PPI treated, H. pylori Gastritis, H. pylori-induced atrophic Gastritis and autoimmune atrophic Gastritis) were selected from a cohort of 1400. RNA extracted from gastric corpus biopsies was analysed using 16S rRNA sequencing (MiSeq). Results: Samples from normal stomachs and patients treated with PPIs demonstrated similarly high microbial diversity. Patients with autoimmune atrophic Gastritis also exhibited relatively high microbial diversity, but with samples dominated by Streptococcus. H. pylori colonisation was associated with decreased microbial diversity and reduced complexity of co-occurrence networks. H. pylori-induced atrophic Gastritis resulted in lower bacterial abundances and diversity, whereas autoimmune atrophic Gastritis resulted in greater bacterial abundance and equally high diversity compared to normal stomachs. Pathway analysis suggested that glucose-6-phosphate 1-dehydrogenase and D-lactate dehydrogenase were over represented in H. pylori-induced atrophic Gastritis versus autoimmune atrophic Gastritis, and that both these groups showed increases in fumarate reductase. Conclusion: Autoimmune and H. pylori-induced atrophic Gastritis were associated with different gastric microbial profiles. PPI treated patients showed relatively few alterations in the gastric microbiota compared to healthy subjects.
