scholarly journals Changes in Gastric Microbial Composition before and after Helicobacter pylori Eradication Therapy

2020 ◽  
Vol 20 (3) ◽  
pp. 177-186
Author(s):  
Chan Hyuk Park
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Microbial Diversity ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Diversity Index ◽  
Eradication Therapy ◽  
Cancer Development ◽  
Microbial Composition ◽  
H Pylori

Owing to advancements in next-generation sequencing and non-culture-based microbial research techniques, we have recognized that many bacterial taxa other than <i>Helicobacter pylori (H. pylori)</i> are present in the human stomach. Gastric microbial composition depends on gastric diseases, including gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Although <i>H. pylori</i> is a major factor associated with gastric cancer development, other bacterial taxa may affect gastric carcinogenesis. Because the risk of gastric cancer development can be reduced through <i>H. pylori</i> eradication, many investigators have studied the changes in the microbial composition in the stomach after <i>H. pylori</i> eradication. The gastric microbiome in patients with <i>H. pylori</i> infection typically shows abundance of <i>H. pylori</i> and a low microbial diversity index. If we treat <i>H. pylori</i>-infected patients with antibiotics, microbial diversity increases, and the relative abundance also increases in many bacterial taxa. Several studies suggested that the microbial composition in patients with <i>H. pylori</i> infection could be restored by <i>H. pylori</i> eradication therapy; however, there have been inconsistent findings of the abundant bacterial taxa after <i>H. pylori</i> eradication in patients with atrophic gastritis and intestinal metaplasia. More studies are required to reach a definitive conclusion on restoration of the microbial composition after <i>H. pylori</i> eradication according to the severity of gastric inflammation.

scholarly journals Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship

2021 ◽  
Vol 12 ◽  
Author(s):  
Mariagrazia Piscione ◽  
Mariangela Mazzone ◽  
Maria Carmela Di Marcantonio ◽  
Raffaella Muraro ◽  
Gabriella Mincione
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Precancerous Lesions ◽  
Eradication Therapy ◽  
Developed Countries ◽  
Gastric Carcinogenesis ◽  
Gastric Disease ◽  
Type I ◽  
H Pylori

Worldwide, gastric cancer (GC) represents the fifth cancer for incidence, and the third as cause of death in developed countries. Indeed, it resulted in more than 780,000 deaths in 2018. Helicobacter pylori appears to be responsible for the majority of these cancers. On the basis of recent studies, and either alone or combined with additional etiological factors, H. pylori is considered a “type I carcinogen.” Over recent decades, new insights have been obtained into the strategies that have been adopted by H. pylori to survive the acidic conditions of the gastric environment, and to result in persistent infection, and dysregulation of host functions. The multistep processes involved in the development of GC are initiated by transition of the mucosa into chronic non-atrophic gastritis, which is primarily triggered by infection with H. pylori. This gastritis then progresses into atrophic gastritis and intestinal metaplasia, and then to dysplasia, and following Correa’s cascade, to adenocarcinoma. The use of antibiotics for eradication of H. pylori can reduce the incidence of precancerous lesions only in the early stages of gastric carcinogenesis. Here, we first survey the etiology and risk factors of GC, and then we analyze the mechanisms underlying tumorigenesis induced by H. pylori, focusing attention on virulence factor CagA, inflammation, oxidative stress, and ErbB2 receptor tyrosine kinase. Moreover, we investigate the relationships between H. pylori eradication therapy and other diseases, considering not only cardia (upper stomach) cancers and Barrett’s esophagus, but also asthma and allergies, through discussion of the “hygiene hypothesis. ” This hypothesis suggests that improved hygiene and antibiotic use in early life reduces microbial exposure, such that the immune response does not become primed, and individuals are not protected against atopic disorders, asthma, and autoimmune diseases. Finally, we overview recent advances to uncover the complex interplay between H. pylori and the gut microbiota during gastric carcinogenesis, as characterized by reduced bacterial diversity and increased microbial dysbiosis. Indeed, it is of particular importance to identify the bacterial taxa of the stomach that might predict the outcome of gastric disease through the stages of Correa’s cascade, to improve prevention and therapy of gastric carcinoma.

scholarly journals Clinical Recommendations of Russian Gastroenterological Association and RENDO Endoscopic Society on Diagnosis and Treatment of Gastritis and Duodenitis

2021 ◽  
Vol 31 (4) ◽  
pp. 70-99
Author(s):  
V. T. Ivashkin ◽  
I. V. Maev ◽  
T. L. Lapina ◽  
E. D. Fedorov ◽  
A. A. Sheptulin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Chronic Gastritis ◽  
Eradication Therapy ◽  
Targeted Biopsy ◽  
High Quality ◽  
Familial History ◽  
History Of ◽  
H Pylori

Aim. The clinical guidelines are intended to supplement specialty decision-making for improved aid quality in patients with gastritis and duodenitis though acknowledging the latest clinical evidence and principles of evidencebased medicine.Key points. Gastritis is an inflammatory disease of stomach mucosa, with a separate definition of acute and chronic gastritis. Chronic gastritis is a cohort of chronic diseases uniting a typical morphology of persistent inflammatory infiltration, impaired cellular renewal with emergent intestinal metaplasia, atrophy and epithelial dysplasia of gastric mucosa. Oesophagogastroduodenoscopy (OGDS) or high-resolution OGDS with magnified or non-magnified virtual chromoendoscopy, including targeted biopsy for atrophy and intestinal metaplasia grading and neoplasia detection, are recommended to verify gastritis and duodenitis, precancer states and/or gastric mucosal changes. All chronic gastritis patients positive for H. рylori should undergo eradication therapy as aetiological and subsidiary for gastric cancer prevention. Chronic gastritis patients with symptoms of dyspepsia (epigastric pain, burning and congestion, early satiety), also combined with functional dyspepsia, are recommended proton pump inhibitors, prokinetics, rebamipide and bismuth tripotassium dicitrate in symptomatic treatment. With focal restricted intestinal metaplasia, follow-up is not required in most cases, mainly when advanced atrophic gastritis is ruled out in high-quality endoscopy with biopsy. However, a familial history of gastric cancer, incomplete intestinal metaplasia and persistent H. pylori infection render endoscopy monitoring with chromoendoscopy and targeted biopsy desirable once in three years. Patients with advanced atrophic gastritis should have high-quality endoscopy every 3 years, and once in 1–2 years if complicated with a familial history of gastric cancer.Conclusion. The recommendations condense current knowledge on the aetiology and pathogenesis of gastritis and duodenitis, as well as laboratory and instrumental diagnostic techniques, main approaches to aetiological H. pylori eradication and treatment of dyspeptic states.

scholarly journals Significance of Helicobacter pylori Eradication on Atrophic Gastritis and Intestinal Metaplasia

2020 ◽  
Vol 20 (2) ◽  
pp. 107-116
Author(s):  
Kichul Yoon ◽  
Nayoung Kim
Keyword(s):  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Precancerous Lesions ◽  
Eradication Therapy ◽  
Diffuse Type ◽  
Helicobacter Pylori Eradication ◽  
Predicting Factors ◽  
Point Of No Return ◽  
H Pylori

There has been an accumulation of data regarding the chemopreventive effects of <i>Helicobacter pylori</i> (<i>H. pylori</i>) eradication. However, it remains unclear how <i>H. pylori</i> infection causes gastric cancer (GC) and how <i>H. pylori</i> eradication can prevent GC. Atrophic gastritis (AG) and intestinal metaplasia (IM) are known as precancerous lesions which mainly lead to intestinal-type GC but to some extent, can also lead to diffuse-type GC. The most important mechanism of AG/IM is <i>H. pylori</i>-induced chronic gastritis. Thus, the reversibility of AG and IM by <i>H. pylori</i> eradication therapy is very important in the prevention of GC. There have been many studies providing data supporting the improvement of AG by the eradication of <i>H. pylori</i> to some extent. In contrast, IM has been regarded as “the point of no return.” However, more recent studies have implied the improvement of IM after eradication, suggesting the importance of early eradication therapy in reversible histological status. In this review, we focused on the reversibility of AG and IM by <i>H. pylori</i> eradication and tried to investigate the predicting factors for the improvement of AG and IM including age, sex, smoking, and diet, as well as <i>H. pylori</i> infection.

scholarly journals Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus

Gut ◽  
2020 ◽  
Vol 69 (12) ◽  
pp. 2093-2112 ◽  
Author(s):  
Jyh-Ming Liou ◽  
Peter Malfertheiner ◽  
Yi-Chia Lee ◽  
Bor-Shyang Sheu ◽  
Kentaro Sugano ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Eradication Therapy ◽  
Population Level ◽  
Cost Effective ◽  
Current Evidence ◽  
Global Consensus ◽  
Vulnerable Subjects ◽  
H Pylori

ObjectiveA global consensus meeting was held to review current evidence and knowledge gaps and propose collaborative studies on population-wide screening and eradication of Helicobacter pylori for prevention of gastric cancer (GC).Methods28 experts from 11 countries reviewed the evidence and modified the statements using the Delphi method, with consensus level predefined as ≥80% of agreement on each statement. The Grading of Recommendation Assessment, Development and Evaluation (GRADE) approach was followed.ResultsConsensus was reached in 26 statements. At an individual level, eradication of H. pylori reduces the risk of GC in asymptomatic subjects and is recommended unless there are competing considerations. In cohorts of vulnerable subjects (eg, first-degree relatives of patients with GC), a screen-and-treat strategy is also beneficial. H. pylori eradication in patients with early GC after curative endoscopic resection reduces the risk of metachronous cancer and calls for a re-examination on the hypothesis of ‘the point of no return’. At the general population level, the strategy of screen-and-treat for H. pylori infection is most cost-effective in young adults in regions with a high incidence of GC and is recommended preferably before the development of atrophic gastritis and intestinal metaplasia. However, such a strategy may still be effective in people aged over 50, and may be integrated or included into national healthcare priorities, such as colorectal cancer screening programmes, to optimise the resources. Reliable locally effective regimens based on the principles of antibiotic stewardship are recommended. Subjects at higher risk of GC, such as those with advanced gastric atrophy or intestinal metaplasia, should receive surveillance endoscopy after eradication of H. pylori.ConclusionEvidence supports the proposal that eradication therapy should be offered to all individuals infected with H. pylori. Vulnerable subjects should be tested, and treated if the test is positive. Mass screening and eradication of H. pylori should be considered in populations at higher risk of GC.

scholarly journals Helicobacter pylori-Induced Signaling Pathways Contribute to Intestinal Metaplasia and Gastric Carcinogenesis

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Soichiro Sue ◽  
Wataru Shibata ◽  
Shin Maeda
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Gastric Carcinogenesis ◽  
Dependent Manner ◽  
Intracellular Signaling Pathways ◽  
H Pylori

Helicobacter pylori(H. pylori) induces chronic gastric inflammation, atrophic gastritis, intestinal metaplasia, and cancer. Although the risk of gastric cancer increases exponentially with the extent of atrophic gastritis, the precise mechanisms of gastric carcinogenesis have not been fully elucidated.H. pyloriinduces genetic and epigenetic changes in gastric epithelial cells through activating intracellular signaling pathways in a cagPAI-dependent manner.H. pylorieventually induces gastric cancer with chromosomal instability (CIN) or microsatellite instability (MSI), which are classified as two major subtypes of gastric cancer. Elucidation of the precise mechanisms of gastric carcinogenesis will also be important for cancer therapy.

scholarly journals ID2012 Helicobacter pylori infection in relation to pre-cancerous lesions in gastritis Vietnamese

2017 ◽  
Vol 4 (S) ◽  
pp. 46
Author(s):  
Truong Xuan Bui
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Atrophic Gastritis ◽  
Intestinal Metaplasia ◽  
High Risk Group ◽  
Gastric Biopsy ◽  
Biopsy Specimens ◽  
Urease Test ◽  
Sydney System ◽  
H Pylori

Gastric cancer is one of the leading cancer lesions in Vietnam. Up to now, Helicobacter pylori (H. pylori) infection is still remaining a major pathogenic factor in patients with peptic disorders in Vietnam. Aims: The aim of the study was evaluated the correlation between H. pylori infection with atrophic gastritis (AG), intestinal metaplasia (IM) and dysplasia (DP) in gastritis Vietnamese. Patients and Methods: A total of 161 gastritis patients including 105 males and 56 females with mean of age of 49.81 ± 11.32 years (21 - 79 years) were enrolled in the study. Upper GI endoscopy was evaluated in all patients and afterward gastric biopsy specimens were taken according to the recommendation of update Sydney system and modified Baylor. The gastric biopsy specimens were analyzed with skilled pathologist who did not know about clinico-endoscopic status. The confirmation of H. pylori infection was evaluated with urease test (clo-test) and Giemsa staining. Results: Of the 161 patients, 96 (59.6%) patients were infected with H. pylori, and about 72.05% (116/161) of patients was suffered from atrophic gastritis. The prevalence of atrophic gastritis in H. pylori infected patients (83/96, 86.45%) was significantly higher than that in non-infected patients (33/65, 50.76%), p = 0.041. In the study, the prevalence of intestinal metaplasia and dysplasia was 84/161 (52.17%) and 17/161 (10.55%), respectively. The prevalence of intestinal metaplasia in H. pylori infected patients was observed significantly higher than that in non-infected patients (61/96, 63.54% vs. 23/65, 35.38%, p = 0.044); and the prevalence of dysplasia in H. pylori infected patients was also higher than that in non-infected patients (14/96, 14.58% vs. 3/65, 4.61%, p = 0.073). Conclusion: In gastritis Vietnamese, H. pylori was related to atrophic gastritis, intestinal metaplasia and dysplasia, so gastritis Vietnamese infected with H. pylori could be categorized into high risk group for screening gastric cancer.

scholarly journals Role of TNF-α-Inducing Protein Secreted by Helicobacter pylori as a Tumor Promoter in Gastric Cancer and Emerging Preventive Strategies

Toxins ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 181
Author(s):  
Masami Suganuma ◽  
Tatsuro Watanabe ◽  
Eisaburo Sueoka ◽  
In Kyoung Lim ◽  
Hirota Fujiki
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Cell Surface Receptor ◽  
Tumor Promoter ◽  
Cancer Development ◽  
Human Gastric Cancer ◽  
Tnf Α ◽  
Surface Receptor ◽  
H Pylori ◽  
Factor Α

The tumor necrosis factor-α (TNF-α)-inducing protein (tipα) gene family, comprising Helicobacter pylori membrane protein 1 (hp-mp1) and tipα, has been identified as a tumor promoter, contributing to H. pylori carcinogenicity. Tipα is a unique H. pylori protein with no similarity to other pathogenicity factors, CagA, VacA, and urease. American H. pylori strains cause human gastric cancer, whereas African strains cause gastritis. The presence of Tipα in American and Euro-Asian strains suggests its involvement in human gastric cancer development. Tipα secreted from H. pylori stimulates gastric cancer development by inducing TNF-α, an endogenous tumor promoter, through its interaction with nucleolin, a Tipα receptor. This review covers the following topics: tumor-promoting activity of the Tipα family members HP-MP1 and Tipα, the mechanism underlying this activity of Tipα via binding to the cell-surface receptor, nucleolin, the crystal structure of rdel-Tipα and N-terminal truncated rTipα, inhibition of Tipα-associated gastric carcinogenesis by tumor suppressor B-cell translocation gene 2 (BTG2/TIS21), and new strategies to prevent and treat gastric cancer. Thus, Tipα contributes to the carcinogenicity of H. pylori by a mechanism that differs from those of CagA and VacA.

Prevalence of Helicobacter pylori infection among blood donors in Saxony-Anhalt, Germany – a region at intermediate risk for gastric cancer

2017 ◽  
Vol 55 (07) ◽  
pp. 653-656 ◽  
Author(s):  
Caspar Franck ◽  
Armin Hoffmann ◽  
Alexander Link ◽  
Christian Schulz ◽  
Kerstin Wuttig ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Blood Donors ◽  
Eradication Therapy ◽  
Surrogate Marker ◽  
University Hospital ◽  
Study Cohort ◽  
Emergency Ward ◽  
Age Related ◽  
H Pylori

Abstract Background In the federal state of Saxony-Anhalt, gastric cancer (GC) incidence ranks among the highest in Germany. Helicobacter pylori prevalence is a surrogate marker for GC risk in a given population. In 2010 we reported an H. pylori seroprevalence of 44.4 % in patients at the emergency ward of the University Hospital of Magdeburg, the capital of Saxony-Anhalt. Our aim is to update these findings in a cohort of healthy blood donors from the same region. Materials and methods The sera of 516 consecutive blood donors (40.1 ± 14.1 years; 286 males and 230 females) were tested for antibodies against H. pylori and CagA. Data on demographics and previous H. pylori eradication therapy were obtained by means of a structured questionnaire. Blood donors with positive serology for H. pylori or CagA and/or history of eradication therapy were classified as H. pylori-positive. Results Overall, 28.9 % of the study cohort were H. pylori-positive. The prevalence was higher in older generations (9 % in 18 – 20 years up to 47 % in 61 – 70 years). In 44.4 % of H. pylori IgG-positive donors, CagA serology was also positive. This proportion was not age-dependent. Study participants with siblings were by trend more often H. pylori-positive (p = 0.066). Conclusion Compared to our previous study in patients at the emergency ward, we found by trend lower age-related H. pylori prevalence rates. In our cohort of healthy blood donors, we confirmed a lower H. pylori prevalence in younger generations.

Pathophysiology of intestinal metaplasia of the stomach: emphasis on CDX2 regulation

2010 ◽  
Vol 38 (2) ◽  
pp. 358-363 ◽  
Author(s):  
Rita Barros ◽  
Vânia Camilo ◽  
Bruno Pereira ◽  
Jean-Noel Freund ◽  
Leonor David ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
De Novo ◽  
Current Knowledge ◽  
Regulatory Mechanisms ◽  
Cancer Development ◽  
Molecular Pathways ◽  
Neoplastic Lesion ◽  
Increased Risk

IM (intestinal metaplasia) of the stomach is a pre-neoplastic lesion that usually follows Helicobacter pylori infection and that confers increased risk for gastric cancer development. After setting the role played by CDX2 (Caudal-type homeobox 2) in the establishment of gastric IM, it became of foremost importance to unravel the regulatory mechanisms behind its de novo expression in the stomach. In the present paper, we review the basic pathology of gastric IM as well as the current knowledge on molecular pathways involved in CDX2 regulation in the gastric context.

Evaluation of the Epidemiologic Efficacy of Eradicating Helicobacter pylori on Development of Gastric Cancer

2019 ◽  
Vol 41 (1) ◽  
pp. 97-108 ◽  
Author(s):  
Fujiao Duan ◽  
Chunhua Song ◽  
Jintao Zhang ◽  
Peng Wang ◽  
Hua Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Population Attributable Risk ◽  
Eradication Therapy ◽  
Attributable Risk ◽  
Chinese Patients ◽  
Controlled Trials ◽  
Mixed Effect ◽  
H Pylori ◽  
Development Of Gastric Cancer

Abstract Eradication of Helicobacter pylori colonization has been reported to affect the progression of gastric cancer. A comprehensive literature search was performed from 1997 to 2017 using electronic databases. All randomized controlled trials (RCTs) and nonrandomized controlled trials (non-RCT) evaluated the effect of H. pylori eradication on development of gastric cancer. Four RCTs and 9 non-RCTs were included (n = 40,740 participants; 321,269 person-years). Overall, H. pylori eradication therapy was associated with a significantly reduced risk of gastric cancer (incidence rate ratio (IRR) = 0.52, 95% confidence interval (CI): 0.41, 0.65). Results of mixed-effect Poisson regression meta-analysis were similar to those of traditional meta-analyses. In stratified analyses, the IRRs were 0.59 (95% CI: 0.41, 0.86) in RCTs and 0.48 (95% CI: 0.36, 0.64) in non-RCTs. The IRRs were 0.45 (95% CI: 0.34, 0.61) in patients and 0.63 (95% CI: 0.44, 0.90) in the general population. Moreover, the relative risk reduction was approximately 77% on the development of noncardiac gastric cancer with H. pylori eradication therapy in China. Attributable risk percentage and population attributable risk percentage for Chinese patients were 77.08% and 75.33%, respectively, and for Japanese patients were 57.80% and 45.99%, respectively. H. pylori eradication therapy reduces the risk of noncardiac gastric cancer development. The findings indicate the importance of early intervention with H. pylori eradication therapy from the perspective of epidemiology.

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