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

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.

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Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study

Clinical and Developmental Immunology ◽

10.1155/2012/640630 ◽

2012 ◽

Vol 2012 ◽

pp. 1-5 ◽

Cited By ~ 7

Author(s):

Anna Alakoski ◽

Teea T. Salmi ◽

Kaisa Hervonen ◽

Hannu Kautiainen ◽

Maarit Salo ◽

...

Keyword(s):

Gastric Cancer ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Dermatitis Herpetiformis ◽

Villous Atrophy ◽

Chronic Atrophic Gastritis ◽

Controlled Study ◽

Gastric Corpus ◽

H Pylori

Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia.Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, andHelicobacter pylori. Duodenal biopsies were taken.Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp.,P<0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%,P=0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P=0.038) andH. pyloriin 17 (18.3%) and 17 (9.3%) (P=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer.Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum.H. pyloriwill partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.

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

The Korean Journal of Helicobacter and Upper Gastrointestinal Research ◽

10.7704/kjhugr.2020.0028 ◽

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 Helicobacter pylori (H. pylori) are present in the human stomach. Gastric microbial composition depends on gastric diseases, including gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Although H. pylori 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 H. pylori eradication, many investigators have studied the changes in the microbial composition in the stomach after H. pylori eradication. The gastric microbiome in patients with H. pylori infection typically shows abundance of H. pylori and a low microbial diversity index. If we treat H. pylori-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 H. pylori infection could be restored by H. pylori eradication therapy; however, there have been inconsistent findings of the abundant bacterial taxa after H. pylori 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 H. pylori eradication according to the severity of gastric inflammation.

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Eradication of Helicobacter pylori and Gastric Cancer: A Controversial Relationship

Frontiers in Microbiology ◽

10.3389/fmicb.2021.630852 ◽

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.

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Clinical and Morphological Manifestations of Gastritis and Serum Cytokine Levels in Schoolchildren with Familial History of Gastric Cancer

Russian Journal of Gastroenterology Hepatology Coloproctology ◽

10.22416/1382-4376-2021-31-3-36-42 ◽

2021 ◽

Vol 31 (3) ◽

pp. 36-42

Author(s):

T. V. Polivanova ◽

E. V. Kasparov ◽

V. A. Vshivkov

Keyword(s):

Gastric Cancer ◽

Cell Immune Response ◽

Serum Cytokine ◽

Cross Sectional ◽

Familial History ◽

Familial Predisposition ◽

Cohort Differences ◽

Cytokine Levels ◽

History Of ◽

H Pylori

Aim. A study of the clinical and morphological traits and cytokine profile of gastritis in schoolchildren with familial history of gastric cancer.Materials and methods. A cross-sectional questionnaire survey was conducted in Siberian regions (Tuva, Even-kiya, Aginskiy Buryat National District, Krasnoyarsk). A total of 3,343 schoolchildren aged 7–17 were surveyed for gastrointestinal complaints and history of gastric cancer in their 1st–2nd degree kindred. Oesophagogastroduo-denoscopy (OGDS) with gastric mucosa biopsy were performed in 463 respondents with complaints. Gastritis was graded in the Sydney classification. Serum cytokine levels (IL-2, IL-4, IL-8, IL-18, IL-1β, IFN-α, TNM-α) were obtained in enzyme immunoassays (ELISA).Results. Schoolchildren with gastritis and familial history of gastric cancer revealed a higher 59.8% rate of dyspeptic complaints vs. 40.8% in negative history (p = 0.001), as well as complaints of weekly heartburn in 14.2 and 8.3% cas-es (p = 0.019), respectively. In positive history and negative H. pylori tests, the cell immune response regulator IL-18 37 was revealed elevated in histology. In histologically verified H. pylori, no cross-cohort differences were observed in serum IL-18 by positive familial history of gastric cancer.Conclusion. Gastritis in schoolchildren with familial predisposition to gastric cancer more often associates with GERD and dyspepsia usually presented in postprandial distress syndrome. The cytokine regulation properties of gastritis in schoolchildren with familial history of gastric cancer have been reported.

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NTESTINAL METAPLASIA AND HELICOBACTER PYLORI INFECTION IN PATIENTS WITH CHRONIC GASTRITIS.

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2011.3.9 ◽

2011 ◽

pp. 63-71

Author(s):

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Significant Relationship ◽

Precancerous Lesion ◽

Chronic Atrophic Gastritis ◽

Helicobacter Pylori Infection ◽

Antral Gastritis

Background: Intestinal metaplasia is a precancerous lesion. Helicobacter pylori is identified as an important cause of gastric cancer. This study is aimed at assessing the intestinal metaplasia and Helicobacter pylori infection and their relation in patients with chronic gastritis. Patients and methods: Study includes 75 patients with chronic gastritis diagnosed by clinical, endoscopic and histopathological criteria. Intestinal metaplasia is diagnosed by HE stain. Hp infection is tested by CLO-test from Viet A Ltd. Results: Hp infecton rate in this study is 66.67% and is highest in patients with antral gastritis. Intestinal metaplasia is found in 29.33% of patients with chronic gastritis with the predominance of complete intestinal metaplasia. The rate of intestinal metaplasia is the highest in the group with chronic atrophic gastritis. There is a significant relationship between intestinal metaplasia and Hp ìnfection. Conclusion: Hp and intestinal metaplasia are found at significant rates in chronic gastritis. The rate of intestinal metaplasia is clearly higher in the group with Hp-positive chronic gastritis.

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A case of Helicobacter pylori-negative early gastric adenocarcinoma with gastrointestinal phenotype

Endoscopy International Open ◽

10.1055/a-1396-3854 ◽

2021 ◽

Vol 09 (06) ◽

pp. E863-E866

Author(s):

Masafumi Takatsuna ◽

Rie Azumi ◽

Takeshi Mizusawa ◽

Hiroki Sato ◽

Ken-Ichi Mizuno ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Intestinal Metaplasia ◽

Bile Reflux ◽

Tumor Lesion ◽

Mucosal Layer ◽

History Of ◽

Well Differentiated ◽

Mucosal Glands ◽

H Pylori

AbstractA 40-year-old man with slightly depressed (0-IIc) type gastric cancer of the pyloric anterior gastric area underwent pre-operative screening for tetralogy of Fallot and endoscopic submucosal dissection (ESD) and was tested for Helicobacter pylori antigens and antibodies. Both tests were negative. He did not have a history of eradication. Pathological diagnosis of ESD showed a well-differentiated adenocarcinoma. The tumor was CD10-positive, MUC5AC-negative, and MUC6-confocal positive; it showed differentiation with gastrointestinal phenotype. Moreover, the tumor cells were lysozyme-positive, resembling Paneth cells. Mucosal glands exhibited intestinal metaplasia on the anal side of the tumor lesion. On the oral side of the tumor, metaplasia was non-existent, with normal pyloric glands present in the mucosal layer. The patient was not infected with H. pylori; however, intestinal metaplasia existed around the early gastric cancer. This suggested that the intestinal metaplasia occurred due to bile reflux, and the gastric neoplasia arose with the metaplasia without an H. pylori infection. This case may potentially help explain gastric cancer development in the absence of H. pylori infection.

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Significance of Helicobacter pylori Eradication on Atrophic Gastritis and Intestinal Metaplasia

The Korean Journal of Helicobacter and Upper Gastrointestinal Research ◽

10.7704/kjhugr.2020.0018 ◽

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 Helicobacter pylori (H. pylori) eradication. However, it remains unclear how H. pylori infection causes gastric cancer (GC) and how H. pylori 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 H. pylori-induced chronic gastritis. Thus, the reversibility of AG and IM by H. pylori 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 H. pylori 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 H. pylori eradication and tried to investigate the predicting factors for the improvement of AG and IM including age, sex, smoking, and diet, as well as H. pylori infection.

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Association of Helicobacter pylori vacA polymorphisms with the risk of gastric precancerous lesions in a Moroccan population

The Journal of Infection in Developing Countries ◽

10.3855/jidc.14435 ◽

2021 ◽

Vol 15 (08) ◽

pp. 1124-1132

Author(s):

Mohamed Reda Jouimyi ◽

Ghizlane Bounder ◽

Imane Essaidi ◽

Hasna Boura ◽

Wafaa Badre ◽

...

Keyword(s):

Helicobacter Pylori ◽

High Risk ◽

Atrophic Gastritis ◽

Intestinal Metaplasia ◽

Chronic Gastritis ◽

Precancerous Lesions ◽

Gastric Lesions ◽

D Region ◽

Reliable Marker ◽

H Pylori

Introduction: Helicobacter pylori infection is the major risk factor of atrophic gastritis and intestinal metaplasia. The vacA gene is one of the most virulence factors of H. pylori and genetic diversity in its s, m, i, and d regions is associated with gastric lesions severity. This study aimed to investigate the association of vacA s, m, i, and d regions with the risk of atrophic gastritis and intestinal metaplasia in a Casablanca population. Methodology: A total of 210 patients suffering from gastric lesions (chronic gastritis, atrophic gastritis, and intestinal metaplasia) were enrolled. The type of lesion was diagnosed by histological examination. Detection of H. pylori infection and genotyping of vacA regions were carried out by PCR. Results: The prevalence of H. pylori was 95%. The most common vacA genotypes were s2 (51.5%), m2 (77%), i2 (60.5%), and d2 (58.5%). VacA s1, m1, and i1 genotypes were associated with a high risk of intestinal metaplasia, while the vacA d1 genotype increases the risk of atrophic gastritis and intestinal metaplasia. The most common vacA combination was s2/m2/i2/d2 (52%), and it was more detected in chronic gastritis. The moderate virulent vacA combination (s1/m2/i1/d1) increases the risk of atrophic gastritis, while the most virulent vacA combination (s1/m1/i1/d1) increases the risk of intestinal metaplasia. Conclusions: Genotyping of vacA d region might be a reliable marker for the identification of vacA virulent strains that represent a high risk of developing precancerous lesions (atrophic gastritis and intestinal metaplasia).

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

Gut ◽

10.1136/gutjnl-2020-322368 ◽

2020 ◽

Vol 69 (12) ◽

pp. 2093-2112 ◽

Cited By ~ 1

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.

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Long-term persistence of gastric dysbiosis after eradication of Helicobacter pylori in patients who underwent endoscopic submucosal dissection for early gastric cancer

Gastric Cancer ◽

10.1007/s10120-020-01141-w ◽

2020 ◽

Author(s):

Toshio Watanabe ◽

Yuji Nadatani ◽

Wataru Suda ◽

Akira Higashimori ◽

Koji Otani ◽

...

Keyword(s):

Gastric Cancer ◽

Helicobacter Pylori ◽

Endoscopic Submucosal Dissection ◽

Eradication Therapy ◽

Bacterial Composition ◽

Submucosal Dissection ◽

History Of ◽

H Pylori

Abstract Background Gastric microbiome, other than Helicobacter pylori, plays a role in the tumorigenesis of gastric cancer (GC). Patients who undergo endoscopic submucosal dissection for early GC have a high risk of developing metachronous GC even after successful eradication of H. pylori. Thus, we investigated the microbial profiles and associated changes in such patients after the eradication of H. pylori. Methods A total of 19 H. pylori-infected patients with early GC who were or to be treated by endoscopic resection, with paired biopsy samples at pre- and post-eradication therapy, were retrospectively enrolled. Ten H. pylori-negative patients were enrolled as controls. Biopsy samples were analyzed using 16S rRNA sequencing. Results H. pylori-positive patients exhibited low richness and evenness of bacteria with the deletion of several genera, including Blautia, Ralstonia, Faecalibacterium, Methylobacterium, and Megamonas. H. pylori eradication partially restored microbial diversity, as assessed during a median follow-up at 13 months after eradication therapy. However, post-eradication patients had less diversity than that in the controls and possessed a lower abundance of the five genera mentioned above. The eradication of H. pylori also altered the bacterial composition, but not to the same extent as that in controls. The microbial communities could be clustered into three separate groups: H. pylori-negative, pre-eradication, and post-eradication. Conclusion Changes in dysbiosis may persist long after the eradication of H. pylori in patients with a history of GC. Dysbiosis may be involved in the development of both primary and metachronous GC after the eradication of H. pylori in such patients.

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