scholarly journals Gastric microbes associated with gastric inflammation, atrophy and intestinal metaplasia 1 year after Helicobacter pylori eradication

Gut ◽  
2020 ◽  
Vol 69 (9) ◽  
pp. 1572-1580 ◽  
Author(s):  
Joseph J Y Sung ◽  
Olabisi Oluwabukola Coker ◽  
Eagle Chu ◽  
Chun Ho Szeto ◽  
Simson Tsz Yat Luk ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Inositol Phosphate ◽  
Eradication Therapy ◽  
Treated Group ◽  
Oral Bacteria ◽  
Microbial Interactions ◽  
Bacterial Taxonomy ◽  
Before And After ◽  
H Pylori

ObjectiveHelicobacter pylori is associated with gastric inflammation, precancerous gastric atrophy (GA) and intestinal metaplasia (IM). We aimed to identify microbes that are associated with progressive inflammation, GA and IM 1 year after H. pylori eradication.DesignA total of 587 H. pylori–positive patients were randomised to receive H. pylori eradication therapy (295 patients) or placebo (292 patients). Bacterial taxonomy was analysed on 404 gastric biopsy samples comprising 102 pairs before and after 1 year H. pylori eradication and 100 pairs before and after 1 year placebo by 16S rRNA sequencing.ResultsAnalysis of microbial sequences confirmed the eradication of H. pylori in treated group after 1 year. Principal component analysis revealed distinct microbial clusters reflected by increase in bacterial diversity (p<0.00001) after H. pylori eradication. While microbial interactions remained largely unchanged after placebo treatment, microbial co-occurrence was less in treated group. Acinetobacter lwoffii, Streptococcus anginosus and Ralstonia were enriched while Roseburia and Sphingomonas were depleted in patients with persistent inflammation 1 year after H. pylori eradication. A distinct cluster of oral bacteria comprising Peptostreptococcus, Streptococcus, Parvimonas, Prevotella, Rothia and Granulicatella were associated with emergence and persistence of GA and IM. Probiotic Faecalibacterium praustznii was depleted in subjects who developed GA following H. pylori eradication. Functional pathways including amino acid metabolism and inositol phosphate metabolism were enriched while folate biosynthesis and NOD-like receptor signalling decreased in atrophy/IM-associated gastric microbiota.ConclusionThis study identified that gastric microbes contribute to the progression of gastric carcinogenesis after H. pylori eradication.

scholarly journals Host Wnt/β-catenin pathway triggered by Helicobacter pylori correlates with regression of gastric intestinal metaplasia after H. pylori eradication

2009 ◽  
Vol 58 (5) ◽  
pp. 567-576 ◽  
Author(s):  
Kuei-Hsiang Hung ◽  
Jiunn-Jong Wu ◽  
Hsiao-Bai Yang ◽  
Li-Ju Su ◽  
Bor-Shyang Sheu
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Glycogen Synthase ◽  
Nucleotide Polymorphisms ◽  
Ags Cells ◽  
Gastric Intestinal Metaplasia ◽  
Before And After ◽  
Cox 2 ◽  
H Pylori ◽  
High Level

Helicobacter pylori eradication can reverse gastric intestinal metaplasia (IM) in some but not all patients. H. pylori induces high levels of nuclear β-catenin staining in IM tissues, as well as overexpression of cyclooxygenase-2 (COX-2). This study investigated whether the Wnt/β-catenin pathway plays a role in IM regression following H. pylori eradication. Sixty-five H. pylori-infected patients with IM who had achieved successful H. pylori eradication provided paired gastric samples before and after eradication to analyse the persistence of IM, and to assess COX-2 and nuclear β-catenin expression. The host genotypes of single nucleotide polymorphisms (SNPs) of the COX-2, β-catenin (CTNNB1) and adenomatous polyposis coli (APC) genes were analysed. In addition, expression of β-catenin, E-cadherin and phosphorylated and unphosphorylated glycogen synthase kinase 3β (GSK-3β) in cell lines challenged with H. pylori isolates from patients with and without IM persistence was compared by immunoanalysis. After a mean 33.9-month follow-up after H. pylori eradication, 44 patients (67.7 %) with IM persistence had a higher rate of high-level nuclear β-catenin expression in IM tissue than those without IM persistence (P=0.008). The patients with IM persistence had a higher rate of AA, GG and AA APC SNP genotypes at positions 4479, 5268 and 5465, respectively, than the patients without IM persistence (P=0.022). The H. pylori isolates from the patients with IM regression after H. pylori eradication induced more phospho-GSK-3β in AGS cells than isolates from patients with IM persistence (P=0.011). It is likely that interactions with H. pylori and the patient's Wnt/β-catenin genetic predisposition determine the outcome of IM persistence following H. pylori eradication.

scholarly journals Impact of Helicobacter pylori Eradication Therapy on Platelet Counts in Patients With Chronic Idiopathic Thrombocytopenic Purpura

2015 ◽  
Vol 8 (7) ◽  
pp. 35 ◽  
Author(s):  
Mohamadreza Amiri
Keyword(s):  
Helicobacter Pylori ◽  
Platelet Count ◽  
Eradication Therapy ◽  
Current Treatment ◽  
Thrombocytopenic Purpura ◽  
Stool Antigen Test ◽  
Platelet Counts ◽  
Before And After ◽  
History Of ◽  
H Pylori

<p>This study was a before and after clinical evaluation of <em>Helicobacter pylori</em> eradication on platelet counts in a group of 23 patients with chronic Idiopathic (Autoimmune) thrombocytopenic purpura (CITP). <em>H. pylori </em>infection was identified in patients by a <sup>13</sup>C-urea breath test and confirmed by an <em>H. pylori</em> stool antigen test. Eradication was conducted in patients testing positive. Infected (<em>n</em> = 10) and uninfected (<em>n</em> = 13) patient groups did not differ with respect to age, gender, history of previous splenectomy, treatment with anti-D, current treatment with corticosteroids, or initial platelet count<strong>s</strong>. <em>H pylori</em> eradication was successful in eight infected CITP patients, with two patients not responsive to treatment. Compared to the uninfected group, patients in the infected group who responded to eradication therapy had significantly increased platelet counts after six months (56.2 ± 22.2 <em>vs.</em> 233 ± 85.6 ×10<sup>3</sup> million cells/L; <em>P </em>&lt; 0.01), whereas platelet counts in the non-responding patients and uninfected group did not differ after this period of time. <em>H. pylori</em> eradication promotes significant platelet count improvement in patients with CITP. Thus, all patients with CITP should be tested and treated for<em> H. pylori </em>infections.</p>

scholarly journals The Reduction in Gastric Atrophy after Helicobacter pylori Eradication Is Reduced by Treatment with Inhibitors of Gastric Acid Secretion

2019 ◽  
Vol 20 (8) ◽  
pp. 1913 ◽  
Author(s):  
Ryota Niikura ◽  
Yoku Hayakawa ◽  
Yoshihiro Hirata ◽  
Keiji Ogura ◽  
Mitsuhiro Fujishiro ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Drug Use ◽  
Intestinal Metaplasia ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Eradication Therapy ◽  
Gastric Atrophy ◽  
H Pylori ◽  
Surveillance Endoscopy

Background: Helicobacter pylori (H. pylori) eradication therapy may improve gastric atrophy and intestinal metaplasia, but the results of previous studies have not always been consistent. The aim of this study was to compare the histological changes of intestinal metaplasia and gastric atrophy among the use of acid-suppressing drugs after H. pylori eradication. Methods: A cohort of 242 patients who underwent successful eradication therapy for H. pylori gastritis and surveillance endoscopy examination from 1996 to 2015 was analyzed. Changes in the histological scores of intestinal metaplasia and atrophy according to drug use (proton-pump inhibitors (PPIs), H2 receptor antagonists (H2RAs), and non-acid suppressant use) were evaluated in biopsies of the antrum and corpus using a generalized linear mixed model in all patients. Results: The mean follow-up period and number of biopsies were 5.48 ± 4.69 years and 2.62 ± 1.67 times, respectively. Improvement in the atrophy scores of both the antrum (p = 0.042) and corpus (p = 0.020) were significantly superior in patients with non-acid suppressant drug use compared with those of PPI and H2RA use. Metaplasia scores in both the antrum and corpus did not improve in all groups, and no significant differences were observed among groups in the antrum (p = 0.271) and corpus (p = 0.077). Conclusions: Prolonged acid suppression by PPIs or H2RAs may limit the recovery of gastric atrophy following H. pylori eradication.

Cell Proliferation and Inflammation on Biopsy Samples With Multifocal Atrophic Gastritis Before and 1 Year After Helicobacter pylori Eradication

2005 ◽  
Vol 129 (11) ◽  
pp. 1451-1456
Author(s):  
Jeannette Guarner ◽  
Jeanine Bartlett ◽  
Roslyn Seitz ◽  
Toni Whistler ◽  
Roberto Herrera-Goepfert ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Helicobacter Pylori ◽  
T Lymphocytes ◽  
Intestinal Metaplasia ◽  
Eradication Therapy ◽  
Ki 67 ◽  
Proliferation Markers ◽  
Helicobacter Pylori Eradication ◽  
Biopsy Specimens ◽  
H Pylori

Abstract Context.—Results of clinical trials that have assessed whether gastric cancer is preventable with Helicobacter pylori eradication therapy remain inconclusive. These trials have used atrophy, intestinal metaplasia, and dysplasia as histopathologic end points that reflect possible preneoplastic lesions. Trial results would be more compelling if cell proliferation and inflammatory markers improved simultaneously with histopathologic lesions. Objective.—To study the presence of cell proliferation markers and type of inflammatory cells in biopsy specimens with gastritis, atrophy, and intestinal metaplasia before and 1 year after H pylori therapy and to determine if immunohistochemistry can be used to study these. Design.—We evaluated 12 subjects with gastritis and 16 with gastritis and multiple foci of atrophy and intestinal metaplasia by using immunohistochemical assays for tumor suppressor protein p53, proliferation marker Ki-67, cell cycle regulator cyclin D1, T and B lymphocytes, macrophages, and TUNEL (terminal deoxynucleotide transferase deoxyuridine triphosphate nick end labeling) assay for apoptosis. The biopsy specimens were selected from a randomized clinical trial that studied improvement of histopathologic gastric lesions after H pylori eradication. Results.—Groups of surface epithelial cells that expressed p53 and Ki-67 were observed more often in subjects with atrophy and intestinal metaplasia compared with those with gastritis alone. T lymphocytes in the lamina propria were frequently observed 1 year after treatment in subjects with atrophy and intestinal metaplasia. Conclusions.—Immunohistochemical assays for cell proliferation and inflammatory cell markers showed different distribution patterns in these gastric biopsy specimens. The presence of T lymphocytes and groups of cells that expressed proliferation markers in subjects with multiple foci of atrophy and intestinal metaplasia needs further study.

Apparent Intracellular Helicobacter pylori Detected by Immunohistochemistry: The Missing Link in Eradication Failure

2020 ◽  
Author(s):  
Andrea Beer ◽  
Helmut Hudler ◽  
Maria Hader ◽  
Michael Kundi ◽  
Susanne Hudler ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Eradication Therapy ◽  
Test Results ◽  
First Line ◽  
Before And After ◽  
Living Bacterium ◽  
Gastric Biopsies ◽  
Polymerase Chain ◽  
H Pylori ◽  
The Impact

Abstract Background Helicobacter pylori is primarily an extracellularly living bacterium. However, seemingly intracellular occurrence can often be detected by immunohistochemical stains. Considering antimicrobial resistance, we investigated the impact of the apparent intracellular H. pylori (aiHp) on treatment failure of first-line triple therapies. Methods Gastric biopsies of 814 patients infected with H. pylori naive to treatment were analyzed before and after eradication therapy by immunohistochemistry. Of these, 373 received treatment consisting of amoxicillin, clarithromycin, and proton pump inhibitor (AC/PPI). Availability of polymerase chain reaction-based clarithromycin susceptibility test results from pretreatment gastric biopsies was a precondition for matching 52 aiHp to 52 non-aiHp cases within the AC/PPI group. Results AiHp were detected mostly in low counts predominantly in corpus biopsies, rarely in antrum biopsies (95.2% vs 24.6%); they were found in 497 (61%) of all patients and in 192 of 373 patients (51.5%) in the AC/PPI group. The eradication rate in aiHp versus non-aiHp cases was 44.4% versus 72.9% in the entire sample and 45.3% versus 66.8% in the AC/PPI group. Among the 104 paired patients, respective values were 46.2% versus 78.8%; in clarithromycin-susceptible cases, 60.6% versus 91.9%. Both aiHp and resistance to clarithromycin proved to be highly significant (P ≤ .001) and independent predictors of eradication failure. Twelve of 13 aiHp cases with a clarithromycin-sensitive strain who failed eradication developed resistance to the antibiotic. Conclusions AiHp found by immunohistochemical staining especially in corpus biopsies proved to be a risk factor for failure of first-line triple therapies; occurrence of aiHp should be considered with regard to therapy options.

scholarly journals Increased Reflux Esophagitis after Helicobacter pylori Eradication Therapy in Cases Undergoing Endoscopic Submucosal Dissection for Early Gastric Cancer

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1779
Author(s):  
Masaki Katsurahara ◽  
Ichiro Imoto ◽  
Yuhei Umeda ◽  
Hiroshi Miura ◽  
Junya Tsuboi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Early Gastric Cancer ◽  
Endoscopic Submucosal Dissection ◽  
Reflux Esophagitis ◽  
Eradication Therapy ◽  
Submucosal Dissection ◽  
Before And After ◽  
H Pylori

Background: The role of Helicobacter pylori in the pathogenesis of reflux esophagitis is controversial. This study investigated the frequency of reflux esophagitis before and after H. pylori eradication in patients having endoscopic submucosal dissection for early gastric cancer. Methods: This study included 160 patients that fulfilled the study’s criteria. Endoscopy was performed before and after H. pylori eradication, and reflux esophagitis was evaluated during the follow-up period. Results: Seropositivity for H. pylori in patients with early gastric cancer was 68.8%, 101 of them received eradication therapy. During the follow-up period, the incidence of reflux esophagitis increased from 3.1% to 18.8% in the successful eradication group but no case of reflux esophagitis was observed in the failed eradication group. The univariate and multivariate analyses showed a significant correlation between successful H. pylori eradication rate and the development of reflux esophagitis. Conclusions: This study demonstrated that a successful H. pylori eradication therapy is a risk factor for newly developed reflux esophagitis in patients with endoscopic submucosal dissection for early gastric cancer.

scholarly journals Анализ изотопического состава выдыхаемого воздуха методами диодной лазерной спектроскопии в районе 2 μm для диагностики Helicobacter pylori-ассоциированных заболеваний-=SUP=-*-=/SUP=-

2019 ◽  
Vol 126 (6) ◽  
pp. 788
Author(s):  
В.Т. Ивашкин ◽  
С.Г. Касоев ◽  
Е.В. Степанов
Keyword(s):  
Helicobacter Pylori ◽  
Gastrointestinal Tract ◽  
Diode Laser ◽  
Breath Test ◽  
Eradication Therapy ◽  
Tunable Diode Laser ◽  
Biopsy Material ◽  
Stomach Body ◽  
Before And After ◽  
H Pylori

Spectral analysis of 13СО2/12СО2 isotope ratio in exhaled air based on tunable diode laser spec-troscopy was applied for diagnostics of digestive organ diseases associated with Helicobacter pylori infection. Special spectrophotometer based on tunable diode laser was developed for the analysis of breath isotope content. Spectral range near 2.05 microns where the rotational-vibration R-branch of the 20013-00001 band of 12CO2 interferes with the P-branch of the 20012-00001 band of 13CO2 was used. The 13C-Urea Breath Test (13C-UDT) was used for the H. pylori infection diagnostic in gastrointestinal tract of 309 tested persons. The results of the isotope breath test were compared with the data of morphological analysis of gastric and duodenal mu-cosa obtained by fibrogastroduodenoscopia. For the first time the total value of the histology analysis results for biopsy material taken in the stomach body, in the distal part of stomach and in the duodenum was proposed to be used for the comparative analysis with 13C-UBT data. A relationship of 13C-UBT data with age, nosology, activity and severity of inflammation process, atrophy degree, and type of eradication therapy was analyzed. Distribution of 13C-UBT data ob-tained before and after therapy was demonstrated to reflect epidemiology of gastroduodenal dis-eases, H.pylori infection incidence, specifics of gastrointestinal tract colonization by H.pylori, parameters of inflammation process, as well as therapy effectiveness and peculiarity of the in-fection restoration at failed eradication therapy.

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 Features That Aid Identification of Autoimmune Gastritis in a Background of Active Helicobacter pylori Infection

2021 ◽  
Author(s):  
Jui Choudhuri ◽  
Sara Hall ◽  
Carlos A. Castrodad-Rodriguez ◽  
Maria Westerhoff ◽  
Tony El Jabbour ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Eradication Therapy ◽  
Autoimmune Gastritis ◽  
Full Thickness ◽  
Cell Hyperplasia ◽  
Oxyntic Mucosa ◽  
Ecl Cell ◽  
Oxyntic Gland ◽  
H Pylori

Context.— Helicobacter pylori–associated and autoimmune gastritis may coexist in a subset of patients who require treatment for both disorders. Objective.— To delineate findings that identify autoimmune gastritis in the background of H pylori infection. Design.— We examined cases of (1) patients with H pylori–associated gastritis who had successful eradication therapy and subsequent biopsies diagnostic of autoimmune gastritis and (2) H pylori–associated gastritis wherein pathologists noted features of autoimmune gastritis during original interpretation. Control patients underwent H pylori eradication but lacked evidence of autoimmune gastritis or H pylori infection after 10 years of follow-up. Results.— Eight subjects had H pylori–associated gastritis followed by H pylori–negative sampling that showed autoimmune gastritis. Review of original samples showed full-thickness inflammation of oxyntic mucosa in 8 of 8 and oxyntic gland loss in 7 of 8 cases. Enterochromaffin-like (ECL) cell hyperplasia, pyloric metaplasia, and intestinal metaplasia were present in 4 of 8 (80% of 5 tested cases), 4 of 8, and 3 of 8 cases, respectively. Features of autoimmune gastritis were noted at the time of their original H pylori diagnosis in 11 study subjects. Ten of 11 samples displayed full-thickness inflammation of oxyntic mucosa and/or partial loss of oxyntic glands, 8 of 11 had ECL cell hyperplasia (all tested cases), 6 of 11 showed pyloric metaplasia, and 4 of 11 harbored intestinal metaplasia. Except for full-thickness oxyntic mucosa inflammation, these features were absent in control cases. Conclusions.— Full-thickness inflammation combined with oxyntic gland loss and ECL cell hyperplasia may help to identify autoimmune gastritis in patients with concomitant H pylori 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.

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