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

Author(s):  
Jui Choudhuri ◽  
Sara Hall ◽  
Carlos A. Castrodad-Rodriguez ◽  
Maria Westerhoff ◽  
Tony El Jabbour ◽  
...  

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.

2019 ◽  
Vol 20 (8) ◽  
pp. 1913 ◽  
Author(s):  
Ryota Niikura ◽  
Yoku Hayakawa ◽  
Yoshihiro Hirata ◽  
Keiji Ogura ◽  
Mitsuhiro Fujishiro ◽  
...  

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.


2005 ◽  
Vol 129 (11) ◽  
pp. 1451-1456
Author(s):  
Jeannette Guarner ◽  
Jeanine Bartlett ◽  
Roslyn Seitz ◽  
Toni Whistler ◽  
Roberto Herrera-Goepfert ◽  
...  

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.


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 ◽  
...  

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.


Author(s):  
Kichul Yoon ◽  
Nayoung Kim

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.


Gut ◽  
2020 ◽  
Vol 69 (12) ◽  
pp. 2093-2112 ◽  
Author(s):  
Jyh-Ming Liou ◽  
Peter Malfertheiner ◽  
Yi-Chia Lee ◽  
Bor-Shyang Sheu ◽  
Kentaro Sugano ◽  
...  

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.


Author(s):  
Chan Hyuk Park

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.


2018 ◽  
Vol 11 (3) ◽  
pp. 187-193 ◽  
Author(s):  
Petruta Violeta Filip ◽  
◽  
Denisa Cuciureanu ◽  
Laura Sorina Diaconu ◽  
Ana Maria Vladareanu ◽  
...  

Primary gastric lymphoma (PGL) represents a rare pathology, which can be easily misdiagnosed because of unspecific symptoms of the digestive tract. Histologically, PGL can vary from indolent marginal zone B-cell lymphoma of the mucosa-associated lymphoid tissue (MALT) to aggressive diffuse large B-cell lymphoma (DLBCL). During the years, clinical trials revealed the important role of Helicobacter pylori (H. pylori) in the pathogenesis of gastric MALT lymphoma. Infection with Helicobacter pylori is an influential promoter of gastric lymphomagenesis initiation. Long-term studies revealed that eradication therapy could regress gastric lymphomas.


2017 ◽  
Vol 55 (07) ◽  
pp. 653-656 ◽  
Author(s):  
Caspar Franck ◽  
Armin Hoffmann ◽  
Alexander Link ◽  
Christian Schulz ◽  
Kerstin Wuttig ◽  
...  

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.


2016 ◽  
Vol 12 (2) ◽  
pp. 122-126 ◽  
Author(s):  
Md Sayeed Hasan ◽  
Md Shirajul Islam Khan ◽  
Jannatun Nayeem

Introduction: Chronic Idiopathic Urticaria (CIU) has an estimated prevalence of 35-65% and impacts 15 to 25% of the population at some point in their lives. Studies have shown the possible involvement of Helicobacter pylori (H. pylori) infection in chronic idiopathic urticaria (CIU), but the relationship remains controversial. Objective: To quantitatively assess the association between H. pylori infection and chronic idiopathic urticaria. Materials and Methods: This was a case-control type of analytical study and 100 patients were enrolled fifty patients of CIU fulfilling inclusion criteria with no identifiable cause were taken as case and patients without urticaria were taken as control, attending in the department of Dermatology & Venereology, CMH Dhaka for treatment from May 2015 to Aug 2016. Helicobacter pylori infection was confirmed by serum IgG for H. pylori test. Results: The result showed that H. pylori infection significantly affected a high percentage of patients 30 (60%) with chronic idiopathic urticaria. Male respondents were more positive 16(53.3%) than female 14(46.7%), in the middle aged 31-50 year about 18(60%) and triple drug therapy was successful in 16(53.33%) patients in whom H. pylori was detected. Conclusion: Urticaria is a common clinical disorder with complex triggering factors. Chronic urticaria has provided evidence that enteric infection with H. pylori may induce the disease. In this case control study, it was evident that chronic idiopathic urticaria was associated with positive serum IgG for H. Pylori. A trial of H. pylori eradication therapy may be offered to patients with CIU and evidence of H. pylori infection. Journal of Armed Forces Medical College Bangladesh Vol.12(2) 2016: 122-126


2010 ◽  
Vol 67 (12) ◽  
pp. 991-997
Author(s):  
Vesna Brzacki ◽  
Aleksandar Nagorni ◽  
Dragan Mihailovic ◽  
Suzana Raicevic-Sibinovic ◽  
Bojan Mladenovic

Background/Aim. The symptoms of gastroesophageal reflux desease (GERD) are among the most common complaints for which patients are indicated for visiting gastroenterologist. It occurs as a result of the effect made by gastric reflux contents that moves into the esophagus. The prevalence of all forms of GERD is 40%. The aim of this study was to analyze the grade of esophagitis, chromendoscopical and histological findings of esophagus in patients with GERD before and after the therapy. Methods. A prospective study included 90 patients with symptoms of GERD, divided into 2 groups depending on whether they had endoscopic signs of gastroezophageal reflux (group ERD), or not (group NERD). All the patients had esophagogastroduodenoscopy, chromoendoscopy staining, test for Helicobacter pylori and histological findings of the esophagus. In the patients with Helicobacter pylori infection eradication therapy was done. Results. Esophagitis-B level was present in most of the patients. Among the groups, roughly the same number responded to positive findings on chromoendoscopy. After the therapy, chromoendoscopy was significantly negative in both groups of the patients comparing to chromoendoscopy before the therapy (p = 0.00001). Multiplication and elongation of papilla, basal cell hyperplasia, vascular dilatation, increasing of mitotic activity and the presence of polymorphonuclear leukocyte cells were statistically more frequent histological findings in the group ERB compared to the group NERB. After the therapy, the patients in both groups had statistically less histological findings of appropriate esophageal parameters. Conclusion. Chromoendoscopy combined with the standard endoscopy increases the sensitivity and specificity for reflux disease. Histology in the reflux disease is associated with endoscopic and clinical findings so that the localization of taking biopsies and histological criteria of pathohistological changes must be clearly defined. Multiplication and elongation of papilla, basal cell hyperplasia and the presence of polymorphonuclear leukocytes are the most relevant criteria in the diagnosis NERD.


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