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 ◽  
...  

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.

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.


F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 1747 ◽  
Author(s):  
David R. Scott ◽  
George Sachs ◽  
Elizabeth A. Marcus

Infection of the stomach by the gastric pathogen Helicobacter pylori results in chronic active gastritis and leads to the development of gastric and duodenal ulcer disease and gastric adenocarcinoma. Eradication of H. pylori infection improves or resolves the associated pathology. Current treatments of H. pylori infection rely on acid suppression in combination with at least two antibiotics. The role of acid suppression in eradication therapy has been variously attributed to antibacterial activity of proton pump inhibitors directly or through inhibition of urease activity or increased stability and activity of antibiotics. Here we discuss the effect of acid suppression on enhanced replicative capacity of H. pylori to permit the bactericidal activity of growth-dependent antibiotics. The future of eradication therapy will rely on improvement of acid inhibition along with current antibiotics or the development of novel compounds targeting the organism’s ability to survive in acid.


2020 ◽  
Vol 8 (10) ◽  
pp. 1457
Author(s):  
Tamaki Ikuse ◽  
Masanori Toda ◽  
Kosuke Kashiwagi ◽  
Kimiko Maruyama ◽  
Masumi Nagata ◽  
...  

Evidence relating to the efficacy of Helicobacter pylori eradication therapy for chronic immune thrombocytopenic purpura (cITP) in childhood is inadequate. The aim of this retrospective study was to determine the efficacy of H. pylori eradication therapy for platelet response in pediatric patients with cITP in our hospital, and to perform a systematic review of previous reports about pediatric patients with cITP who were positive for H. pylori infection and were treated with H. pylori eradication therapy. Analysis of the data of pediatric patients with cITP in our hospital and a systematic review of digital literature databases of studies in pediatric patients with cITP were performed. Data of 33 pediatric patients with cITP from our hospital records showed that the prevalence of H. pylori infection and the rate of response to platelet therapy were 15% and 33.3%, respectively. Data of 706 pediatric patients from 18 previous reports showed that the prevalence of H. pylori infection and rate of platelet response were 23% and 43.8%, respectively. Eradication therapy for H. pylori infection in pediatric cITP patients can be expected to result in a response equivalent to that in the adult population, with fewer adverse effects than other treatments for cITP.


2020 ◽  
Vol 9 (9) ◽  
pp. 3007 ◽  
Author(s):  
Mitsushige Sugimoto ◽  
Masaki Murata ◽  
Hitomi Mizuno ◽  
Eri Iwata ◽  
Naoyoshi Nagata ◽  
...  

Backgrounds: The etiology of gastroesophageal reflux disease (GERD) including reflux esophagitis and non-erosive reflux disease is multifactorial and a recent meta-analysis showed no association between the development of GERD and Helicobacter pylori eradication in both Western and East-Asian populations. However, the problem remains that various inclusion criteria are used in these studies, which hinders meta-analysis. With a focus on reflux esophagitis with endoscopic mucosal injury, we meta-analysed to evaluate the association between eradication and reflux esophagitis and symptoms using a clearly defined set of inclusion criteria. Methods: We conducted a meta-analysis of studies published up until March 2020, which compared the incidence of reflux esophagitis and symptoms between patients undergoing H. pylori eradication therapy in a randomized placebo-controlled trial (Category A); between patients with successful and failed eradication (Category B); and between patients with successful vs. failed eradication, receipt of placebo, or no-treatment H. pylori-positives (Category C). Results: A total of 27 studies were included. Significant statistical effects were found for development of endoscopic reflux esophagitis [relative risk (RR): 1.46, 95% confidence interval (CI): 1.16–1.84, p = 0.01] or de novo reflux esophagitis (RR: 1.42, 95% CI: 1.01–2.00, p = 0.03) in the case group that received eradication in all studies, especially in Western populations. There was no significant difference in the incidence of symptoms after eradication between patient and control groups, regardless of category, location of population, or baseline disease. Conclusions: Eradication therapy for H pylori increases the risk of reflux esophagitis, irrespective of past history of esophagitis. In contrast, no effect was seen on reflux-related symptoms.


2016 ◽  
Vol 6 (1) ◽  
pp. 19-24
Author(s):  
DB. Namiot ◽  
K. Leszczyńska ◽  
A. Namiot ◽  
A. Kemona ◽  
R. Bucki ◽  
...  

Purpose: The aim of this study was to evaluate the presence of H. pylori antigens in the oral cavity (dental plaque and saliva) of patients undergoing systemic eradication therapy. Materials and methods: The study was conducted in 49 subjects with H. pylori stomach infection. H. pylori antigens in dental plaque and saliva were evaluated with immunological method. Results: In subjects with initial H. pylori oral infection, the presence of H. pylori antigens in the oral cavity 6 weeks after successful or unsuccessful H. pylori eradication therapy in the stomach was 47.0% and 50.0%, respectively. In subjects without initial oral infection with H. pylori, the presence of H. pylori antigens in the oral cavity 6 weeks after successful and unsuccessful eradication therapy in the stomach was 30.0% and 20.0%, respectively. Conclusions: The immunological method detecting H. pylori antigens in the dental plaque and saliva cannot be recommended to evaluate the efficacy of H. pylori eradication in the oral cavity.


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.


2019 ◽  
Vol 8 (9) ◽  
pp. 1324 ◽  
Author(s):  
Seung Joo Kang ◽  
Boram Park ◽  
Cheol Min Shin

Background: Previous studies on the effect of Helicobacter pylori eradication on functional dyspepsia (FD) are conflicting. We performed a comprehensive meta-analysis on this issue according to region and prevalence of H. pylori. Methods: Randomized controlled trials (RCTs) evaluating the effect of eradication of H. pylori on functional dyspepsia up to December 2018 were searched through PubMed, EMBASE, and the Cochrane Library. Subgroup analyses by the outcome measure, region, and prevalence of H. pylori were performed. All data were analyzed with Review Manager 5.3. Results: Eighteen RCTs were included in our meta-analysis. Overall, the H. pylori eradication group showed significant improvement of symptoms compared with the control group (risk ratio (RR) = 1.18; 95% confidence interval (CI): 1.07–1.30, p < 0.01). There was moderate heterogeneity among studies (I2 = 34%) and the number needed to treat (NNT) was 15.0. Helicobacter pylori eradication improved dyspeptic symptoms both in low (<50%) and high (≥50%) H. pylori prevalence regions (RR = 1.21 and 1.17; 95% CI: 1.02–1.44 and 1.06–1.29, I2 = 49% and 5%, respectively.) In the analysis of studies from Asia, however, the effect of eradication on improvement of dyspepsia was not significant (RR = 1.14; 95% CI: 0.99–1.33, p = 0.08, I2 = 37%). Conclusion: Overall, H. pylori eradication provides significant improvement of symptoms in functional dyspepsia patients regardless of H. pylori prevalence. However, in the analysis of studies from Asia, the eradication did not significantly improve dyspeptic symptoms. In this region, eradication for dyspepsia can be individualized.


2019 ◽  
Vol 9 (3-4) ◽  
pp. 523-530
Author(s):  
L. B. Drygina ◽  
V. N. Ellenidi ◽  
N. A. Bardysheva ◽  
M. M. Bogoslovskiy

Effective eradication of Helicobacter pylori infection is an important means to reduce the risk of precancerous changes in the gastric mucosa and prevention of gastric cancer. A search for non-invasive diagnostic tools for Helicobacter pylori infection, evaluation of the effectiveness of eradication remains of high importance.The aim of the study was to assess an informative value of detecting pepsinogen I and II as well as serum antibodies to Helicobacter pylori while assessing an efficacy of treated chronic Helicobacter gastritis and identifying preneoplastic changes in the stomach mucosa. There enrolled 113 male patients with chronic gastritis aged 41 to 76, average age- (56.7±0.7) years. Examination of patients was carried out at admission to the clinic, as well as at 2 and 12 months after administering a standard eradication therapy. It was found that Helicobacter pylori infection was detected in 101 (89.4%) patients. Groups of patients with effective eradication therapy were noted. A time-dependent level of antibodies to Helicobacter pylori, as well as measured concentration of pepsinogen I and II after the onset of eradication treatment were determined. Which were analyzed in connection with the results of histology examination of gastric mucosa biopsy specimens and expression of oncoproteins Ki-67, Bcl-2, c-erbB-2, p16 in the gastric mucosa depending on efficacy of eradication therapy. It is shown that effective eradication therapy was characterized by significantly decreased serum level of IgG antibodies to Helicobacter pylori 2 months after the onset of treatment. Moreover, a significantly decreased pepsinogen II and serum IgG antibodies to Helicobacter pylori during eradication therapy were accompanied by a significant decrease in Ki-67 expression in the gastric epithelium. Decreased concentration of pepsinogen II within the first year after Helicobacter pylori eradication therapy was due to a greater decrease in activity of inflammatory changes in the gastric mucosa than to dynamic changes in gastric atrophy and metaplasia. An inverse relation between the serum level of pepsinogen I and atrophy as well as intestinal metaplasia within the gastric mucosa were found.


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