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.

Outcome of gastric atrophy and intestinal metaplasia in patients with or without Helicobacter pylori infection during a ten year follow-up

2003 ◽  
Vol 124 (4) ◽  
pp. A606
Author(s):  
Renzo Suriani ◽  
Alba Rocco ◽  
Dario Mazzucco ◽  
Ivo Venturini ◽  
Gabriele Budillon ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
Gastric Atrophy ◽  
Helicobacter Pylori Infection

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.

Prospective Study of Helicobacter pylori Eradication Therapy in Stage IE High-Grade Mucosa-Associated Lymphoid Tissue Lymphoma of the Stomach

2001 ◽  
Vol 19 (22) ◽  
pp. 4245-4251 ◽  
Author(s):  
Li-Tzong Chen ◽  
Jaw-Town Lin ◽  
Rong-Yaun Shyu ◽  
Chang-Ming Jan ◽  
Chi-Long Chen ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Prospective Study ◽  
Lymphoid Tissue ◽  
Remission Rate ◽  
Early Stage ◽  
Eradication Therapy ◽  
Stage I ◽  
High Grade ◽  
H Pylori

PURPOSE: High-grade mucosa-associated lymphoid tissue (MALT) lymphomas of the stomach are generally believed to be Helicobacter pylori–independent, autonomously growing tumors. However, anecdotal cases of regression of high-grade lymphomas after the cure of H pylori infection had been described. The present prospective study was conducted to evaluate the effect of anti–H pylori therapy in stage IE high-grade gastric MALT lymphomas. PATIENTS AND METHODS: Sixteen patients with H pylori infection and stage IE gastric high-grade MALT lymphoma consented to a brief antibiotic therapy as first-line treatment from June 1995 through April 2000. Then, patients underwent intensive endoscopic follow-up examinations (± endoscopic ultrasonography) with biopsy to evaluate tumor response. Patients with significant improvement of gross lesions that accompanied regression of large cells were followed up without additional treatment. Patients without significant improvement were immediately referred to systemic chemotherapy. RESULTS: Eradication of H pylori was achieved in 15 patients and was accompanied by rapid gross tumor regression and disappearance of large cells in 10. All 10 of these patients with early response had subsequent complete histologic remission of lymphoma. The complete remission rate was 62.5% (95% confidence interval, 35.8% to 89.1%). The response rate was not affected by the tumor grading (proportion of large blast cells within the tumor) but was adversely affected by the depth of tumor invasion. At a median follow-up of 43.5 months (range, 21.1 to 67.4 months), all 10 of these patients remained lymphoma-free. The median duration of complete response was 31.2 months (range, 14.4 to 49.1 months). CONCLUSION: These results suggest that high-grade transformation is not necessarily associated with the loss of H pyloridependence in early-stage MALT lymphomas of the stomach.

scholarly journals Precancerous gastric conditions in high Helicobacter pylori prevalence areas: comparison between Eastern European (Lithuanian, Latvian) and Asian (Taiwanese) patients

Medicina ◽  
2007 ◽  
Vol 43 (8) ◽  
pp. 623 ◽  
Author(s):  
Laimas Jonaitis ◽  
Audrius Ivanauskas ◽  
Dainius Jančiauskas ◽  
Konrads Funka ◽  
Agnese Sudraba ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Intestinal Metaplasia ◽  
The Elderly ◽  
Gastric Atrophy ◽  
Eastern European ◽  
Urease Test ◽  
Gastric Biopsies ◽  
The Mean ◽  
H Pylori ◽  
Positive Results

The aim of the study was to compare the prevalence and severity of precancerous condition – gastric atrophy and intestinal metaplasia (IM) between Eastern European (Lithuania and Latvia) and Asian (Taiwan) countries in population older than 55 years. Methods. Patients aged 55 years and older, referred for upper endoscopy due to dyspeptic symptoms, were included in the study. Gastric biopsies were histological investigated according modified Sydney classification. Helicobacter pylori (H. pylori) was detected if any two of three methods (urease test, histology, and serology) were positive. Results. Overall 322 patients included: 52 from Taiwan (TW), 171 from Latvia (LV) and 99 from Lithuania (LT). There were 227 (70%) females and 95 (30%) males. The mean age of TW patients was significantly lower (61.0±5.8 years), than of LV (68.1±7.3 years) and LT (66.5±7.5 years) patients. H. pylori was established in 224 (69.6%) patients. H. pylori positivity was established in 43 (82.7%) TW patients, in 112 (65.5%) LV patients, and in 69 (69.7%) LT patients (P>0.05). In H. pylori-infected patients, any atrophy either in the corpus or in the antrum of the stomach was detected in 26 (60.5%) TW patients, in 40 (35.7%) LV patients, and in 36 (52.2%) LT patients (between TW and LV patients P<0.005). Severe atrophy (grade 2 or 3) detected in 8 (18.6%) TW patients, in 17 (15.2%) LV patients, and in 18 (26.1%) LT patients (P>0.05). Intestinal metaplasia was detected in 22 (51.2%) TW patients, in 37 (33.0%) LV patients and in 31 (44.9%) LT patients among countries (P>0.05). There were no significant differences in proportions of different degrees of both atrophy and intestinal metaplasia among countries. Intestinal metaplasia was found in 79 (77.5%) of 102 patients with any degree of atrophy and in 11 (9.0%) of 122 patients without atrophy (P<0.0001). We found strong statistically significant correlations between atrophy and intestinal metaplasia in antrum (r=0.89), P<0.01, and corpus (r= 0.73), P<0.01. Conclusions. The prevalence of H. pylori in the elderly population is still high in LT, LV, and TW. There are no significant differences in prevalence of gastric atrophy and intestinal metaplasia among TW, LT, and LV. There is a strong correlation between gastric atrophy and intestinal metaplasia.

scholarly journals Detection of Helicobacter pylori in Stool Specimens by PCR and Antigen Enzyme Immunoassay

1998 ◽  
Vol 36 (9) ◽  
pp. 2772-2774 ◽  
Author(s):  
Athanasios Makristathis ◽  
Eva Pasching ◽  
Kurt Schütze ◽  
Margit Wimmer ◽  
Manfred L. Rotter ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Enzyme Immunoassay ◽  
Eradication Therapy ◽  
Diagnostic Tools ◽  
Pcr Assay ◽  
Highly Sensitive ◽  
Stool Specimens ◽  
H Pylori ◽  
Seminested Pcr

A highly sensitive seminested PCR assay to detectHelicobacter pylori DNA in feces was developed. PCR with stool specimens and a novel antigen enzyme immunoassay (EIA) forH. pylori detection in feces were evaluated as diagnostic tools and in follow-up with samples from 63 infected and 37 noninfected persons. Infected individuals received eradication therapy followed by endoscopic follow-up 35 days after the start of treatment. At that time, a second stool specimen was obtained from 55 of these patients. Before eradication, the sensitivity of PCR was 93.7% and that of EIA 88.9%. Specificities were 100 and 94.6%, respectively. Of the 55 follow-up specimens, 41 originated from patients from whom H. pylori had been eradicated. Of these, 21 were still positive by PCR and 13 were positive by EIA, indicating that 1 month may be too short a period for follow-up evaluation of stool specimens by these tests.

scholarly journals Helicobacter pylori and Gastric Metaplasia: Their Status after Eradication Therapy

1970 ◽  
Vol 15 (2) ◽  
pp. 59-63
Author(s):  
Maleeha Hussain ◽  
Mian Ahmad Mashud ◽  
Hazera Khatun ◽  
Tareak Al Nasir
Keyword(s):  
Duodenal Ulcer ◽  
Helicobacter Pylori ◽  
Eradication Therapy ◽  
Ulcer Recurrence ◽  
Ulcer Margin ◽  
Gastric Metaplasia ◽  
H Pylori ◽  
The Relationship

This study was carried out with an aim to investigate the relationship between gastricmetaplasia with H. pylori and the effect of eradication therapy. A total of 210 patients withhistory of dyspepsia were included in the study of which 50 were enrolled in the eradicationtherapy. After the eradication therapy 35 patients came for follow-up endoscopy. Pairedendoscopic biopsies were taken from antrum and duodenal ulcer margin and were examined forH. pylori and for duodenitis and gastric metaplasia. Gastric metaplasia was significantlyassociated with H. pylori. After eradication H. pylori showed further extension of gastricmetaplasia. It can be recommended that these patients can be further followed up to see thecourse of gastric metaplasia and what impact it has on ulcer recurrence and re-infection.doi: 10.3329/taj.v15i2.3908TAJ December 2002; Vol.15(2):59-63

scholarly journals Helicobacter pylori eradication therapy is effective in the treatment of early-stage H pylori–positive gastric diffuse large B-cell lymphomas

Blood ◽  
2012 ◽  
Vol 119 (21) ◽  
pp. 4838-4844 ◽  
Author(s):  
Sung-Hsin Kuo ◽  
Kun-Huei Yeh ◽  
Ming-Shiang Wu ◽  
Chung-Wu Lin ◽  
Ping-Ning Hsu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Confidence Interval ◽  
B Cell ◽  
De Novo ◽  
Early Stage ◽  
Eradication Therapy ◽  
B Cell Lymphomas ◽  
H Pylori ◽  
Large B Cell

Abstract An explorative study evaluates the efficacy of Helicobacter pylori (HP) eradication (HPE) therapy on early-stage gastric diffuse large B-cell lymphomas (DLBCLs) without features of mucosa-associated lymphoid tissue (MALT), the pure (de novo) DLBCLs, in comparison with its efficacy on high-grade transformed gastric MALT lymphomas, the DLBCL(MALT). In total, 50 patients of stage IE/IIE1 HP-positive gastric DLBCLs with frontline HPE treatment were included. HP infection was successfully eradicated in 100% (16/16) of the pure (de novo) DLBCL patients and 94.1% (32/34) of the DLBCL(MALT) patients. In total, 68.8% (11/16) of pure (de novo) DLBCL patients and 56.3% (18/32) of DLBCL(MALT) patients achieved complete pathologic remission (pCR) after HPE therapy. The median time to pCR was 2.1 months (95% confidence interval, 0.6%-3.7%) for pure (de novo) DLBCLs and 5.0 months (95% confidence interval, 2.8%-7.5%; P = .024) for DLBCL(MALT). At a median follow-up of 7.7 years, all patients with pCR after HPE therapy were alive and free of lymphomas, except for one patient with pure (de novo) DLBCL who died of lung cancer. Similar to DLBCL(MALT), a substantial portion of early-stage HP-positive gastric pure (de novo) DLBCLs remains HP-dependent and responds to antibiotic treatment. Prospective studies to validate the findings are warranted.

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 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 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.

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