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Background & Aims: The immune compartment is critical for maintaining tissue homeostasis. A weak immune response increases susceptibility to infection, but immune hyperactivation causes tissue damage, and chronic inflammation may lead to cancer development. In the stomach, inflammation damages the gastric glands and drives the development of potentially preneoplastic metaplasia. Glucocorticoids are potent anti-inflammatory steroid hormones that are required to suppress gastric inflammation and metaplasia. However, these hormones function differently in males and females. Here, we investigate the impact of sex on the regulation of gastric inflammation., Methods: Endogenous glucocorticoids and male sex hormones were removed from mice using adrenalectomy and castration, respectively. Mice were treated with 5α-dihydrotestosterone (DHT) to test the effects of androgens on regulating gastric inflammation. Single-cell RNA sequencing of gastric leukocytes was used to identify the leukocyte populations that were the direct targets of androgen signaling. Type 2 innate lymphoid cells (ILC2s) were depleted by treatment with CD90.2 antibodies., Results: We show that adrenalectomized female mice develop spontaneous gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM) but that the stomachs of adrenalectomized male mice remain quantitatively normal. Simultaneous depletion of glucocorticoids and sex hormones abolished the male-protective effects and triggered spontaneous pathogenic gastric inflammation and SPEM. Treatment of female mice with DHT prevented gastric inflammation and SPEM development when administered concurrent with adrenalectomy and also reversed the pathology when administered after disease onset. Single-cell RNAseq of gastric leukocytes revealed that ILC2s expressed abundant levels of both the glucocorticoid receptor (Gr) and androgen receptor (Ar). We demonstrated that DHT treatment potently suppressed the expression of the proinflammatory cytokines Il13 and Csf2 by ILC2s. Moreover, ILC2 depletion protected the stomach from SPEM development., Conclusions: Here, we report a novel mechanism by which glucocorticoids and androgens exert overlapping effects to regulate gastric inflammation. Androgen signaling within ILC2s prevents their pathogenic activation by suppressing the transcription of proinflammatory cytokines. This work revealed a critical role for sex hormones in regulating gastric inflammation and metaplasia., (Published by Elsevier Inc.)

Background & Aims: The association between cellular senescence and Helicobacter pylori-induced atrophic gastritis is not clear. Here, we explore the role of cellular senescence in H pylori-induced atrophic gastritis and the underlying mechanism., Methods: C57BL/6J mice were infected with H pylori for biological and mechanistic studies in vivo. Gastric precancerous lesions from patients and mouse models were collected and analyzed using senescence-associated beta-galactosidase, Sudan Black B, and immunohistochemical staining to analyze senescent cells, signaling pathways, and H pylori infection. Chromatin immunoprecipitation, luciferase reporter assays, and other techniques were used to explore the underlying mechanism in vitro., Results: Gastric mucosa atrophy was highly associated with cellular senescence. H pylori promoted gastric epithelial cell senescence in vitro and in vivo in a manner that depended on C-X-C motif chemokine receptor 2 (CXCR2) signaling. Interestingly, H pylori infection not only up-regulated the expression of CXCR2 ligands, C-X-C motif chemokine ligands 1 and 8, but also transcriptionally up-regulated the expression of CXCR2 via the nuclear factor-κB subunit 1 directly. In addition, CXCR2 formed a positive feedback loop with p53 to continually enhance senescence. Pharmaceutical inhibition of CXCR2 in an H pylori-infected mouse model attenuated mucosal senescence and atrophy, and delayed further precancerous lesion progression., Conclusions: Our study showed a new mechanism of H pylori-induced atrophic gastritis through CXCR2-mediated cellular senescence. Inhibition of CXCR2 signaling is suggested as a potential preventive therapy for targeting H pylori-induced atrophic gastritis. GEO data set accession numbers: GSE47797 and GSE3556., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: A 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)., Methods: 28 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., Results: Consensus 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 ., Conclusion: Evidence 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., Competing Interests: Competing interests: J-ML reports receiving lecture fees from Takeda Pharmaceuticals (Taiwan) and Abbott Laboratories. PM reports receiving advisory and lecture fees from Bayer, Mayoly Spindler and Nordmark. DYG is a consultant for RedHill Biopharma and Phathom Pharmaceuticals regarding novel H. pylori therapies and has received research support for culture of Helicobacter pylori., (© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Helicobacter pylori is a significant risk factor for gastric cancer. Recent trials show eradication decreases the incidence of gastric cancer in patients with early-stage gastric cancer. However, data on gastric cancer prevention are inconsistent for patients with precancerous lesions such as atrophic gastritis and intestinal metaplasia., Aim: The aim of the study is to assess the efficacy of H. pylori eradication in gastric cancer prevention in patients with varying risk factors for gastric cancer at baseline., Methods: A systematic review and meta-analysis were performed according to Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. PubMed, Medline, and Google Scholar were searched from inception through March 2019 for randomized controlled trials (RCTs) studying H. pylori eradication on gastric cancer prevention. We estimated the odds ratio (OR) with 95% confidence interval (CI) for each outcome using a random-effects model. P values of less than 0.05 were considered significant., Results: Nine RCTs with total of 6967 patient were included in the analysis. There was significant reduction in gastric cancer incidence in the H. pylori group for patients with early gastric cancer status post endoscopic mucosal resection OR, 0.47; 95% CI, 0.33-0.67; P < 0.0001; I = 0%. There was no difference in gastric cancer incidence in patients with atrophic gastritis and intestinal metaplasia at baseline for H. pylori arm OR, 0.67; 95% CI, 0.42-1.07; P = 0.09; I = 0%). Atrophic gastritis and intestinal metaplasia improved from baseline in the H. pylori arm compared to placebo OR, 2.61; 95% CI, 1.41-4.81; P = 0.002; I = 88 and OR, 2.61; 95% CI, 1.66-4.11; P ≤ 0.0001; I = 0%, respectively., Conclusions: H. pylori eradication is associated with reduced gastric cancer incidence in patients with early-stage gastric cancer and improvement in atrophic gastritis and intestinal metaplasia. There was no difference in gastric cancer incidence in patients with atrophic gastritis and intestinal metaplasia at baseline.

Ethnopharmacological Relevance: Gastrodiae Rhizoma (GR), a well-known and commonly-used TCM (Traditional Chinese Medicine) for treating headache, dizziness, tetanus, epilepsy, and etc., has been proven to relieve chronic atrophic gastritis (CAG). Due to its complex ingredients, the active fractions responsible for the treatment of CAG remain largely unknown., Aim of the Study: To explore the underlying material and interpret its underlying mechanism, the therapeutic effect of extract from different polar parts of Gastrodiae Rhizoma on autoimmune CAG was studied based on the 1 H NMR metabolomics., Materials and Methods: The rat model of CAG was established by autoimmune method. The modeled CAG rats were then treated with 4 polar parts (T1-4 in descending polarity, corresponding to water, n-butanol, ethyl acetate and petroleum ether extracts, respectively) of Gastrodiae Rhizoma for 21 consecutive days. The stomach and serum samples were collected and then subjected to histopathology observation, biochemical measurement (MDA, SOD, GSH, NO, XOD and pepsin), 1 H NMR metabolic profiling and multivariate/univariate statistical analysis., Results: The results showed that T1 had the best therapeutic effect, T2 the second, and T3 and T4 the poorest with no obvious therapeutic effect, demonstrating that the effective components of Gastrodiae Rhizoma should be compounds of high polarity. T1 achieved good therapeutic effects due to the anti-inflammatory and anti-oxidant activities, and by rectifying the disturbed energy and amino acid metabolism in CAG model., Conclusion: This integrated metabolomics approach proved the validity of the therapeutic effect of extract from different polar parts of Gastrodiae Rhizoma on autoimmune CAG, providing new insights into the underlying mechanisms, and demonstrating the feasibility of metabolomics to evaluate efficacy of herbal drug, which is often difficult by traditional means., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Chronic atrophic gastritis (CAG) is one of the most common digestive system diseases worldwide which defined by WHO as initial step of cancer. Gastrodia elata Blume (GEB) is a traditional herbal with multiple pharmacological activities which was widely used in Asian countries. This study aims to explore the preventive and therapeutical effects of Gastrodia elata Blume on auto-immune induced CAG in rats. Tissues of stomachs were collected and submitted to 1 H NMR-based metabolomics analysis and histopathological inspection. The biochemical indexes of MDA, SOD, GSH, NO and XOD were measured. Gastrodia elata Blume could apparently ameliorate the damaged gastric glands and the biochemical parameters, enhance gastric acid secretion, and significantly relieve the inflammation of the stomach. Orthogonal signal correction-partial least squares-discriminant analysis (OSC-PLS-DA) of NMR profiles and correlation network analysis revealed that Gastrodia elata Blume could effectively treat CAG via regulating energy and purine metabolisms, and by anti-oxidation and anti-inflammation effects., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Helicobacter pylori pathogenesis results from the inflammation induced by chronic infection. CBA mice are nonresponsive to gastric Helicobacter infection, providing a useful model for examining host regulation of Helicobacter-induced gastritis. We examined whether gastric Helicobacter nonresponsiveness impacts upon vaccine efficacy and whether immune-mediated protection could occur in the absence of inflammation., Methods: Mice were vaccinated prior to challenge with Helicobacter felis or H. pylori. Gastritis and H. felis colonization was evaluated histologically. H. pylori colonization was quantified by colony-forming assay., Results: Immunizations protected CBA mice against challenge with either H. felis or H. pylori. Protection against H. felis was marked by a loss of nonresponsiveness and development of an atrophic gastritis with mucus metaplasia. However, vaccine-induced protection against H. pylori was only associated with cell infiltration into the gastric mucosa., Conclusions: Nonresponsiveness to gastric Helicobacter infection did not interfere with vaccination-induced protection. Vaccine-induced protective immunity against H. pylori was linked with the induction of cellular infiltration, but importantly not atrophic gastritis., (© 2015 John Wiley & Sons Ltd.)

Assessment of health status of the population - the most important issue in preventive medicine. The objective of this work - to determine the possibility of nonendoscopic screening for gastroduodenal pathology, by the example of atrophic gastritis, in mass medical examinations of working residents in Moscow. Minimally invasive diagnostic test system GastroPanel ("Biohit", Finland) has been used. It allows with the ELISA method to determine both serum indicators of the function of the stomach -pepsinogen 1, gastrin 17 and the presence of H. pylori infection. 758 persons have been examined. The performed study confirms the possibility with the use of a set of mentioned indicators to identify individuals suspected for the presence of gastroduodenal disorders, especially atrophic gastritis, recognized as a precancerous condition. The use in preventive medicine complex diagnostic system, firstly, will make assessment of the health of the population more correct, increase the effectiveness of preventive measures and quality of life, and secondly, will contribute to the diagnosis of diseases of the stomach and duodenum in the early stages.

Context: Gastric type I carcinoid is a rare neoplasm, deriving from enterochromaffin-like cells (ECL), mainly affecting women with autoimmune gastritis. The approach to treatment, either endoscopic, medical or surgical, is not well defined, particularly in multifocal tumours or carcinoids with rapid growth/frequent recurrence., Objective: To determine whether an anti-G17 vaccination might interfere on the natural history of gastric type I carcinoid., Setting: Padua teaching Hospital, outpatient clinic., Design and Patients: Three patients with type I gastric carcinoid in autoimmune gastritis were administered, after informed consent and ethic committee approval, with a vaccine against gastrin 17 (G17), a synthetic peptide that stimulates specific and high-affinity anti-G17 antibodies, and followed up endoscopically and clinically for a mean of 36 months., Main Outcome Measures: Gastric histology and specifically carcinoid growth/recurrence and trend in time in gastrin, G17, pepsinogens, chromogranin A and clinical parameters., Results: Following vaccination, carcinoid regression was observed in 2/3 patients and, in one of the patients, even the disappearance of ECL hyperplasia, with a reduced ECL cells stimulation, confirmed by a significant reduction in chromogranin A levels. Regression was observed in the two patients that showed a more clear local response to the vaccine. Increased autoantibody titre was observed, but no appearance of new autoimmune diseases., Conclusions: Anti-G17 vaccination induced regression of type I gastric carcinoid and could be considered for the treatment of this tumour, when endoscopic removal is not indicated.

To investigate the effect of a high-protein diet on corpus atrophic gastritis in Helicobacter pylori-infected Mongolian gerbils, H. pylori was administered orally to 5-wk-old Mongolian gerbils; and the animals were then fed a control diet (Group C); a high-fat diet (Group F: 40% fat); a high-protein diet (Group P: 32% protein); or a high-fat, high-protein diet (Group FP: 40% fat, 32% protein) for 50 wk beginning at 7 wk of age. In uninfected animals, the mucosal thickness of the corpus was significantly greater in Group P and Group FP than in Group C (P < 0.05). In infected animals, the serum gastrin level was significantly decreased in Group FP and marginally significantly decreased in Group P (P = 0.057) in comparison to Group C. The mucosal thickness of the corpus was significantly greater in Group P and Group FP than in Group C (P < 0.05). Mean inflammation and atrophy scores in the corpus were significantly lower in the high-protein groups (Groups P and FP) than in the control groups (Groups C and F; both inflammation and atrophy: P < 0.05). In conclusion, long-term administration of a high-protein diet suppresses corpus atrophic gastritis in H. pylori-infected Mongolian gerbils.

Objective: Pre-selection of individuals with epidemiological risk factors for Helicobacter pylori infection and atrophic gastritis could increase the efficiency of serologic screening to prevent peptic ulcer disease and gastric cancer in Western countries. The aim of this study was to determine the prevalence of and risk factors for H. pylori infection and atrophic gastritis in a migrant community in The Netherlands., Material and Methods: Inhabitants from an urban district in Rotterdam, The Netherlands with a large proportion of immigrants were randomly selected. Information was collected on demographic factors, socio-economic status, lifestyle, history of dyspeptic symptoms and medication use. In addition, serologic H. pylori and CagA status and the presence of atrophic gastritis were evaluated., Results: In total, 288 subjects were included. Surinamese or Antillean, Turkish, Cape Verdian and Moroccan subjects were H. pylori-infected in 65%, 82%, 86% and 96% of cases, respectively, whereas the infection rate in Dutch subjects was 46% (all p<0.05). Within multivariate logistic regression analysis, ethnicity and number of persons in a household were identified as independent risk factors for H. pylori infection. In addition, mean pepsinogen I level and pepsinogen I/II ratio were significantly lower in subjects of non-Dutch origin as compared to Dutch subjects (both p<0.001). No Dutch subjects suffered from atrophic gastritis, as compared with 12 subjects of non-Dutch origin (p=0.13)., Conclusions: The prevalence of H. pylori is high in migrant populations in The Netherlands. Furthermore, markers of atrophic gastritis are increased in subjects of foreign origin. Therefore, these migrant communities may constitute a target group for serologic screening to prevent H. pylori-related complications in Western countries.

Aim: To investigate the effect of H pylori eradication on atrophic gastritis and intestinal metaplasia (IM)., Methods: Two hundred and fifty-nine patients with atrophic gastritis in the antrum were included in the study, 154 patients were selected for H pylori eradication therapy and the remaining 105 patients served as untreated group. Gastroscopy and biopsies were performed both at the beginning and at the end of a 3-year follow-up study. Gastritis was graded according to the updated Sydney system., Results: One hundred and seventy-nine patients completed the follow-up, 92 of them received H pylori eradication therapy and the remaining 87 H pylori-infected patients were in the untreated group. Chronic gastritis, active gastritis and the grade of atrophy significantly decreased in H pylori eradication group (P<0.01). However, the grade of IM increased in H pylori -infected group (P<0.05)., Conclusion: H pylori eradication may improve gastric mucosal inflammation, atrophy and prevent the progression of IM.

Helicobacter pylori infection has been recognized as the most important pathogenetic principal of peptic ulcer disease, atrophic gastritis, gastric adenocarcinoma and MALT lymphoma. At the moment efforts are made to clarify it's role in functional dyspepsia, and gastro-esophageal reflux disease. The complex interactions between H. pylori infection and NSAIDs is another field of ongoing research. Diagnosis and eradication therapy are standardized. Established indications are peptic ulcer disease, low-grade gastric MALT lymphoma, early gastric cancer treated by mucosal resection and partial gastrectomy for gastric cancer. Atrophic gastritis, known to be a precancerous lesion, as well as first degree relatives of patients with gastric cancer is another widely accepted indication for eradication therapy. The recommended eradication regimens combine a proton pump inhibitor with clarithromycin and either amoxicillin or metronidazole--for a week.

Objective: To investigate the mechanism of isinglass in the prevention and treatment of chronic atrophic gastritis (CAG) in rats., Method: Animal models of SD rats with CAG were made in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while CAG rat model was being made. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed. Then the length of the proliferation zone of the gastric mucosa and serum epidermal growth factors (EGF) and growth hormones (GH)level were studied., Result: In isinglass prevention groups and high dose isinglass reverse group, the length of the proliferation zone of the gastric mucosa was very close to that in normal control group (P > 0.05), much better than model control group (P < 0.01). In low dose isinglass reverse group, it was lower than that in normal control group (P < 0.01), but much better than model control group (P < 0.01). In both prevention and reverse groups, serum EGF level was higher than that in normal (P < 0.01) and model control group (P < 0.05). Serum GH level was the same in every group (P > 0.05)., Conclusion: The mechanism of isinglass in the prevention and treatment of CAG rats lies in revitalizing and proliferating gastric mucosal cells by stimulating endogenous EGF secretion.

Previous in vitro and animal experiments have shown that sulforaphane, which is abundant in broccoli, inhibits Helicobacter pylori (H. pylori) infection and blocks gastric tumor formation. This suggests that broccoli consumption prevents chronic atrophic gastritis (CAG) introduced by H. pylori infection and, therefore, gastric cancer. For an epidemiological investigation of the relationship between the broccoli consumption and CAG, a cross-sectional study of 438 male employees, aged 39 to 60 years, of a Japanese steel company was conducted. CAG was serologically determined with serum cut-off values set at pepsinogen I < or = 70 ng/ml and a ratio of serum pepsinogen I/pepsinogen II < or = 3.0. Broccoli consumption (weekly frequency) and diet were monitored by using a 31-item food frequency questionnaire. The prevalence of CAG among men who ate broccoli once or more weekly was twice as high as that among men who consumed a negligible amount (P < 0.05). Multiple logistic regression analysis indicated that broccoli consumption once or more weekly significantly increased the risk for CAG (odds ratio, 3.06; 95% confidence interval, 1.12-8.38; P < 0.05), after controlling for age, education, cigarette smoking, and alcohol consumption. The present study failed to show an expected association between frequent broccoli consumption and a low prevalence of CAG.

Objective: To evaluate the effect of isinglass on the prevention and treatment of chronic atrophic gastritis in rats., Method: Animal model of SD rats with CAG was established in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while we were establishing CAG rat model. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy., Result: In isinglass prevention groups and reverse groups, inflammation grades of gastric antrum were less than these in model control group (P < 0.01) while the means of ratios of the thickness of gastric mucosal gland and muscularis mucos (L1/L2), the number of gastric glands in 1-mm lengths of mucosal layer were much better than those in model control group (P < 0.01). They were very close to normal control group (P > 0.05)., Conclusion: Isinglass can prevent the gastric mucosal atrophy in the CAG model and can improve and cure the gastric mucosal atrophy of the SD rats with GAG.

Background/aims: The effects of Helicobacter pylori infection on the development of atrophic gastritis and intestinal metaplasia in relation to lifestyle and diet and the effect of the bovine milk on H. pylori adherence to gastric antral mucosa were investigated., Methodology: H. pylori infection was investigated in 63 patients without endoscopic evidence of gastroduodenal disease. Presence of H. pylori infection was assessed by culture and histologic examination of antral and corpus biopsy samples. Grades of atrophic gastritis and intestinal metaplasia were judged with chromoendoscopy (Congo red-methylene blue test). Adherence of H. pylori was evaluated with scanning electron microscopic examination of antral mucosa in Mongolian gerbils., Results: Cross-sectional analysis of lifestyle and diet showed that a high intake of bovine milk was significantly related to prevention of H. pylori infection and the developments of atrophic gastritis and intestinal metaplasia. H. pylori adherence to the gastric mucosa was inhibited by bovine milk in a dose-dependent manner., Conclusions: Bovine milk prevents the development of atrophic gastritis and intestinal metaplasia through its defense mechanisms against the attachment of H. pylori to the gastric mucosa.

Background: Helicobacter pylori gastritis may progress to glandular atrophy and intestinal metaplasia, conditions that predispose to gastric cancer. Profound suppression of gastric acid is associated with increased severity of H pylori gastritis. This prospective randomised study aimed to investigate whether H pylori eradication can influence gastritis and its sequelae during long term omeprazole therapy for gastro-oesophageal reflux disease (GORD)., Methods: A total of 231 H pylori positive GORD patients who had been treated for > or =12 months with omeprazole maintenance therapy (OM) were randomised to either continuation of OM (OM only; n = 120) or OM plus a one week course of omeprazole, amoxycillin, and clarithromycin (OM triple; n = 111). Endoscopy with standardised biopsy sampling as well as symptom evaluation were performed at baseline and after one and two years. Gastritis was assessed according to the Sydney classification system for activity, inflammation, atrophy, intestinal metaplasia, and H pylori density., Results: Corpus gastritis activity at entry was moderate or severe in 50% and 55% of the OM only and OM triple groups, respectively. In the OM triple group, H pylori was eradicated in 90 (88%) patients, and activity and inflammation decreased substantially in both the antrum and corpus (p<0.001, baseline v two years). Atrophic gastritis also improved in the corpus (p<0.001) but not in the antrum. In the 83 OM only patients with continuing infection, there was no change in antral and corpus gastritis activity or atrophy, but inflammation increased (p<0.01). H pylori eradication did not alter the dose of omeprazole required, or reflux symptoms., Conclusions: Most H pylori positive GORD patients have a corpus predominant pangastritis during omeprazole maintenance therapy. Eradication of H pylori eliminates gastric mucosal inflammation and induces regression of corpus glandular atrophy. H pylori eradication did not worsen reflux disease or lead to a need for increased omeprazole maintenance dose. We therefore recommend eradication of H pylori in GORD patients receiving long term acid suppression.

Chronic atrophic gastritis (CAG) is well known as a precancerous lesion of the stomach, and Helicobacter pylori (H. pylori) infection increases the risk of CAG. While recent studies have reported that green tea consumption decreases the risk of gastric cancer, there has been no study analyzing the relationship between green tea consumption and the both risks H. pylori infection and CAG. We conducted a cross-sectional study on 636 subjects living in a farming village in Japan to examine the relationship among green tea consumption, H. pylori infection, and CAG. Smoking, alcohol drinking, consumption of four beverages, including green tea, and of five foods were investigated as lifestyle factors that may affect H. pylori infection and CAG. The measurement of H. pylori-IgG antibodies was used to define H. pylori infection, and serum pepsinogens were used to define of CAG. The unconditional logistic regression model was used for analyzing each odds ratio (OR). H. pylori infection was positively associated with the risk of CAG (OR = 3.73; 95% confidence interval [CI], 2.59-5.36). High green tea consumption (more than 10 cups per day) was negatively associated with the risk of CAG, even after adjustment for H. pylori infection and lifestyle factors associated with green tea consumption (OR = 0.63; 95% CI, 0.43-0.93). These results support the hypothesis that high green tea consumption prevents CAG.

Background: We have previously observed that profound acid suppressive therapy in Helicobacter pylori positive patients with gastro-oesophageal reflux disease is associated with increased corpus inflammation and accelerated development of atrophic gastritis., Aim: To investigate if H pylori eradication at the start of acid suppressive therapy prevents the development of these histological changes., Patients/methods: In a prospective randomised case control study, patients with reflux oesophagitis were treated with omeprazole 40 mg once daily for 12 months. H pylori positive patients were randomised to additional double blind treatment with omeprazole 20 mg, amoxicillin 1000 mg and clarithromycin 500 mg twice daily or placebo for one week. Biopsy sampling for histology, scored according to the updated Sydney classification, and culture were performed at baseline, and at three and 12 months., Results: In the persistently H pylori positive group (n=24), active inflammation increased in the corpus and decreased in the antrum during therapy (p=0.032 and p=0.002, respectively). In contrast, in the H pylori positive group that became H pylori negative as a result of treatment (n=33), active and chronic inflammation in both the corpus and antrum decreased (p

The pattern of Helicobacter pylori gastritis depends on acid secretion. Profound acid suppressive therapy with proton pump inhibitors leads to a decrease of antral gastritis, but an increased severity of corpus gastritis. As such, maintenance therapy with these drugs for gastroesophageal reflux disease has consistently been associated with an increased incidence of atrophic gastritis in H. pylori infected patients. For this reason, the preventive effect of H. pylori eradication in these patients needs to be considered; this is being studied in prospective trials.

The rate of detection of helicobacterium pylori (HP) in chronic atrophic gastritis (CAG) is 67%, HP being a slightly aerobic Gram-negative bacterium. Some drugs of traditional Chinese medicine (TCM) for clearing away heat and for removing blood stasis have significant effect on inhibition of HP. The drugs in both the recipe for nourishing yin, clearing away heat and invigorating blood circulation and the recipe for clearing away heat and invigorating blood circulation have inhibitory action on HP in vitro. All patients with CAG have symptoms of damp-heat and blood stasis. Radix et Rhizoma Rhei and Rhizoma Coptidis Decoction for Purging Stomach-Fire ([symbol: see text]) as the basic recipe and "Huo Wei" ([symbol: see text]) No. 2 recipe as the supplementary have good inhibitory effect on HP in inhibition tests. The results show several forms of the medicine all resulted in significant good therapeutic effect.

The total detectable rate of Helicobacter pylori (HP) of 485 patients suffering from gastric diseases was 59.6%. The HP in gastric mucosa of chronic atrophic gastritis (CAG) patients was separated from the cell culture in vitro and transferred successively. The mice were perfused with exciccate alum, and the rabbits with aspirin to injure their gastric mucosa, then HP was perfused. Result showed that the change of experimental animals was identical with that of CAG patients by means of bacteriological and pathological examination. It revealed that HP was in agreement with Robert Koch's three principles about pathogenic bacteria. According to the bacterial infectious hypothesis of CAG, 53 Chinese medicinal herbs and prescriptions were investigated with bacteriostatic test. Panax notogenseng and Magnolia officinalis were discovered to be sensitive, Prunus mume and Corydalis yanhusuo were moderate sensitive, and Coptis chinensis and Rheum palmatum highly sensitive to HP. Decoction of Clearing up the Heat and Relieving the Blood Stasis and No.2 recipe of Huowei were used to treat 70 CAG patients with Stomach Heat Syndrome. The effective rate of gastroscopic examination was 85.7%, that of pathological study was 80%. In comparing with the group of Shanjiu Weitai, there was significant difference between the traditional Chinese medicine treated group and Shanjiu Weitai control group, the former being markedly better.

A few recent reports suggest the protective effect of antacids against gastric mucosal injury. This study was aimed to examine the influence of some antacids on ethanol induced gastric mucosal damage in rats. We have found that Polish antacids (Alugastrin, Gelatum Aluminii Phosphorici, Gastrin) and calcium carbonate diminished gastric mucosal lesions produced by ethanol. Moreover, Alugastrin and Gelatum Aluminii Phosphorici decreased volume of gastric contents, and its pH, as well as lowered sodium, potassium and protein levels and decreased LDH activity in gastric contents. These findings indicate that antacids protect rat gastric mucosa against injury caused by ethanol. We have found also that aspirin given prior to Alugastrin abolished the protective ability of Alugastrin. This suggest that prostaglandins might be involved in antacid cytoprotection. Our studies indicate that antacids can be used prophilactically in the gastric mucosal injuries.