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Background Chronic atrophic gastritis (CAG) is related to the body’s microbial and metabolic systems. Combined studies of microbiome and metabolomics can clarify the mechanisms of disease occurrence and progression. We used 16S rRNA sequencing, metagenomics sequencing and metabolomics sequencing to depict the landscapes of bacterium and metabolites, construct correlation networks of different bacterium and metabolites describe potential pathogenic mechanisms of chronic atrophic gastritis. Methods The gastric juices of 30 non-atrophic gastritis (NAG) patients and 30 CAG patients were collected. Gastric microflora was analyzed by 16S rRNA sequencing and metagenomics sequencing. Gastric metabolites were analyzed by LC–MS analysis. Different bioinformatics methods were used to analyze the data of microbiome and metabolome, and to analyze the relationship between them. Results In atrophic gastritis, bacteria diversity decreased. The genera with a mean decrease in Gini greater than 1.5 included peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides . KEGG pathway included renal cell carcinoma, proximal tubule bicarbonate reclamation, citrate cycle and aldosterone synthesis and secretion with significant enrichment of differential metabolites. Peptostreptococcus , fusobacterium, prevotella and sphingomonas were in pivot positions of the correlation network of differential metabolites and differential bacterium. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism were enriched in chronic atrophic gastritis based on the metagenomic sequencing data. Conclusion Peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides were the essential features that distinguish atrophic gastritis from non-atrophic gastritis, and caused disease by altering various metabolic pathways. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism may be related to the occurrence and progression of CAG.

To assess the efficacy and safety of LiWei Capsule (LWC) in the treatment of chronic non-atrophic gastritis (CNG) with erosions and damp-heat stasis syndrome, based on Traditional Chinese Medicine (TCM) principles. This phase II, multicenter, randomized, double-blind, placebo- and positive-controlled trial enrolled patients diagnosed with CNG with erosions and damp-heat stasis syndrome. Participants were allocated to LWC, Sanjiu Weitai Capsule (SJWT, positive control), and placebo groups (2:1:1 ratio) and received corresponding treatment for 4 weeks, followed by a 16-week follow-up. The primary outcome was the curative rate of epigastric pain/bloating. Secondary outcomes included improvement in endoscopic examination, histopathological examination, and TCM symptom scores. Of 301 enrolled participants from five centers, 189 completed the study (95, 45, 49 cases in LWC, SJWT, and placebo groups, respectively). After 4 weeks of treatment, the curative rates of epigastric pain/bloating were 76.84%, 42.22%, and 22.45% in LWC, SJWT, and placebo groups, respectively ( P  < 0.001). The healing rates of endoscopic erosions were 65.3%, 46.7%, and 30.6% in LWC, SJWT, and placebo groups, respectively ( P  < 0.001). LWC effectively and safely alleviates epigastric pain/bloating and promotes endoscopic erosion healing in CNG patients with erosions (damp-heat stasis syndrome). LWC may be a promising treatment option for this condition. Trial registration : ChiCTR2100052010, assigned by the Chinese Clinical Trial Registry, registration date 13/10/2021.

Objective: Chronic non-atrophic gastritis (CNAG) is a common clinical gastrointestinal disease with a long and recurrent course. In China, Wuzhuyu decoction (WZYD) has been used for centuries to treat gastrointestinal disorders. To unravel the efficacy and mechanism of WZYD for CNAG, a clinical study was conducted. And metabolomics was used to explore the mechanism of WZYD for CNAG patients. Methods: Twenty patients in total were recruited in this study (Nos. ChiCTR2200062296) and the protocol was approved by the Ethics Committee (Approval number: KY-2022-2-6-1) and complied with the Declaration of Helsinki. The formula granule of WZYD were assessed by UHPLC-QQQ-TOF to discern the main potential active compounds. The endoscopy evaluation and histopathological changes were detected as effective indicators. Serum samples from patients were used for metabolomics. Inflammatory factors in patients' serum were determined by ELISA. Metabolomics revealed a series of differential metabolites and signaling pathways. Results: WZYD was capable to prevent CNAG by ameliorating score of endoscopy evaluation including erosion, hemorrhage, as well as chronic inflammation and active chronic inflammation score after treatment were decreased. The results indicated that 10 core metabolic components were associated with the treatment of WZYD. Moreover, these metabolic components proved that pyrimidine metabolism and thiamine metabolism were critically responsible for CNAG. In addition, WZYD treatment effectively reduced serum levels of TNF-[alpha], IL-10, and COX-2. Conclusion: Altogether, WZYD can effectively alleviate CNAG by inhibiting inflammation and regulating related metabolic processes, which might be the molecular mechanism of WZYD treatment of CNAG. More studies are warranted to be conducted in this area. Trial Registration: ChiCTR, ChiCTR2200062296. Registered 1 August 2022, Keywords: Wuzhuyu decoction, chronic non-atrophic gastritis, metabolomics, natural product

Objectives: To investigate the effects of sucralfate suspension gel on gastroscopic pathology and inflammatory cytokine levels in patients with Helicobacter pylori (Hp)-positive chronic non-atrophic gastritis. Methodology: A retrospective analysis was conducted on 80 outpatients treated at Beijing Hospital of Integrated Traditional Chinese and Western Medicine between January 2022 to January 2025. Patients were divided into a control group (n = 40) and an observation group (n = 40). The control group received standard quadruple therapy, while the observation group received additional treatment with sucralfate suspension gel on top of the standard regimen. Clinical outcomes, gastroscopic pathological scores, gastrointestinal hormone levels, inflammatory cytokine levels and incidence of adverse events were compared between the two groups. Results: The observation group demonstrated a significantly higher overall response rate compared with the control group(P< 0.05). Post-treatment gastroscopic pathological scores were significantly lower in the observation group than in the control group(P< 0.05). Levels of gastrointestinal hormones were significantly elevated in the observation group(P< 0.05). Furthermore, post-treatment levels of interleukin-2, matrix metalloproteinase-9 and tumor necrosis factor-α were significantly reduced in the observation group compared with the control group(P< 0.05, respectively). The incidence of adverse events did not differ significantly between the two groups(P> 0.05). Conclusion: The addition of sucralfate suspension gel to standard therapy in the treatment of Hp-positive chronic non-atrophic gastritis yields favorable clinical outcomes. It can significantly improve gastroscopic pathology, reduce inflammatory cytokine levels and enhance gastrointestinal hormone secretion without compromising treatment safety.

According to a systematic review [11], estimates of the prevalence of CAG worldwide were 23.9% and 27.0% in the general population and in individual groups, respectively, using serology, and 33.4% in the general population, and 31.6 % in selected groups based on biopsies. According to the manufacturer's instructions, a PGI <30 pg / L was taken as a positive marker of gastric atrophy; for inflammation of the coolant, the amount of PGII was considered above 22 pg / l; a PGI to PGII ratio (PGI / PGII) less than 2.5 was considered positive for atrophy. [...]analysis of the obtained data showed that the content of pepsinogens and their ratio significantly decreased in patients with atrophy of the coolant in comparison with those without atrophy (Table 3). Since the degree of atrophy was assessed by the indicators of pepsinogens, with a pronounced degree of atrophy, the PGI was 8.7 ± 0.1 pg / l and the PGI / PGII was 1.1 ± 0.1, respectively; with moderate atrophy 16.6 ± 0.9 pg / l and 1.6 ± 0.1; with mild atrophy 27.2 ± 1.5 and 2.3 ± 0.2, respectively. [...]we can say that the risk factor for both severe atrophic gastritis of the gastric corpus and of a mild and moderate degree was age over 55 years.

Different lines of evidence support an association between Epstein-Barr virus (EBV) and gastric cancer (GC). The main understood risk factor to develop GC is infection by Helicobacter pylori (H. pylori), which triggers a local inflammatory response critical for progression from gastritis to GC. The role of EBV in early inflammatory gastric lesions has been poorly studied. A recent study proposed a cutoff value of 2000 EBV particles to identify patients with increased chances of infection of the gastric epithelium, which may favor the inflammatory process. To better understand the role of EBV in cancer progression, we analyzed 75 samples of GC, 147 control samples of non-tumor gastric tissue derived from GC patients and 75 biopsies from patients with non-atrophic gastritis (NAG). A first-round PCR was used for EBV detection in tumor and non-tumor controls and a more sensitive nested PCR for gastritis samples; both PCRs had lower detection limits above the proposed cutoff value. With this strategy 10.67% of GC, 1.3% of non-tumor controls and 8% of gastritis samples were found positive. An EBER1 in situ hybridization showed EBV infection of epithelial cells in GC and in a third of NAG samples, while in the other NAGs infection was restricted to the mononuclear cell infiltrate. EBV-positive GCs were enriched in lace and cribriform patterns, while these rare patterns were not observed in EBV negative samples. Our results support a role for EBV in GC and early precursor lesions, either as directly oncogenic infecting epithelial cells or indirectly as an inflammatory trigger.

Background Chronic gastritis (CG), a poorly understood entity, is a very common disease of the digestive tract and is difficult to cure. Chronic non-atrophic gastritis (CNG) is the most common type of CG. Even if treated with current standard chemotherapy, some patients will not be freed from this confusing disease. Many studies have shown traditional Chinese medicine (TCM) is more effective compared to chemotherapy in the treatment of chronic gastritis and no serious side effects have been identified. However, the studies that have been carried out were not scientifically rigorous trials. Our aim is to design a high-quality trial for a new TCM drug, the Jian-Wei-Qu-Tong Pills (JWQTP), to investigate the efficacy and safety of this new drug in treating chronic non-atrophic gastritis patients with spleen and stomach qi deficiency with damp-heat stasis syndrome (SSQDDSS). Methods/Design This is a phase II, multicenter, parallel-group, double-blind, randomized and placebo-controlled trial. A total of 240 participants will be assigned to a high-dose group, a low-dose group or a placebo control group with a 1:1:1 ratio at five sites. Then, one dose (six 1-g pills), with a variable ratio between real drug and dummy drug according to the intervention protocol, will be taken three times a day before each meal for 8 weeks. The primary outcome is the eradication rate of epigastric pain. The secondary outcome includes the changes of endoscopic examination, histopathological examination, traditional Chinese medicine symptom scores and patient-reported outcome instrument scores for chronic gastrointestinal diseases and the eradication rate of Helicobacter pylori (HP). Discussion Many CNG patients suffer from frequent, recurrent bouts of dyspeptic symptoms. This is the first clinical trial to evaluate the safety and efficacy of JWQTP in treating CNG with SSQDDSS in a multicenter, parallel-group, double-blind, randomized and placebo-controlled manner. This trial may not only provide evidence for a phase III clinical trial, but also a vision of an alternative option for CNG treatment. Trial registration The registration number, ChiCTR-TRC-14004088 , was assigned by the Chinese Clinical Trial Registry on 7 January 2014.

Background and aims: The development of atrophic chronic gastritis (ACG) is multifactorial, involving environment as well as host responses to Helicobacter pylori infection. The aim of this study was to determine factors involved in ACG in a European dyspeptic population. Methods: Data concerning sociodemographics, social behaviour, biological aspects, diet, and virulence factors of H pylori strains were collected in a cross sectional study from 19 European centres in 14 countries. Dyspeptic H pylori positive patients with ACG or non-ACG (NACG) at histology were included. Anti-CagA antibodies were evaluated by two immunoblot tests and anti-VacA antibodies by one. Logistic regression models were constructed, and estimated odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated from the coefficients. Results: Of the 451 patients included in the study, 267 were analysed: 202 had NACG and 65 ACG. Mean age was 44.4 years and 63% were women. Risk factors for atrophy identified by multivariate analysis were: age over 60 years (OR 4.14, 95% CI 1.79–9.58), coffee consumption (OR 2.35, 95% CI 1.07–5.16), sedative consumption (OR 2.17, 95% CI 1.04–4.52), and harbouring anti-CagA and anti-VacA antibodies simultaneously (OR 3.09, 95% CI 1.26–7.56), while the odds were significantly reduced for those with an anxiety score of 6 or more (OR 0.45, 95% CI 0.21–0.99). Conclusion: The simultaneous presence of anti-CagA and anti-VacA antibodies enhanced the risk of ACG in European dyspeptic patients. Failure to discern diet and family history as risk factors for ACG may suggest that diet is homogeneous in Europe and that most of the risk factors for ACG identified so far are identical to risk factors for H pylori infection.

Background:Helicobacter pylori infection induces progressive inflammatory changes in the gastric mucosa that may lead to gastric cancer. Understanding long term effects resulting from the cure of this infection is needed to design cancer prevention strategies. Methods: A cohort of 795 adults with preneoplastic gastric lesions was randomised to receive anti-H pylori treatment and/or antioxidants. At the end of six years of intervention, those who did not receive anti-H pylori treatment were offered it. Gastric biopsies were obtained at baseline, and at 3, 6, and 12 years. A histopathology score was utilised to document changes in gastric lesions. Non-linear mixed models were used to estimate the cumulative effect of H pylori clearance on histopathology scores adjusted for follow up time, interventions, and confounders. Results: Ninety seven per cent of subjects were H pylori positive at baseline, and 53% were positive at 12 years. Subjects accumulated 1703 person years free of infection. A multivariate model showed a significant regression in histopathology score as a function of the square of H pylori negative time. Subjects who were H pylori negative had 14.8% more regression and 13.7% less progression than patients who were positive at 12 years (p = 0.001). The rate of healing of gastric lesions occurred more rapidly as years free of infection accumulated, and was more pronounced in less advanced lesions. Conclusions: Preneoplastic gastric lesions regress at a rate equal to the square of time in patients rendered free of H pylori infection. Our findings suggest that patients with preneoplastic gastric lesions should be treated and cured of their H pylori infection.