Epithelial cell proliferation and glandular atrophy in lymphocytic gastritis: Effect of H pylori treatment

AIM:Lymphocytic gastritis is commonly associated with Helicobacter pylori infection.The presence of glandular atrophy and foveolar hyperplasia in lymphocytic gastritis suggests abnormalities in cell proliferation and differentiation, forming a potential link with the suspected association with gastric cancer.Our aim was to compare epibhelial cell proliferation and morphology in H pylori associated lymphocytic gastritis and H pylori gastritis without features of lymphocytic gastritis, and to evaluate the effect of H pylori treatment. METHODS:We studied 14 lymphocytic gastritis patients with H pylori infection.For controls,we selected 14 matched dyspeptic patients participating in another treatment trial whose H pylori infection had successfully been eradicated. Both groups were treated with a triple therapy and followed up with biopsies for 6-18 months (patients) or 3 months (controls).Blinded evaluation for histopathological features was carried out.To determine the cell proliferation index, the sections were labeled with Ki-67 antibody. RESULTS:Before treatment,lymphocytic gastritis was characterized by foveolar hyperplasia (P=0.001) and glandular atrophy in the body (P=0.008),and increased proliferation in both the body (P=0.001) and antrum (P=0.002).Proliferation correlated with foveolar hyperplasia and inflammation activity.After eradication therapy,the number of intraepithelial lymphocytes decreased in the body (P=0.004) and antrum (P=0.065),remaining higher than in controls (P<0.001).Simultaneously,the proliferation index decreased in the body from 0.38 to 0.15 (P=0.043),and in the antrum from 0.34 to 0.20 (P=0.069),the antral index still being higher in lymphocytic gastritis than in controls (P=0.010). Foveolar hyperplasia and glandular atrophy in the body improved (P=0.021),reaching the non-LG level.CONCLUSION: In lymphocytic gastritis, excessive epithelialcell proliferation is predominantly present in the body, where it associates with foveolar hyperplasia and glandular atrophy. These characteristic changes of lymphocytic gastritis are largely related to H pylori infection, as shown by their improvement after eradication. However, some residualdeviation was still seen in lymphocytic gastritis, indicating either an abnormally slow improvement or the presence of some persistent abnormality.

Gastric Atrophy, Intestinal Metaplasia in Helicobacter pylori Gastritis: Prevalence and Predictors Factors

Gastric atrophy and intestinal metaplasia represent the most important premalignant lesions in gastric carcinogenesis. The severity of gastric mucosal inflammation depends on the bacterium Helicobacter pylori (HP), on the host and on environmental factors. The aim of our study is to determine the prevalence and factors associated with Gastric atrophy and intestinal metaplasia in patients infected with Helicobacter pylori. Methods: This is a prospective study over a period of 4 years (May 2009 - January 2015) conducted in the service of Hepatology and Gastroenterology in hospital university Hassan II of Fez in collaboration with microbiology and molecular biology laboratory and epidemiology service of Faculty of Medicine and Pharmacy Fes. We included in our study all patients aged over 15 years, having ulcerative dyspepsia, peptic ulcer disease, gastritis or esophagitis. Results: During the study period, 1190 patients were included of which 70% had HP infection (N = 833). The average age was 48.21 years [16 - 99 years], sex ratio M/F was 1, 11. 60% of patients were older than 45 years. Chronic smoking was found in 12% of patients. Gastric atrophy was observed in 84% (N = 699) of patients infected with HP. Gastric atrophy was localized in 70% in the antrum and 30% in the fundus and 24% in both. The activity of gastritis (p = 0.0001) and the density of the HP (p = 0.005) were factors associated with atrophy. Intestinal metaplasia was observed in 13.5% of patients (N = 112). The density of HP (p = 0.037) and severe atrophy (p = 0.001) were factors associated with metaplasia. Other factors studied: age, sex, smoking, CagA+ genotype were not associated with either gastric atrophy or intestinal metaplasia. Conclusion: In our study, the prevalence of atrophic gastritis and intestinal metaplasia in patients infected with Helicobacter pylori was 84% and 13.5% respectively, which was a high prevalence. The activity of gastritis, and density of HP were factors associated with atrophy. The density of HP and severe atrophy were factors associated with metaplasia.

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

Mucosal patterns of Helicobacter pylori-related gastritis without atrophy in the gastric corpus using standard endoscopy

AIM:To identify the mucosal patterns of Helicobacter pylori(H.pylori )-related gastritis in the gastric corpus using standard endoscopy and to evaluate their reproducibility.METHODS:A total of 112 consecutive patients underwent upper gastrointestinal endoscopy.The endoscopists classified the endoscopic findings into 4 patterns.In the second part of the study,90 images were shown to 3 endoscopists in order to evaluate the inter-observer and intra-observer variability in image assessment.RESULTS:The mucosal patterns of the gastric bodywere categorized into 4 types.Type 1 pattern was defined as cleft-like appearance,type 2 as regular arrangement of red dots,type 3 pattern as the mosaic mucosal pattern and type 4 pattern as the mosaic pattern with a focal area of hyperemia.Type 1 and type 2 mucosal patterns were statistically significant in predicting H.pylorinegative status as compared with other mucosal types(χ 2 = 12.79 and 61.25 respectively,P < 0.01).Type 3 and type 4 mucosal patterns were statistically significant in predicting a H.pylori-positive status as compared with other mucosal types(χ 2 = 21.22 and 11.02 respectively,P < 0.01).Furthermore,the sensitivity,specificity,positive and negative predictive values of type 3 plus type 4 patterns for predicting H.pylori-positive gastric mucosa were 100%,86%,94%,and 100%,respectively.The mean κ values for inter-and intra-observer agreement in assessing the various endoscopic patterns were 0.808(95% CI,0.678-0.938) and 0.826(95% CI,0.727-0.925) respectively.CONCLUSION:Our study suggests that mucosal patterns in H.pylori-infected gastric mucosa without atrophy can be reliably identified using standard endoscopy in the gastric corpus.

Association between autoimmune gastritis and gastric polyps:Clinical characteristics and risk factors

BACKGROUND The relationship between autoimmune gastritis(AIG)and gastric polyps(GPs)is not well understood.AIM To explore the clinical characteristics and risk factors of AIG with GPs in patients.METHODS This double center retrospective study included 530 patients diagnosed with AIG from July 2019 to July 2023.We collected clinical,biochemical,serological,and demographic data were of each patient.Logistic regression analyses,both multivariate and univariate,were conducted to pinpoint independent risk factors for GPs in patients with AIG patients.Receiver operating characteristic curves were utilized to establish the optimal cutoff values,sensitivity,and specificity of these risk factors for predicting GPs in patients with AIG.RESULTS Patients with GPs had a higher median age than those without GPs[61(52.25-69)years vs 58(47-66)years,P=0.006].The gastrin-17 levels were significantly elevated in patients with GPs compared with those without GPs[91.9(34.2-138.9)pmol/mL vs 60.9(12.6-98.4)pmol/mL,P<0.001].Additionally,the positive rate of parietal cell antibody(PCA)antibody was higher in these patients than in those without GPs(88.6%vs 73.6%,P<0.001).Multivariate and univariate analyses revealed that PCA positivity[odds ratio(OR)=2.003,P=0.017],pepsinogen II(OR=1.053,P=0.015),and enterochromaffin like cells hyperplasia(OR=3.116,P<0.001)were significant risk factors for GPs,while pepsinogen I was identified as a protective factor.CONCLUSION PCA positivity and enterochromaffin like cells hyperplasia are significant risk factor for the development of GPs in patients with AIG.Elevated gastrin-17 levels may also play a role in this process.These findings suggest potential targets for further research and therapeutic intervention in managing GPs in patients with AIG.

Traditional Chinese medicine in the treatment of Helicobacter pylorirelated gastritis:The mechanisms of signalling pathway regulations

Helicobacter pylori-associated gastritis(HPAG)is a common condition of the gastrointestinal tract.However,extensive and long-term antibiotic use has resulted in numerous adverse effects,including increased resistance,gastrointestinal dysfunction,and increased recurrence rates.When these concerns develop,traditional Chinese medicine(TCM)may have advantages.TCM is based on the concept of completeness and aims to eliminate pathogens and strengthen the body.It has the potential to prevent this condition while also boosting the rate of Helicobacter pylori eradication.This review elaborates on the mechanism of TCM treatment for HPAG based on cellular signalling pathways,which reflects the flexibility of TCM in treating diseases and the advantages of multi-level,multipathway,and multi-target treatments for HPAG.

Insights into spinal muscular atrophy from molecular biomarkers

Spinal muscular atrophy is a devastating motor neuron disease characterized by severe cases of fatal muscle weakness.It is one of the most common genetic causes of mortality among infants aged less than 2 years.Biomarker research is currently receiving more attention,and new candidate biomarkers are constantly being discovered.This review initially discusses the evaluation methods commonly used in clinical practice while briefly outlining their respective pros and cons.We also describe recent advancements in research and the clinical significance of molecular biomarkers for spinal muscular atrophy,which are classified as either specific or non-specific biomarkers.This review provides new insights into the pathogenesis of spinal muscular atrophy,the mechanism of biomarkers in response to drug-modified therapies,the selection of biomarker candidates,and would promote the development of future research.Furthermore,the successful utilization of biomarkers may facilitate the implementation of gene-targeting treatments for patients with spinal muscular atrophy.

Reduced mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor contributes to neurodegeneration in a model of spinal and bulbar muscular atrophy pathology

Spinal and bulbar muscular atrophy is a neurodegenerative disease caused by extended CAG trinucleotide repeats in the androgen receptor gene,which encodes a ligand-dependent transcription facto r.The mutant androgen receptor protein,characterized by polyglutamine expansion,is prone to misfolding and forms aggregates in both the nucleus and cytoplasm in the brain in spinal and bulbar muscular atrophy patients.These aggregates alter protein-protein interactions and compromise transcriptional activity.In this study,we reported that in both cultured N2a cells and mouse brain,mutant androgen receptor with polyglutamine expansion causes reduced expression of mesencephalic astrocyte-de rived neurotrophic factor.Overexpressio n of mesencephalic astrocyte-derived neurotrophic factor amelio rated the neurotoxicity of mutant androgen receptor through the inhibition of mutant androgen receptor aggregation.Conversely.knocking down endogenous mesencephalic astrocyte-derived neurotrophic factor in the mouse brain exacerbated neuronal damage and mutant androgen receptor aggregation.Our findings suggest that inhibition of mesencephalic astrocyte-derived neurotrophic factor expression by mutant androgen receptor is a potential mechanism underlying neurodegeneration in spinal and bulbar muscular atrophy.

Chronic active and atrophic gastritis as significant contributing factor to the development of gastric cystica profunda

Gastric cystica profunda(GCP)is an uncommon but underestimated gastric lesion.Its precancerous potential determines its significance.In addition to previous mucosa injury due to operations,biopsy or polypectomy,chronic active and atrophic gastritis may also lead to the development of GCPs.By carefully examining the stomach and taking biopsy samples from the susceptible regions,the stage of atrophy can be determined.Chronic atrophic gastritis is a risk factor for cancer evolvement and it can also contribute to GCPs formation.GCPs frequently occur close to early gastric cancers(EGCs)or EGC can arise from the cystic glands.Endoscopic resection is an effective and minimally invasive treat-ment in GCP.

Update understanding on diagnosis and histopathological examination of atrophic gastritis:A review

Chronic atrophic gastritis(CAG)is a complex syndrome in which long-term chronic inflammatory stimulation causes gland atrophy in the gastric mucosa,reducing the stomach's ability to secrete gastric juice and pepsin,and interfering with its normal physiological function.Multiple pathogenic factors contribute to CAG incidence,the most common being Helicobacter pylori infection and the immune reactions resulting from gastric autoimmunity.Furthermore,CAG has a broad spectrum of clinical manifestations,including gastroenterology and extraintestinal symptoms and signs,such as hematology,neurology,and oncology.Therefore,the initial CAG evaluation should involve the examination of clinical and serological indicators,as well as diagnosis confirmation via gastroscopy and histopathology if necessary.Depending on the severity and scope of atrophy affecting the gastric mucosa,a histologic staging system(Operative Link for Gastritis Assessment or Operative Link on Gastritis intestinal metaplasia)could also be employed.Moreover,chronic gastritis has a higher risk of progressing to gastric cancer(GC).In this regard,early diagnosis,treatment,and regular testing could reduce the risk of GC in CAG patients.However,the optimal interval for endoscopic monitoring in CAG patients remains uncertain,and it should ideally be tailored based on individual risk evaluations and shared decision-making processes.Although there have been many reports on CAG,the precise etiology and histopathological features of the disease,as well as the diagnosis of CAG patients,are yet to be fully elucidated.Consequently,this review offers a detailed account of CAG,including its key clinical aspects,aiming to enhance the overall understanding of the disease.

Gene therapy for spinal muscular atrophy:perspectives on the possibility of optimizing SMN1 delivery to correct all neurological and systemic perturbations

Spinal muscular atrophy(SMA)is a genetic condition that results in selective lower motor neuron loss with concomitant muscle weakness and atrophy.The genetic cause of SMA was understood in 1995 when loss or impairment of the survival motor neuron 1(SMN1)gene was identified as the main contributing factor(Lefebvre et al.,1995).This,in combination with the discovery that humans have a“back-up”gene,SMN2,which can produce low levels(approximately 10%)of the full-length functional SMN protein,has led to the generation of SMA-specific gene therapies.SMA was traditionally classified according to age of symptom onset and developmental milestones achieved,with life expectancy and severity varying between individuals.Now,SMN2 copy number is used as a proxy for the prediction of disease severity,with higher SMN2 copy number typically being associated with reduced severity of SMA,although this relationship is not absolute:some individuals with low SMN2 copy number have less severe SMA phenotypes and vice versa.Additionally,the etiology of SMA is further complicated by other factors,such as non-typical nucleotide variants and SMN2-independent modifiers of disease severity.

Metabolic dynamics in chronic gastritis:Examining urinary profiles post Helicobacter pylori eradication

Chronic gastritis is the persistent and insidious inflammation of the gastric lining.Helicobacter pylori(H.pylori)has been identified as the most common cause of chronic gastritis and consequently elimination of H.pylori can lead to its cure.This editorial explores the use of urinary metabolic profiles before and after eradication to identify biomarkers that can aid in prognosis and treatment.Despite providing promising insights,there are limitations such as a small sample size(17 patients),a narrow treatment period of 2 wk,and treatment heterogeneity,which raise concerns.Nevertheless,these findings have opened a gateway to enhancing the treatment and prognosis of chronic gastritis through urinary metabolomics.

Efficacy and safety of rebamipide/nizatidine in patients with erosive gastritis: A randomized, multicenter, phase 4 study

BACKGROUND For the treatment of gastritis,rebamipide,a mucoprotective agent,and nizatidine,a gastric acid suppressant,are commonly employed individually.AIM To compare the efficacy of Mucotra®SR(rebamipide 150 mg)and Axid®(nizatidine 150 mg)combination therapy with the sole administration of Axid®in managing erosive gastritis.METHODS A total of 260 patients diagnosed with endoscopically confirmed erosive gastritis were enrolled in this open-label,multicenter,randomized,phase 4 clinical trial,allocating them into two groups:Rebamipide/nizatidine combination twice daily vs nizatidine twice daily for 2 weeks.The full-analysis set analysis encompassed 239 patients(rebamipide/nizatidine,n=121;nizatidine,n=118),while the per-protocol analysis included 218 patients(n=110 vs 108).Post-treatment assessments comprised primary(erosion improvement rate)and secondary(erosion and edema cure rates,erythema improvement rates,hemorrhage,and gastrointestinal symptoms)endpoints.Furthermore,drug-related adverse effects were evaluated.RESULTS Primary efficacy assessment showed a statistically significant improvement rate in mucosal erosions in the combination group compared to the control group in the full-analysis set(rebamipide/nizatidine 62.0%,nizatidine 49.2%,P=0.046),with a similar trend noted in the per-protocol analysis(62.7%vs 50.0%,P=0.058).Both groups were effective in curing erosion and edema and improvement of bleeding,erythema,and gastrointestinal symptoms,whereas no inter-group differences were noted.When confined to the participants with gastritis symptoms,improvement of erosion was more optimal in the combination group(63.0%vs 49.5%,P=0.046).No adverse events related to the drugs were observed.CONCLUSION Rebamipide/nizatidine combination is effective in treatment of erosive gastritis.

Efficacy of fexuprazan compared with rebamipide in Korean patients with gastritis:A matching-adjusted indirect comparison

BACKGROUND Gastritis is one of the most frequently diagnosed diseases requiring medical treatment in South Korea.Fexuprazan,a novel potassium-competitive acid blocker,has been approved for treating gastritis and erosive esophagitis.Meanwhile,rebamipide is the most commonly used mucoprotective agent for acute and chronic gastritis in real-world settings in South Korea.However,there have been no studies comparing the efficacy of these two drugs yet.AIM To compare the efficacy of fexuprazan with that of rebamipide for acute and chronic gastritis.METHODS This was a matching-adjusted indirect comparison.Individual patient data from a phase III study of fexuprazan(10 mg BID)were compared with cumulative data from two matching studies of rebamipide(100 mg TID).Erosion improvement and healing rates were compared between two weeks of fexurapan,two weeks of rebamipide,and four weeks of rebamipide.The two main outcome variables were presented as percentages,and the risk differences(RD)and 95%confidence intervals(CI)were calculated for the relative treatment effects.RESULTS In the primary analysis,the erosion improvement and healing rates after a twoweek treatment with fexuprazan were 64.5%and 53.2%,respectively,while a twoweek treatment with rebamipide resulted in erosion improvement and healing rates of 43.6%(RD:21.0%;95%CI:9.6-32.3;P<0.01)and 35.6%(RD:17.6%;95%CI:6.1-29.2;P=0.003),respectively.In the additional analysis,the erosion improvement and healing rates for the two-week fexuprazan treatment(64.2%and 51.2%,respectively)were similar to those obtained during a four-week treatment with rebamipide(60.6%;RD:3.6%;95%CI:-9.8,17.0;P=0.600 and 53.5%;RD:-2.3%;95%CI:-16.1,11.5;P=0.744,respectively).CONCLUSION The two-week fexuprazan treatment was superior to the two-week rebamipide treatment and similar to the fourweek rebamipide treatment for patients with gastritis.

Clinical manifestation,lifestyle,and treatment patterns of chronic erosive gastritis:A multicenter real-world study in China

BACKGROUND Although chronic erosive gastritis(CEG)is common,its clinical characteristics have not been fully elucidated.The lack of consensus regarding its treatment has resulted in varied treatment regimens.AIM To explore the clinical characteristics,treatment patterns,and short-term outcomes in CEG patients in China.METHODS We recruited patients with chronic non-atrophic or mild-to-moderate atrophic gastritis with erosion based on endoscopy and pathology.Patients and treating physicians completed a questionnaire regarding history,endoscopic findings,and treatment plans as well as a follow-up questionnaire to investigate changes in symptoms after 4 wk of treatment.RESULTS Three thousand five hundred sixty-three patients from 42 centers across 24 cities in China were included.Epigastric pain(68.0%),abdominal distension(62.6%),and postprandial fullness(47.5%)were the most common presenting symptoms.Gastritis was classified as chronic non-atrophic in 69.9%of patients.Among those with erosive lesions,72.1%of patients had lesions in the antrum,51.0%had multiple lesions,and 67.3%had superficial flat lesions.In patients with epigastric pain,the combination of a mucosal protective agent(MPA)and proton pump inhibitor was more effective.For those with postprandial fullness,acid regurgitation,early satiety,or nausea,a MPA appeared more promising.CONCLUSION CEG is a multifactorial disease which is common in Asian patients and has non-specific symptoms.Gastroscopy may play a major role in its detection and diagnosis.Treatment should be individualized based on symptom profile.

History of chronic gastritis:How our perceptions have changed

Currently,the diagnostic strategy for chronic gastritis(CG)is aimed not just at fixing the presence of gastric mucosal inflammation,but also at gastric cancer(GC)risk stratification in a particular patient.Modern classification approach with the definition of the stage of gastritis determines the need,activities and frequency of dynamic monitoring of a patient.However,this attitude to the patient suffering from CG was far from always.The present publication is a literature review describing the key milestones in the history of CG research,from the description of the first observations of inflammation of the gastric mucosa,assessment of gastritis as a predominantly functional disease,to the advent of endoscopy of the upper digestive tract and diagnostic gastric biopsy,assessment of the role of Helicobacter pylori infection in progression of inflammatory changes to atrophy,intestinal metaplasia,dysplasia and GC.

Immune checkpoint inhibitor-associated gastritis:Patterns and management

Immune checkpoint inhibitors(ICIs)are widely used due to their effectiveness in treating various tumors.Immune-related adverse events(irAEs)are defined as adverse effects resulting from ICI treatment.Gastrointestinal irAEs are a common type of irAEs characterized by intestinal side effects,such as diarrhea and colitis,which may lead to the cessation of ICIs.Although irAE gastritis is rarely reported,it may lead to serious complications such as gastrorrhagia.Furthermore,irAE gastritis is often difficult to identify early due to its diverse symptoms.Although steroid hormones and immunosuppressants are commonly used to reverse irAEs,the best regimen and dosage for irAE gastritis remains uncertain.In addition,the risk of recurrence of irAE gastritis after the reuse of ICIs should be considered.In this editorial,strategies such as early identification,pathological diagnosis,mana-gement interventions,and immunotherapy rechallenge are discussed to enable clinicians to better manage irAE gastritis and improve the prognosis of these patients.

Urinary metabolic profiles during Helicobacter pylori eradication in chronic gastritis

BACKGROUND Helicobacter pylori(H.pylori)infection is a major risk factor for chronic gastritis,affecting approximately half of the global population.H.pylori eradication is a popular treatment method for H.pylori-positive chronic gastritis,but its mecha-nism remains unclear.Urinary metabolomics has been used to elucidate the mechanisms of gastric disease treatment.However,no clinical study has been conducted on urinary metabolomics of chronic gastritis.AIM To elucidate the urinary metabolic profiles during H.pylori eradication in patients with chronic gastritis.METHODS We applied LC–MS-based metabolomics and network pharmacology to in-vestigate the relationships between urinary metabolites and H.pylori-positive chronic gastritis via a clinical follow-up study.RESULTS Our study revealed the different urinary metabolic profiles of H.pylori-positive chronic gastritis before and after H.pylori eradication.The metabolites regulated by H.pylori eradication therapy include cis-aconitic acid,isocitric acid,citric acid,L-tyrosine,L-phenylalanine,L-tryptophan,and hippuric acid,which were involved in four metabolic pathways:(1)Phenylalanine metabolism;(2)phenylalanine,tyrosine,and tryptophan biosynthesis;(3)citrate cycle;and(4)glyoxylate and dicarboxylate metabolism.Integrated metabolomics and network pharmacology revealed that MPO,COMT,TPO,TH,EPX,CMA1,DDC,TPH1,and LPO were the key proteins involved in the biological progress of H.pylori eradication in chronic gastritis.CONCLUSION Our research provides a new perspective for exploring the significance of urinary metabolites in evaluating the treatment and prognosis of H.pylori-positive chronic gastritis patients.

Effectiveness of serological markers of gastric mucosal atrophy in the gastric precancer screening and in cancer prevention

BACKGROUND New markers are needed to improve the effectiveness of serological screening for atrophic gastritis.AIM To develop a cost-effective method for serological screening of atrophic gastritis with a high level of sensitivity.METHODS Of the 169 patients with atrophic gastritis,selected by the visual endoscopic Kimura-Takemoto method,165 showed histological mucosal atrophy using the updated Kimura-Takemoto method.All 169 patients were examined for postprandial levels of gastrin-17(G17)and pepsinogen-1(PG1)using Gastro-Panel®(Biohit Plc,Helsinki,Finland).RESULTS We used the histological standard of five biopsies of the gastric mucosa,in accordance with the Kimura-Takemoto classification system to assess the sensitivity of G17 in detecting gastric mucosal atrophy.We also compared the morphofunctional relationships between the detected histological degree of gastric mucosal atrophy and the serological levels of G17 and PG1,as the markers of atrophic gastritis.The sensitivity of postprandial G17 was 62.2%for serological levels of G17(range:0-4 pmol/L)and 100%for serological G17(range:0-10 pmol/L)for the detection of monofocal severe atrophic gastritis.No strong correlation was found between the levels of PG1 and degree of histological atrophy determined by the Kimura-Takemoto classification system to identify the severity of mucosal atrophy of the gastric corpus.In the presented clinical case of a 63-year-old man with multifocal atrophic gastritis,there is a pronounced positive long-term dynamics of the serological marker of atrophy-postprandial G17,after five months of rennet replacement therapy.CONCLUSION Serological screening of multifocal atrophic gastritis by assessment of postprandial G17 is a cost-effective method with high sensitivity.Postprandial G17 is an earlier marker of regression of atrophic gastritis than a morphological examination of a gastric biopsy in accordance with the Sydney system.Therefore,postprandial G17 is recommended for dynamic monitoring of atrophic gastritis after treatment.

Clinical Efficacy Observation of a Jing Ethnic Prescription in Treating Chronic Atrophic Gastritis

Objective: To observe the clinical efficacy of a Jing ethnic prescription in treating chronic atrophic gastritis (CAG). Methods: A total of 182 CAG patients admitted to our hospital were randomly divided into a control group (91 cases) and a treatment group (91 cases) based on their admission order. The control group received conventional treatment, while the treatment group was treated with a Jing ethnic prescription. The clinical efficacy, changes in gastric mucosa-related indicators, and systemic inflammatory markers were compared between the two groups. Results: After treatment, the overall effective rate in the treatment group was higher than that in the control group, but the difference was not statistically significant (P > 0.05). The levels of trefoil factor 2 (TFF2) in the gastric mucosa increased, and the levels of nuclear factor-kappa B (NF-κB) decreased in both groups. However, the improvement in these indicators was significantly better in the treatment group (P Conclusion: The custom formula of the Jing ethnic group shows comparable clinical efficacy to conventional treatment for chronic atrophic gastritis (CAG), but it demonstrates significantly better effects in reducing systemic inflammatory responses. Specifically, the treatment group showed superior results in the following aspects compared to the control group: increased levels of TFF2, decreased levels of NF-κB, and reduced serum levels of IL-6, IL-8, and hs-CRP.