Pylori Infection Research Articles

Helicobacter pylori infection in psoriatic patients and its relation to psoriasis severity: Cross Sectional Study.

Psoriasis is a prevalent inflammatory skin condition that can be recognized by silvery-white scales on plaques and erythematous papules, despite the fact that psoriasis appears to have multiple causes. Helicobacter pylori (H. pylori) has been investigated recently as a potential infectious etiological component. The objective of the study was to evaluate the prevalence of H. pylori infection in psoriatic patients compared to that of healthy controls and determine whether the degree of psoriasis and H. pylori infection were related. The dermatology, venerology, and andrology department at South Valley University Outpatient Clinic carried out this cross-sectional study. Psoriatic patients of both sexes and ages were included. In addition to the control group, H. Pylori antigen was measured from psoriatic and control groups by using H. pylori stool antigen-enzyme linked immunosorbent assay (HpSA-ELISA), a test for H. pylori stool antigen. More than 20ng/mL of antigen proved positive, or less than 15ng/mL proved negative. There was a significant difference between psoriatic patients and control regarding H. pylori infection (p=0.046): (30.66%) positive in controls, (45.33%) positive in psoriatic patients. Both groups were matched for age (p=0.908), that is, the mean age of psoriatic patients was 37.44±15.79 years, and the control group was 37.15±15.15 years. Twenty-five psoriatic patients in each group: mild, moderate, and severe psoriasis according to the Psoriasis Area Severity Index (PASI) score. No significant correlation between H. pylori infection and PASI, age, or duration of illness in psoriatic patients. Patients with psoriasis had greater rates of H. pylori infection but didn't affect the severity of psoriasis.

Data-driven rapid detection of Helicobacter pylori infection through machine learning with limited laboratory parameters in Chinese primary clinics

BackgroundHelicobacter pylori (H. pylori) is a significant global health concern, posing a high risk for gastric cancer. Conventional diagnostic and screening approaches are inaccessible, invasive, inaccurate, time-consuming, and expensive in primary clinics. ObjectiveThis study aims to apply machine learning (ML) models to detect H. pylori infection using limited laboratory parameters from routine blood tests and to investigate the association of these biomarkers with clinical outcomes in primary clinics. MethodsA retrospective analysis with three ML and five ensemble models was conducted on 1409 adults from Hubei Provincial Hospital of Traditional Chinese Medicine. evaluating twenty-three blood test parameters and using the C14 urea breath test as the gold standard for diagnosing H. pylori infection. ResultsIn our comparative study employing three different feature selection strategies, Random Forest (RF) model exhibited superior performance over other ML and ensemble models. Multiple evaluation metrics underscored the optimal performance of the RF model (ROC = 0.951, sensitivity = 0.882, specificity = 0.906, F1 = 0.906, accuracy = 0.894, PPV = 0.908, NPV = 0.880) without feature selection. Key biomarkers identified through importance ranking and shapley additive Explanations (SHAP) analysis using the RF model without feature selection include White Blood Cell Count (WBC), Mean Platelet Volume (MPV), Hemoglobin (Hb), Red Blood Cell Count (RBC), Platelet Crit (PCT), and Platelet Count (PLC). These biomarkers were found to be significantly associated with the presence of H. pylori infection, reflecting the immune response and inflammation levels. ConclusionAbnormalities in key biomarkers could prompt clinical workers to consider H. pylori infection. The RF model effectively identifies H. pylori infection using routine blood tests, offering potential for clinical application in primary clinics. This ML approach can enhance diagnosis and screening, reducing medical burdens and reliance on invasive diagnostics.

Hereditary Gastric Cancer Is Linked With Hereditary Breast and Ovarian Cancer.

Helicobacter pylori (H. pylori), a bacterium which chronically infects the stomach of approximately half the world's population, is a risk factor for the development of gastric cancer (GC). However, the underlying mechanism whereby H. pylori infection induces GC development remains unclear. Intermittent injection of the H. pylori cytotoxin-associated gene A antigen (CagA) protein into its host cell inhibits nuclear translocation of BRCA1/BRCA2, DNA repair proteins involved in the development of breast cancer/ovarian cancer. Interestingly, hereditary breast and ovarian cancer (HBOC) syndrome is associated with GC development. Here, we aimed to clarify the molecular link between H. pylori infection, BRCA1/2 pathogenic variants (PVs), GC and higher GC incidence in HBOC families. We retrospectively reviewed data from Japanese patients undergoing precision treatment using cancer genomic medicine. We found a higher GC incidence in HBOC families having germline pathogenic variants (GPVs) of BRCA1/2 (2.95% vs. 0.78% in non-HBOC families). Next, we found that 96.1% of H. pylori-infected patients received cancer genomic medicine for advanced GC, and > 16% advanced GC patients had gBRCA2 PVs. Furthermore, expressing wild-type BRCA1/2 in Gan mice (a mouse model of human GC) inhibited GC development. Thus, gBRAC1/2 PVs and H. pylori infection synergistically increase the risk of GC development. Our study highlights the need to investigate the potential of therapeutic agents against BRCA1/2 PVs to avoid the development of GC in HBOC families. In addition, our results suggest that poly (ADP-ribose) polymerase (PARP) inhibitors could potentially inhibit GC development and progression with gBRCA1/2 PVs.

Chilean consensus by expert panel using the Delphi technique for primary and secondary prevention of gastric cancer

IntroductionGastric cancer (GC) is the first cause of cancer-related death in Chile and 6th in Latin America and the Caribbean (LAC). Helicobacter pylori (H. pylori) is the main gastric carcinogen, and its treatment reduces GC incidence and mortality. Esophageal-gastro-duodenoscopy (EGD) allows for the detection of premalignant conditions and early-stage GC. Mass screening programs for H. pylori infection and screening for premalignant conditions and early-stage GC are not currently implemented in LAC. The aim of this study is to establish recommendations for primary and secondary prevention of GC in asymptomatic standard-risk populations in Chile. MethodsTwo on-line synchronous workshops and a seminar were conducted with Chilean experts. A Delphi panel consensus was conducted over 2 rounds to achieve >80% agreement on proposed primary and secondary prevention strategies for the population stratified by age groups. Results10, 12, and 12 experts participated in two workshops and a seminar, respectively. In the Delphi panel, 25 out of 37 experts (77.14%) and 28 out of 52 experts (53.85%) responded. For the population aged 16–34, there was no consensus on non-invasive testing and treatment for H. pylori, and the use of EGD was excluded. For the 35–44 age group, non-invasive testing and treatment for H. pylori is recommended, followed by subsequent test-of-cure using non-invasive tests (stool antigen test or urea breath test). In the ≥45 age group, a combined strategy is recommended, involving H. pylori testing and treatment plus non-invasive biomarkers (H. pylori IgG serology and serum pepsinogens I and II); subsequently, a selected group of subjects will undergo EGD with gastric biopsies (Sydney Protocol), which will be used to stratify surveillance according to the OLGA classification (Operative Link for Gastritis Assessment); every 3 years for OLGA III–IV and every 5 years for OLGA I–II. ConclusionA “test-and-treat” strategy for H. pylori infection based on non-invasive studies (primary prevention) is proposed in the 35–44 age group, and a combined strategy (serology and EGD) is recommended for the ≥45 age group (primary and secondary prevention). These strategies are potentially applicable to other countries in LAC.

Quadruple therapies show a higher eradication rate compared to standard triple therapy for Helicobacter pylori infection within the LEGACy consortium. A multicenter observational study in European and Latin American countries.

Gastric cancer (GC) is one of the most lethal malignancies worldwide. Helicobacter pylori is the primary cause of GC; therefore, its eradication reduces the risk of developing this neoplasia. There is extensive evidence regarding quadruple therapy with relevance to the European population. However, in Latin America, data are scarce. Furthermore, there is limited information about the eradication rates achieved by antibiotic schemes in European and Latin American populations. To compare the effectiveness of standard triple therapy (STT), quadruple concomitant therapy (QCT), and bismuth quadruple therapy (QBT) in six centers in Europe and Latin America. A retrospective study was carried out based on the LEGACy registry from 2017 to 2022. Data from adult patients recruited in Portugal, Spain, Chile, Mexico, and Paraguay with confirmed H. pylori infection who received eradication therapy and confirmatory tests at least 1month apart were included. Treatment success by each scheme was compared using a mixed multilevel Poisson regression, adjusting for patient sex and age, together with country-specific variables, including prevalence of H. pylori antibiotic resistance (clarithromycin, metronidazole, and amoxicillin), and CYP2C19 polymorphisms. 772 patients were incorporated (64.64% females; mean age of 52.93years). The total H. pylori eradication rates were 75.20% (255/339) with STT, 88.70% (159/178) with QCT, and 91.30% (191/209) with QBT. Both quadruple therapies (QCT-QBT) showed significantly higher eradication rates compared with STT, with an adjusted incidence risk ratio (IRR) of 1.25 (p: <0.05); and 1.24 (p: <0.05), respectively. The antibiotic-resistance prevalence by country, but not the prevalence of CYP2C19 polymorphism, showed a statistically significant impact on eradication success. Both QCT and QBT are superior to STT for H. pylori eradication when adjusted for country-specific antibiotic resistance and CYP2C19 polymorphism in a sample of individuals residing in five countries within two continents.

Efficacy and Safety of Vonoprazan-Based Quadruple Therapy for the Eradication of Helicobacter pylori in Patients with Peptic Ulcers: A Pooled Analysis of Two Randomized, Double-Blind, Double-Dummy, Phase 3 Trials.

Helicobacter pylori eradication is crucial in the treatment of peptic ulcers caused by H. pylori infection, a disease highly prevalent in Asia. We present a pooled analysis of two randomized, double-blind, double-dummy, phase 3 studies evaluating the efficacy and safety of vonoprazan-based bismuth-containing quadruple therapy for H. pylori eradication. Patients aged ≥18 years with endoscopically confirmed duodenal or gastric ulcers were randomized 1 : 1 to receive vonoprazan 20 mg or lansoprazole 30 mg once daily for up to 6 (duodenal ulcers) or 8 weeks (gastric ulcers). H. pylori-positive patients received vonoprazan- or lansoprazole-based bismuth-containing quadruple therapy for the first 2 weeks. H. pylori eradication was determined using the carbon-13 urea breath test at a follow-up visit 4 weeks post-treatment. The H. pylori eradication rate was 90.6% with vonoprazan vs. 85.2% with lansoprazole (difference: 5.4%; 95% confidence interval (CI): -0.1, 10.8). H. pylori eradication rates were 7.1% (95% CI: 1.4, 12.8) and 12.6% (95% CI: 3.9, 22.0) higher in patients aged <65 years and current smokers, respectively, with vonoprazan vs. lansoprazole. In the Chinese subpopulation, the H. pylori eradication rate was 92.0% with vonoprazan vs. 86.0% with lansoprazole (difference: 6.1%; 95% CI: 0.5, 11.7). Treatment-emergent adverse events occurred in 72.7 vs. 62.6% of H. pylori-positive patients at baseline in the vonoprazan vs. lansoprazole arm. H. pylori eradication with vonoprazan-based quadruple therapy was noninferior to lansoprazole-based quadruple therapy and exceeded 90%, a clinically relevant threshold for determining the efficacy of H. pylori eradication regimens (ClinicalTrials.gov identifier: NCT03050359; NCT03050307).

Maintaining H. pylori Negativity After Eradication Can Consolidate Its Benefit in Gastric Cancer Prevention: A Meta-Analysis.

Several studies have reported the role of Helicobacter pylori eradication in gastric cancer (GC) prevention. However, for individuals with unsatisfactory management of their H. pylori infection status after eradication, the risk of GC remains unclear. An exhaustive search strategy of the incidence of GC (including primary gastric cancer and metachronous gastric cancer) incidence in patients with unsuccessful eradication or H. pylori reinfection was implemented in the PubMed, Embase, Cochrane Library, and Web of Science. The hazard ratios (HRs) and cumulative incidence of total GC in patients with failed eradication or H. pylori reinfection (FE-Hp (+)) group were compared with that in patients with successful eradication and no H. pylori reinfection (SE-Hp (-)) group and patients with noneradication (NE) group. Seven eligible studies (including 8,767 patients with H. pylori infection) were identified. In the FE-Hp (+) group, the total GC risk was 1.86-fold of that in the SE-Hp (-) group (HR = 1.86, 95% confidence interval [CI]: 1.14-3.04, P = 0.013). The total GC risk in the NE group was also higher than that in the FE-Hp (+) group (HR = 1.98, 95% CI: 1.11-3.52, P = 0.002). On further analysis with different end points showed that the pooled GC risk increased over time (5-year follow-up: HR = 2.92, 1.34-6.34; 10-year follow-up: HR = 4.04, 2.56-6.37). Compared with the SE-Hp (-) group, the FE-Hp (+) group had a higher risk of gastric carcinoma. Long-term monitoring of H. pylori infection status could consolidate the benefit of eradicating H. pylori for preventing GC prevention in patients after eradication.

Predictive biomarkers for metachronous gastric cancer development after endoscopic resection of early gastric cancer.

We aimed to identify predictive markers for metachronous gastric cancer (MGC) in early gastric cancer (EGC) patients curatively treated with endoscopic submucosal dissection (ESD). From EGC patients who underwent ESD, bulk RNA sequencing was performed on non-cancerous gastric mucosa samples at the time of initial EGC diagnosis. This included 23 patients who developed MGC, and 23 control patients without additional gastric neoplasms for over 3 years (1:1 matched by age, sex, and Helicobacter pylori infection state). Candidate differentially-expressed genes were identified, from which biomarkers were selected using real-time quantitative polymerase chain reaction and cell viability assays using gastric cell lines. An independent validation cohort of 55 MGC patients and 125 controls was used for marker validation. We also examined the severity of gastric intestinal metaplasia, a known premalignant condition, at initial diagnosis. From the discovery cohort, 86 candidate genes were identified of which KDF1 and CDK1 were selected as markers for MGC, which were confirmed in the validation cohort. CERB5 and AKT2 isoform were identified as markers related to intestinal metaplasia and were also highly expressed in MGC patients compared to controls (p<0.01). Combining these markers with clinical data (age, sex, H. pylori and severity of intestinal metaplasia) yielded an area under the curve (AUC) of 0.91 (95% CI, 0.85-0.97) for MGC prediction. Assessing biomarkers in non-cancerous gastric mucosa may be a useful method for predicting MGC in EGC patients and identifying patients with a higher risk of developing MGC, who can benefit from rigorous surveillance.

Prevalence of Iron Deficiency Among Patients With Helicobacter pylori Infection at a Tertiary Care Hospital.

Background and objective Iron deficiency and iron deficiency anemia are related but distinct conditions. Iron deficiency refers to a state where the body has insufficient iron stores, which can lead to anemia if not addressed. Iron deficiency anemia, on the other hand, is a more severe condition where the lack of iron has resulted in decreased hemoglobin levels, impacting oxygen transport in the blood. Helicobacter pylori (H. pylori) infection can contribute to iron deficiency through mechanisms such as chronic gastrointestinal bleeding and impaired iron absorption, potentially progressing to iron deficiency anemia. The objective of this study was to determine the prevalence of iron deficiency, including its potential progression to iron deficiency anemia, among patients diagnosed with H. pylori infection. Methodology This cross-sectional study was conducted at Bolan Medical Complex Hospital, Quetta, and included 200 patients diagnosed with H. pylori infection via endoscopic biopsy or urea breath test, from January to June 2023. Participants were aged 18 years and older, excluding those with chronic diseases affecting iron metabolism, current iron supplement users, and pregnant women. Data were collected through questionnaires and medical records, and blood samples were analyzed for serum ferritin and hemoglobin levels. Statistical analysis included chi-square testsand logistic regression was performed in SPSS (version 27; IBM Corp, Armonk, NY); p-value <0.05 was significant. Results Out of 200 patients, 80 (40%) were iron deficient. The prevalence was highest among those over 60 years (n = 15, 75%) compared to the 18-30 age group (n = 10, 20%). Males had a slightly higher prevalence of iron deficiency (n = 50, 45.5%) compared to females (n = 30, 33.3%). Patients with H. pylori infection for more than three years exhibited a higher prevalence of iron deficiency (n = 30, 50%) compared to those with less than one year of infection (10/60, 16.7%). Dietary habits also played a role, with vegetarians showing a higher prevalence (n = 20, 50%) compared to non-vegetarians (n = 60, 37.5%). Hemoglobin levels were significantly lower in iron-deficient participants, averaging 10.8 ± 0.9 g/dL, and logistic regression indicated significant associations between iron deficiency and both age (OR = 1.05, p = 0.001) and infection duration (OR = 1.10, p < 0.001). Conclusions The study revealed a significant prevalence of iron deficiency among H. pylori-infected patients, particularly in older adults, males, those with longer infection duration, and vegetarians. The findings underscore the need for routine monitoring and targeted treatment of iron deficiency in this population.

Progranulin inhibits autophagy to facilitate intracellular colonization of Helicobacter pylori through the PGRN/mTOR/DCN axis in gastric epithelial cells.

Helicobacter pylori (H. pylori) infection is the primary risk factor for the progress of gastric diseases. The persistent stomach colonization of H. pylori is closely associated with the development of gastritis and malignancies. Although the involvement of progranulin (PGRN) in various cancer types has been well-documented, its functional role and underlying mechanisms in gastric cancer (GC) associated with H. pylori infection remain largely unknown. This report demonstrated that PGRN was up-regulated in GC and associated with poor prognosis, as determined through local and public database analysis. Additionally, H. pylori induced the up-regulation of PGRN in gastric epithelial cells both in vitro and in vivo. Functional studies have shown that PGRN promoted the intracellular colonization of H. pylori. Mechanistically, H. pylori infection induced autophagy, while PGRN inhibited autophagy to promote the intracellular colonization of H. pylori. Furthermore, PGRN suppressed H. pylori-induced autophagy by down-regulating decorin (DCN) through the mTOR pathway. In general, PGRN inhibited autophagy to facilitate intracellular colonization of H. pylori via the PGRN/mTOR/DCN axis. This study provides new insights into the molecular mechanisms underlying the progression of gastric diseases, suggesting PGRN as a potential therapeutic target and prognostic predictor for these disorders.

Programmed cell death in Helicobacter pylori infection and related gastric cancer.

Programmed cell death (PCD) plays a crucial role in maintaining the normal structure and function of the digestive tract in the body. Infection with Helicobacter pylori (H. pylori) is an important factor leading to gastric damage, promoting the Correa cascade and accelerating the transition from gastritis to gastric cancer. Recent research has shown that several PCD signaling pathways are abnormally activated during H. pylori infection, and the dysfunction of PCD is thought to contribute to the development of gastric cancer and interfere with treatment. With the deepening of studies on H. pylori infection in terms of PCD, exploring the interaction mechanisms between H. pylori and the body in different PCD pathways may become an important research direction for the future treatment of H. pylori infection and H. pylori-related gastric cancer. In addition, biologically active compounds that can inhibit or induce PCD may serve as key elements for the treatment of this disease. In this review, we briefly describe the process of PCD, discuss the interaction between different PCD signaling pathways and the mechanisms of H. pylori infection or H. pylori-related gastric cancer, and summarize the active molecules that may play a therapeutic role in each PCD pathway during this process, with the expectation of providing a more comprehensive understanding of the role of PCD in H. pylori infection.

The overview of Clarithromycin treatment for Helicobacter pylori infection

Helicobacter pylori (H. pylori) is a Gram-negative bacillus that causes infections worldwide. Helicobacter pylori's drug resistance and infectivity are vital factors causing Helicobacter pylori infection. The virulence factors of Helicobacter pylori include acid escape virulence factors and epithelial cell colonizing factors, which can directly or indirectly cause chronic gastritis or gastric ulcer. As the resistance of Helicobacter pylori increases, a combination of multiple antibiotics is now the recommended therapy, and clarithromycin is one of them. The production process of clarithromycin and its effectiveness are essential points of discussion.

Treatment outcomes and CYP3A4*1G genotype distribution in children with peptic ulcers

Many factors, including the role of the cytochrome P450 system such as CYP3A4*1G, may influence the effectiveness of peptic ulcer treatment. The study aimed to describe the treatment outcomes and distribution of CYP3A4*1G genotype in children with peptic ulcers. A descriptive cross-sectional study, longitudinal follow-up before and after six weeks of treatment was conducted on 100 children with peptic ulcers from October 2022 to February 2024. Children with peptic ulcers without H. pylori infection had a higher rate of anemia, and pyloric and duodenal deformation, compatible with children with H. pylori. The ulcer healing rate was lower in children with deep peptic ulcers, excess eosinophils in mucosal biopsies, and poor therapeutic compliance. The distribution of CYP3A4*1/*1, CYP3A4*1/CYP3A4*1G, CYP3A4*1G/CYP3A4*1G in the study was 43.2%, 48.1%, and 8.6%, respectively, with no difference by gender. There were no difference in ulcer healing rates according to the presence of the CYP3A4*1G variant. In conclusion, the degree of peptic ulcer healing in children varies according to several characteristics. However, there were no difference in ulcer healing rates according to the presence of the CYP3A4*1G variant.

Vitamin B12 (cobalamin) deficiency in gastroenterological diseases - review

Introduction: Vitamin B12 is a water-soluble vitamin found primarily in animal-derived products such as red meat, dairy, and eggs. An essential substance for its absorption is the intrinsic factor, produced by the parietal cells of the stomach. After absorption in the distal ileum, cobalamin acts as a coenzyme in DNA synthesis and the metabolism of fatty acids and homocysteine. In addition to its well-known influence on the nervous system, it has been associated with gastrointestinal diseases according to numerous authors. Objective: The objective of this study is to gather and analyze literature regarding the associations between vitamin B12 deficiency and gastrointestinal diseases, including gastroesophageal reflux disease (GERD), gastritis, inflammatory bowel disease (IBD), small intestinal bacterial overgrowth (SIBO), and hepatitis C (HCV). Materials and Methods: A literature review was conducted using the PubMed database with the following search terms: vitamin B12, cobalamin, deficiency, gastrointestinal diseases, GERD, IBD, SIBO, HCV. Current Knowledge: Vitamin B12 deficiency can be caused by autoimmune factors, dietary insufficiencies, toxin exposure, and malabsorption disorders related to gastrointestinal diseases. Gastrointestinal conditions such as GERD and IBD can both lead to and be exacerbated by cobalamin deficiency. Furthermore, vitamin B12 deficiency may be worsened by prolonged use of proton pump inhibitors (PPIs) and Helicobacter pylori infection. Conclusions: An adequate amount of vitamin B12 is crucial for gastrointestinal health. Deficiency can significantly impact the course and symptoms of many gastrointestinal diseases. Therefore, monitoring and supplementation of vitamin B12 should be an integral part of managing patients with gastrointestinal conditions.

Efficacy and Mechanism of Core Traditional Chinese Medicines for Treating Malignant Lymphoma based on Efficacy Studies: A Study Supported by Network Pharmacology and Molecular Docking.

The burden of malignant lymphoma in China is greater than the global equivalent. The randomized controlled trials provide medical evidence that TCM can improve the response and survival in patients with lymphoma. However, the mechanisms underlying remain undefined. Evidence-based data mining for traditional Chinese medicine (TCM) on improving response and survival in malignant lymphoma treatment was performed in this study. In addition, the mechanisms of TCM through network pharmacology and molecular docking were explored. The China national knowledge infrastructure, Wanfang Data, China Science and Technology Journal Database, PubMed, and Web of Science databases were searched to select TCM formulas with response and survival benefits in the treatment of malignant lymphomas. We then analyzed and visualized the tropism of taste, frequency of drug use, dosage, clustering, association rules mining (minimum support threshold as 0.20, the minimum confidence threshold as 0.80 and lift >1), and complex networks for potential core herb compositions using Excel, IBM SPSS Statistics 26, and IBM SPSS Modeler 18. TCM systems pharmacology, GeneCards, Online Mendelian Inheritance in Man, and other databases were used to screen potential core active ingredients and malignant lymphoma-related targets. The intersection targets were used to construct a protein interaction network using Cytoscape to obtain the key targets. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment were used to analyze the core target, and molecular docking of key components and targets was performed using CB-Dock2. Twenty-four Chinese herbal formulae were included, encompassing 107 herbs with mainly cold and warm properties and bitter and sweet flavors. They were associated with the yin meridians of the liver, spleen, and lungs. The TCMs underwent association rule analysis, identified 27 association rules, including 12 herb pairs and 13 angle medicine, and clustered into eight classes by clustering analysis. Combined with the results from mining analysis, Pinelliae (Ban-xia), Poria (Fu-ling), Atractylodis macrocephalae (Bai-zhu), Curcumae (E-zhu), and Sparganii (San-leng) were the potential core herbs According to network pharmacology and molecular docking, the main core components of the potential core drugs are hederagenin, cerevisterol, 14- acetyl-12-senecioyl-2E,8E,10E-atractylentriol, 12,13-epoxy-9-hydroxynonadeca-7,10-dienoic acid, cavidine, and baicalein. These core drugs are mainly involved in the pathways of EGFR tyrosine kinase inhibitor resistance, PD-1/L1, natural killer cell-mediated cytotoxicity, NF-κB, epithelial cell signaling in H. pylori infections, and Th17 cell differentiation. They aid in regulating the transmembrane receptor protein tyrosine kinase signaling pathway, ERBB signaling pathway, PI3K signaling pathway, and phosphorylation process. Ten key components and eight key targets, including baicalein and hederagenin, demonstrated strong binding activity. Collectively, some core herbs exerted anti-tumor effects through immune and inflammatory pathway modulation, inhibition of immune escape, and induction of cell apoptosis. These findings support future evidence-based research on malignant lymphoma treatment using TCM.

Evaluation of In Vitro Biofilm Formation of Helicobacter pylori in Different Culture Media

Objective: Biofilms are surface-attached cell communities that play a role in the survival of bacteria. Helicobacter pylori, a gram-negative pathogen that colonizes the human gastric mucosa, forms biofilms, causing treatment failure and the risk of developing peptic ulcers, gastritis and gastric cancer in infected individuals. The aim of the study is to evaluate the biofilm formation abilities of H. pylori ATCC 26695 and three clinical strains in different culture media. Material and Method: Biofilm formation characteristics of H. pylori strains using different culture media were evaluated, and the crystal violet (CV) staining method (measured at OD 595 ) was used. Various media were used for incubating H. pylori strains: Brucella broth (BB), TSB with 10% FBS, BHI with 10% FBS, BB with 10% FBS, BB with 10% FBS + 0.25% glucose, and BB with 10% FBS + 1% glucose (incubated for 3 days). Additionally, BB with 1% FBS, BB with 10% FBS, and BB with 5% inactivated human serum were incubated for 2 and 4 days at 37°C under microaerophilic conditions. Results: It was observed that 5% inactived human serum was more effective in biofilm formation of H. pylori ATCC 26695 and three clinical strains. However, there was no biofilm production in the strains cultured with Brucella broth alone and that the strains cultured with TSB + 10% FBS could not form a strong biofilm compared to other media. Conclusion: Different culture media used for H. pylori ATCC 26695 and three clinical strains affect biofilm formation. It is thought that in vitro experiments to prevent biofilm formation may provide a solution to the prevention of H. pylori infection.

The metabolites mainly composed of lipids in tongue coating are non-invasive potential biomarkers for chronic gastritis

The changes in tongue coating metabolites in patients with chronic gastritis (CG) under different gastroscopy indicators were analyzed, and these metabolites were screened for potential non-invasive biomarkers to assist in the diagnosis of chronic gastritis. The technology of gas chromatography and liquid chromatography combined with mass spectrometry has been used to more comprehensively detect tongue coating metabolites of 350 CG patients. Spearman correlation analysis and random forest algorithm were used to screen metabolites that can serve as potential biomarkers. Compared with healthy individuals, CG group showed significant changes in the content of 101 metabolites, with an increase in the content of 54 metabolites and a decrease in the content of 47 metabolites. These differential metabolites are mainly composed of 47 lipids and lipid like substances. 1 metabolite was associated with bile reflux, 1 metabolite was associated with gastric mucosal erosion, 10 metabolites were associated with atrophy, 10 metabolites were associated with intestinal metaplasia, and 3 metabolites were associated with Helicobacter pylori infection. The ROC model composed of 5 metabolites can distinguish between CG group and healthy individuals, with an accuracy of 95.4%. The ROC model composed of 5,6-Dihydroxyindole can distinguish between chronic superficial gastritis group and chronic atrophic gastritis group, with an accuracy of 75.3%. The lipids and lipid like metabolites were the main abnormal metabolites in patients with chronic gastritis. It was worth noting that the content of Sphinganine 1-phase, 4-Ipomenol, and Nervonic acid in tongue coating increased, and the content of 1-Methyladenosine and 3-Hydroxycapric acid decreased, which helped to identify CG patients. The decrease in the content of 5,6-dihydroxyindole reminded patients that the development trend of CG was shifting from superficial to atrophic or even intestinal metaplasia. The detection of these metabolic markers of tongue coating was expected to be developed as a non-invasive and convenient technology in the future to assist us in monitoring and diagnosing the occurrence and development of CG.

Modern approaches to diagnosing and preventing malignization of peptic ulcer in the practice of the general practitioner from the perspective of evidence-based medicine

Background: Peptic ulcer disease (PUD) is a prevalent gastrointestinal disorder that affects millions globally and has the potential to transform into gastric cancer (GC). GC ranks as the fifth most common cancer and is notably lethal. A significant correlation exists between PUD and Helicobacter pylori infection, which disrupts the stomach lining, leading to ulcers that may become malignant if not properly managed. Methods and Materials: This study employed a systematic analysis and meta-analysis approach, gathering data from multiple medical databases including Medscape, Medline, Scopus, Pubmed, and various gastrointestinal guidelines from regions such as Malaysia, Europe, and the United States. The primary methods involved comparing the risk of malignization between gastric and duodenal ulcers, assessing the sensitivity of different diagnostic methods, and determining optimal prevention strategies. Results: The findings indicate that gastric ulcers have a higher risk of malignization compared to duodenal ulcers. Diagnostic methods such as endoscopic biopsy demonstrated higher sensitivity for early malignization detection. Screening programs, especially those targeting H. pylori eradication, significantly reduce the incidence and mortality rates associated with gastric cancer. Conclusion: Early diagnosis and prevention of PUD malignization are vital for improving patient outcomes. Effective strategies include the use of sensitive diagnostic methods and comprehensive screening programs for H. pylori. Lifestyle modifications and vigilant monitoring by healthcare professionals are also crucial in reducing the risk of peptic ulcer malignization and subsequent gastric cancer development.

Association of Helicobacter pylori infection with colorectal polyps/adenomas: A single-center cross-sectional study

BackgroundHelicobacter pylori (H. pylori) infection may be associated with colorectal polyps/adenomas, but the current evidence remains controversial. MethodsWe retrospectively screened the medical records of 655 participants who underwent both colonoscopy and H. pylori test from June 15, 2020 to April 30, 2023. The number, size, location, and pathological type of colorectal polyps/adenomas were compared between H. pylori positive and negative groups. Adjusting for age, gender, smoking, drinking, hypertension, diabetes, fatty liver, body mass index, and inflammatory and metabolic indicators, multivariate logistic regression analyses were performed to evaluate the association of H. pylori infection with the number, size, location, and pathological type of colorectal polyps/adenomas, where no polyp/adenoma was used as reference. ResultsOverall, 508 participants were included, of whom 154 and 354 were divided into H. pylori positive and negative groups, respectively. H. pylori positive group had significantly higher colorectal polyps/adenomas (74.7 % vs. 65.8 %, P=0.048), low-grade adenomas (55.7 % vs. 47.6 %, P=0.026), advanced adenomas (22.6 % vs. 13.3 %, P=0.008), and colorectal polyps/adenomas with sizes of ≥6 mm (61.7 % vs. 48.5 %, P=0.002) and ≥10 mm (25.2 % vs. 14.6 %, P=0.004) than H. pylori negative group. In multivariate logistic regression analyses, H. pylori infection was independently associated with low-grade adenomas (OR=2.677, 95 %CI=1.283–5.587, P=0.009), advanced adenomas (OR=3.017, 95 %CI=1.007–9.036, P=0.049), right-side colon polyps/adenomas (OR=5.553, 95 %CI=1.679–18.360, P=0.005), and colorectal polyps/adenomas with sizes of ≥10 mm (OR=4.436, 95 %CI=1.478–13.310, P=0.008), but not number of colorectal polyps/adenomas. ConclusionH. pylori infection is associated with increased risk of colorectal polyps/adenomas, especially low-grade adenomas, advanced adenomas, right-side colon polyps/adenomas, and large colorectal polyps/adenomas.

Helicobacter pylori infection exacerbates metabolic dysfunction-associated steatotic liver disease through lipid metabolic pathways: a transcriptomic study

BackgroundThe relationship between Helicobacter pylori (H. pylori) infection and metabolic dysfunction-associated steatotic liver disease (MASLD) has attracted increased clinical attention. However, most of those current studies involve cross-sectional studies and meta-analyses, and experimental mechanistic exploration still needs to be improved. This study aimed to investigate the mechanisms by which H. pylori impacts MASLD.MethodsWe established two H. pylori-infected (Cag A positive and Cag A negative) mouse models with 16 weeks of chow diet (CD) or high-fat diet (HFD) feeding. Body weight, liver triglyceride, blood glucose, serum biochemical parameters, inflammatory factors, and insulin resistance were measured, and histological analysis of liver tissues was performed. Mouse livers were subjected to transcriptome RNA sequencing analysis.ResultsAlthough H. pylori infection could not significantly affect serum inflammatory factor levels and serum biochemical parameters in mice, serum insulin and homeostatic model assessment for insulin resistance levels increased in CD mode. In contrast, H. pylori Cag A + infection significantly aggravated hepatic pathological steatosis induced by HFD and elevated serum inflammatory factors and lipid metabolism parameters. Hepatic transcriptomic analysis in the CD groups revealed 767 differentially expressed genes (DEGs) in the H. pylori Cag A + infected group and 1473 DEGs in the H. pylori Cag A- infected group, and the “nonalcoholic fatty liver disease” pathway was significantly enriched in KEGG analysis. There were 578 DEGs in H. pylori Cag A + infection combined with the HFD feeding group and 820 DEGs in the H. pylori Cag A- infected group. DEGs in the HFD groups were significantly enriched in “fatty acid degradation” and “PPAR pathway.” Exploring the effect of different Cag A statuses on mouse liver revealed that fatty acid binding protein 5 was differentially expressed in Cag A- H. pylori. DEG enrichment pathways were concentrated in the “PPAR pathway” and “fatty acid degradation.”ConclusionsClinicians are expected to comprehend the impact of H. pylori on MASLD and better understand and manage MASLD. H. pylori infection may exacerbate the development of MASLD by regulating hepatic lipid metabolism, and the H. pylori virulence factor Cag A plays a vital role in this regulation.