Introduction

The association between chronic Helicobacter pylori infection and hormone levels affecting food intake and obesity remains controversial. Thus, our aim was to investigate the long-term effect of H. pylori eradication on changes in ghrelin and leptin levels.

Aims & Methods

A total of 72 patients meeting the inclusion and exclusion criteria were enrolled (July 2020 to November 2022). Participants were randomly assigned to two treatment groups (group 1: 14-day regimen with esomeprazole, amoxicillin, and clarithromycin; group 2: 14-day regimen with esomeprazole, amoxicillin, metronidazole and colloidal bismuth subcitrate). We evaluated changes in insulin resistance (HOMA-IR score), body mass index (BMI) and serum levels of ghrelin and leptin (ELISA test) at baseline, two months, and one year following successful H. pylori eradication.

Results

Of the 72 patients included, 13.9% (10/72) did not complete the study protocol. Both treatment groups were similar at enrolment and showed no statistically significant differences (p = 0.332 for OLGIM stages; p = 0.583 and p= 0.696 for antrum and corpus atrophy respectively, p = 0.177 and p = 0.296 for antrum and corpus intestinal metaplasia respectively). No statistically significant changes were present in BMI (p = 0.910) and insulin resistance (p = 0.342) after H. pylori eradication. A statistically significant decrease in ghrelin serum levels was observed in both treatment groups (p < 0.001), but not in leptin serum levels (p = 0.309), as shown in Table 1.

Table 1. Changes in various parameters over time in the entire cohort.

Conclusion

Successful eradication of chronic H. pylori gastritis decreased serum ghrelin levels regardless of the presence of gastric mucosal atrophy. Furthermore, no changes in BMI or waist circumference were detected after one year of follow-up, proving that H. pylori eradication is not related to weight gain through hormonal changes as previously hypothesized. These results reduce the fear that massive H. pylori eradication from the population could be associated with obesity.

References

1. Martin-Nunez GM, Cornejo-Pareja I. Clemente-Postigo M, Tinahones FJ, Moreno-Indias I. Helicobacter pylori Eradication Therapy Affect the Gut Microbiota and Ghrelin Levels. Front Med 2021;8:712908.
2. Yanagi H, Tsuda A, Matsushima M, Takahashi S, Ozawa G, Koga Y, et al. Changes in the gut microbiota composition and the plasma ghrelin level in patients with Helicobacter pylori-infected patients with eradication therapy. BMJ Open Gastro 2017;4:e000182.
3. Roper J, Francois F, Shue PL, Mourad MS, Pei Z, Olivares de Perez AZ, et al. Leptin and ghrelin in relation to Helicobacter pylori status in adult males. J Clin Endocrinol Metab 2008;93: 2350-2357.
4. Nwokolo CU, Freshwater DA, O'Hare P, Randeva HS. Plasma ghrelin following cure of Helicobacter pylori. Gut 2003;52:637–40.

Disclosure

None of the authors have any conflict of interest regarding this study.
KT was a speaker for Abbvie, Pfizer, Krka, Altamedics, Viatris, Eli Lilly.
BT served as a speaker or received research grant from KRKA, Ewopharma, Swixx pharma, Infai GmbH.
RO was speaker for Abbvie, Lek Sandoz, Medis, Ewopharma, Polymetria, Nutricia.
ML, UPF, GA and DŠ have no conflict of interest to declare.

Introduction

Aims & Methods

Results

Conclusion

Introduction

Helicobacter pylori (HP) infection is the most significant environmental factor contributing to gastric carcinogenesis. However, the rising prevalence of antibiotic resistance in HP has become a global concern. Currently, there is limited research on the correlation between HP antibiotic resistance and early gastric cancer (EGC). This study aimed to detect HP resistance genes in EGC patients using qRT-PCR on paraffin-embedded ESD specimens and explore the association between HP resistance and EGC.

Aims & Methods

A total of 150 EGC patients who underwent endoscopic submucosal dissection (ESD) between January 1, 2023, and December 31, 2024, were enrolled. HP resistance genes were detected in post-ESD gastric mucosal paraffin sections. Resistance rates to various antibiotics were compared, and correlations between resistance and clinicopathological features were analyzed.

Results

Among the 150 EGC patients, 28 (18.67%) were HP-positive, with 18 (64.3%, 95% CI: 44.1%–81.4%) showing antibiotic resistance. Levofloxacin had the highest resistance rate (50.0%), followed by clarithromycin (38.9%), tetracycline (11.1%), and amoxicillin (5.6%). No resistance to furazolidone was observed. Multidrug resistance analysis revealed common combinations, including clarithromycin + quinolone (22.2%) and clarithromycin + quinolone + tetracycline (5.6%). No significant correlations were found between resistance and clinicopathological features such as tumor location, size, histologic type, differentiation, depth of invasion, or mucosal status (all *p* > 0.05).

Conclusion

HP antibiotic resistance is prevalent in EGC patients, with high resistance rates to levofloxacin and clarithromycin. However, no significant association was observed between HP resistance and clinicopathological characteristics of EGC. Further studies are needed to elucidate the role of resistant HP strains in gastric carcinogenesis.

References

[1]Yang L, Kartsonaki C, Yao P, de Martel C, Plummer M, Chapman D, Guo Y, Clark S, Walters RG, Chen Y, Pei P, Lv J, Yu C, Jeske R, Waterboer T, Clifford GM, Franceschi S, Peto R, Hill M, Li L, Millwood IY, Chen Z; China Kadoorie Biobank Collaborative Group. The relative and attributable risks of cardia and non-cardia gastric cancer associated with Helicobacter pylori infection in China: a case-cohort study. Lancet Public Health. 2021 Dec;6(12):e888-e896. doi: 10.1016/S2468-2667(21)00164-X.
[2]Lee YC, Chiang TH, Chou CK, Tu YK, Liao WC, Wu MS, Graham DY. Association Between Helicobacter pylori Eradication and Gastric Cancer Incidence: A Systematic Review and Meta-analysis. Gastroenterology. 2016 May;150(5):1113-1124.e5. doi: 10.1053/j.gastro.2016.01.028. Epub 2016 Feb 2.
[3]Dingsdag SA, Hunter N. Metronidazole: an update on metabolism, structure-cytotoxicity and resistance mechanisms. J Antimicrob Chemother. 2018 Feb 1;73(2):265-279. doi: 10.1093/jac/dkx351.
[4]Dingsdag SA, Hunter N. Metronidazole: an update on metabolism, structure-cytotoxicity and resistance mechanisms. J Antimicrob Chemother. 2018 Feb 1;73(2):265-279. doi: 10.1093/jac/dkx351.
[5]Lee SM, Kim N, Kwon YH, Nam RH, Kim JM, Park JY, Lee YS, Lee DH. rdxA, frxA, and efflux pump in metronidazole-resistant Helicobacter pylori: Their relation to clinical outcomes. J Gastroenterol Hepatol. 2018 Mar;33(3):681-688. doi: 10.1111/jgh.13906.

Introduction

Endoscopic diagnosis of gastric dysplasia (GD) and early gastric cancer (EGC) remains challenging. Raman spectral analysis is a biomolecular specific vibrational analytical technique which measures inelastic light scattering process within samples. This technique detects disease via biomolecular "fingerprinting", which may be applied to objectively diagnose gastric lesions.

Aims & Methods

We aim to develop a machine learning model based on Raman spectra to diagnose intestinal metaplasia (IM), GD and EGC with biomarker correlations. Raman spectra were prospectively collected prior to endoscopic resection and correlated with histopathology. GD and EGC were classified as high-risk (HR) lesions; while IM and gastritis as low-risk (LR). Two methods were employed to identify significant Raman wavenumber for group differentiation: Partial Least Squares-Discriminant Analysis with Variance Importance in Projection analysis, and a theory-based statistical approach. Next, these features were tested using XGBoost model for best accuracy. A similar approach was applied to differentiate IM versus LGD, and the model was tested with leave-one-out cross-validation (LOOCV) method for the Support Vector Machine (SVM).

Results

20 participants were recruited from April 2022 to July 2023. A total of 1961 Raman spectra were collected from 33 lesions for HR versus LR differentiation. The results are as shown in Table 1. The diagnostic accuracy and F1 score for PLS-DA VIP and theory-based ranking were similar at 75.5% and 0.8318, respectively. XGBoost testing revealed that the model attained peak performance with the top 400 wavenumbers from PLS-DA VIP sorting, and the top 200 wavenumbers from the theory-based ranking. An overlap of 192 wavenumbers emerged, and the model achieved a peak F1 Score of 0.84 and 76.9% accuracy. These 192 wavenumbers were then mapped to the Raman spectrum and can be correlated with 8 Raman peaks of biochemicals related to gastric cancer including lipids, proteins, phospholipids and leucine. For LGD versus IM, we utilized 487 Raman signals from 25 lesions. was an overlap of 100 wavenumbers with accuracy of 74.1%.
The diagnostic accuracy and F1 score for PLS-DA VIP and theory-based ranking were similar at 74.4% and 0.79 respectively. LOOCV with SVM testing revealed that the model attained peak performance with the top 200 wavenumbers from PLS-DA VIP sorting, and the top 100 wavenumbers from the theory-based ranking. An overlap of 100 wavenumbers emerged, and the model achieved a peak F1 Score of 0.80 and 74.7% accuracy.

Table 1 Current AI model (XGBoost for differentiaton high risk and low risk lesions; LOOC method with SVM performance: intestinal metaplasia ) performance with selected wavenumbers for differentiation between gastric lesions.

Conclusion

A Raman spectroscopy-based AI algorithm may be useful for real time diagnosis of GIM, GD and EGC.

Introduction

In addition to gluten and a genetic predisposition, other external factors dictate the onset of coeliac disease (CeD). These, including the microbiota, have not yet been well characterised, but could explain why the disease occurs later in life in a large proportion of patients. Microbiota-associated barrier defects may contribute to this process.

Aims & Methods

Our aim was to investigate the potential of microorganisms to alter small intestinal epithelial polarity as well as epithelial barrier function - in particular with regard to epithelial gluten peptide uptake.
The study was designed in two phases. In the screening phase, the cell lines Caco2-Bbe and Caco2-PIP2 were exposed to different microorganisms. Caco2-PIP2 was stably transfected with a GFP-labelled PIP2 binding unit, which allowed for analysis of cell polarity. Read-outs in the screening phase included transepithelial resistance (TER), tight junction (TJ) integrity and epithelial polarity (IF and confocal imaging) and paracellular permeability by sandwich assay. In experimental phase II, the microorganisms (including a invasio-defective ALS3-mutant) were selected for a detailed analysis using human duodenal organoid 2D monolayers (isolated from healthy individuals and CeD patients). Read-outs included: TER, TJ integrity, epithelial polarity, 33mer-gliadin translocation and differential transcriptome analysis of bulk-RNA isolated from microbiota-exposed duodenal organoids.

Results

​Pseudomonas aeruginosa and Candida albicans were selected in phase I. They caused a decrease in TER by 90% and 95% of the original TER, respectively. Escherichia coli K12 and Saccharomyces cerevisiae were used as controls for P. aeruginosa and C. albicans, respectively. In phase II, both candidates revealed a reduced TER, an abolition of epithelial polarity and disrupted TJs as well as an increased epithelial 33mer uptake in CeD and control 2D organoids. Candida invaded – in an ALS3-dependent manner – the 2D organoid duodenal epithelia and thereby interacted with epithelial dynamin. On the other hand, differential gene expression of P. aeruginosa-exposed epithelia revealed altered apoptosis, barrier function and ion transport.

Conclusion

Our results suggest that distinct microorganisms can cause an epithelial barrier defect and increase 33mer transport in epithelial monolayers, thereby contributing to CeD immune pathology.

Introduction

Gastric cancer is a major cause of cancer-related mortality, and early detection improves outcomes. However, organized gastric cancer screening programs are largely absent in Europe, and vulnerable groups often have low awareness of preventive services. Roma communities face pronounced health disparities and barriers to healthcare, including social exclusion and low literacy, which may limit their use of preventive services [1].

Aims & Methods

We aimed to explore the knowledge, attitudes, and preferences regarding gastric cancer screening among Roma adults with low health literacy in Cluj-Napoca, Romania, to inform culturally tailored outreach strategies, as part of the TOGAS project. Approximately 40 Roma adults (18–72 years) were recruited via community centers for three focus groups (two urban, one rural) in Cluj-Napoca. All participants first attended a brief educational session on digestive health and gastric cancer to ensure baseline understanding. Guided by trained moderators, groups discussed their awareness of gastric cancer and perceptions of screening methods (endoscopy, blood tests, stool tests). All discussions were audio-recorded, transcribed, and thematically analyzed.

Results

Baseline awareness of gastric cancer screening was minimal. Most participants had never heard of any screening test or program for gastric cancer, indicating a major knowledge gap. Nevertheless, after receiving information, many expressed interest in screening for early detection. A prominent theme was communication preferences: nearly all participants preferred to receive health information via mobile phone or social media (e.g., messaging) and also through traditional channels like primary care providers. Overall, participants were open to screening if it was offered conveniently and respectfully.

Conclusion

Outreach is needed to improve engagement in cancer prevention among underserved populations. The lack of awareness in this Roma community echoes reports of poor knowledge of cancer prevention in other Roma groups and signals the need for targeted health promotion to reduce inequalities. As European health authorities consider implementing gastric cancer screening, input from vulnerable communities will be vital for equitable uptake.

References

1. Leja M. Where are we with gastric cancer screening in Europe in 2024? Gut. 2024 Nov 11;73(12):2074-2082.

Introduction

Increased intestinal permeability, mediated by zonulin, has been implicated in the pathogenesis of insulin resistance, dyslipidemia, and non-alcoholic fatty liver disease (NAFLD). Small intestinal bacterial overgrowth (SIBO) may further contribute to metabolic dysfunction through endotoxin-induced inflammation.

Aims & Methods

The aim was to determine zonulin concentrations in patients with dyslipidemia and NAFLD and analyze their relationships with metabolic parameters and the prevalence of small intestinal bacterial overgrowth (SIBO). A total of 342 patients with dyslipidemia were enrolled; NAFLD was confirmed in 152 of them based on ultrasound and steatometry. Fecal zonulin levels were measured using ELISA; SIBO was assessed by hydrogen breath test. Lipid profiles, high-sensitivity C-reactive protein (hsCRP), and HDL-C levels were also analyzed.

Results

Zonulin levels in patients with NAFLD (115±2.76 ng/g) exceeded the normal range (≤107 ng/g), compared to 87±0.28 ng/g in the dyslipidemia group without NAFLD (p<0.05). SIBO was present in 45% of dyslipidemic patients and 53.2% of those with NAFLD. A positive correlation was found between zonulin and hsCRP (r=0.65) and triglycerides (r=0.58), and a negative correlation between SIBO and HDL-C (r=–0.78) in the dyslipidemia group.

Conclusion

Elevated zonulin and increased intestinal permeability are associated with higher cardiometabolic risk in patients with NAFLD and dyslipidemia. Both zonulin and SIBO may serve as potential therapeutic targets for preventing progression of NAFLD and related metabolic disturbances.