Introduction

As well in the world Helicobacter pylori is the microorganism more prevalent in humans. Although the infection is a necessary factor but not enough to develop gastric cancer, the risk of disease develops varies among continents, countries and regions. Despite of there is a high Helicobacter pylori prevalence its role as pathogen or mutualist define the gastric cancer risk in regions from Colombia. Our study hypothesis postulate that the Helicobacter pylori role as pathogen or mutualist define the gastric cancer risk in Andean mountains or coastal regions in Colombia.

Aims & Methods

This study aimed to investigate the complex interaction between the genetic makeup of both the host and the pathogen in the development of Helicobacter pylori-associated diseases. An analysis was conducted on the human genetic composition, immune response, Helicobacter pylori genetics, and virulence factors to determine if there is a symbiotic or pathogenic process of the microorganism with the host in Colombia.

Results

The human and Helicobacter pylori coevolution observed in coastal region from Colombia: low gastric cancer risk and the disrupted coevolution found in the Andean mountain from Colombia: high gastric cancer risk; a virulent genotypes prevalence of Helicobacter pylori of (85,9%) in the mountain region, significative higher than (75,9%) found in the coastal region p=0,04; the type of inflammatory immune response to Helicobacter pylori (th1) observed in (83%) of participants from mountain region, in contrast to (81%) of participants with inflammatory immune response type 2 (th2) found in the coastal region and the human susceptibility to gastric cancer (IL1β, IL10). The frequency of genotype risk IL-1B-511TT was significantly higher in the mountain population (54,4%) compared to the frequency in the coastal population (36,6%), p=0,006 along with individuals that reside in mountain population and carriers the mutated genotype IL-10-1082AG have a 5,45 higher risk of develop precursor lesions of gastric cancer than those carrying the wild type genotype IL-10-1082AA (OR: 5.45; CI95% 1-7.59), all these findings explain the role of Helicobacter pylori as pathogen o mutualist associated to gastric cancer in Colombia.

Conclusion

Helicobacter pylori has a mutualist role mainly in low gastric cancer risk areas (coast from Colombia). However, in high gastric cancer risk areas (Mountains from Colombia) its role as pathogen deserve its eradication, being this a valid strategy to mitigate the high incidence of gastric cancer in Colombia.

References

1. Cover, T. L., & Blaser, M. J. (2009). Helicobacter pylori in health and disease. Gastroenterology, 136(6), 1863-1873.
2. Blaser, M. J., & Atherton, J. C. (2004). Helicobacter pylori persistence: biology and disease. Journal of clinical investigation, 113(3), 321-333.

Introduction

Gastrointestinal (GI) hemorrhage accounts for 30% of acute decompensations in cirrhotic patients, with 60% originating from variceal bleeding. Each decompensation episode carries an in-hospital mortality rate of 13%, and a 6-week mortality rate of 20%, commonly assed using Child Pugh (CP) and MELD scores. The ALBI (Albumin-Bilirubin) score, which includes only two variables, offers a simplified evaluation of liver function. However, there is limited data on its utility in predicting short-term mortality in cirrhotic patients with GI hemorrhage.

Aims & Methods

This study aimed to evaluate the association between ALBI Score with short-term mortality in cirrhotic patients with GI hemorrhage. We conducted a prospective, cross-sectional study between January and December of 2023 at Hospital Roosevelt, Guatemala, including cirrhotic patients admitted for GI hemorrhage. Informed consent was obtained from all participants. Categorical variables were analyzed using the chi-square test, normally distributed continuous variables with Student’s t-test, and non-normally distributed variables with the Mann-Whitney U test. Logistic binary regression and AUROC analysis were used to assess associations with short-term mortality. Statistical analyses were performed using SPSS.

Results

A total of 187 patients were included: 50.8% female and 49.2% male, with a mean age of 56 among survivors and 58 among non-survivors. Of these, 52.9% had a prior diagnosis of cirrhosis, while 47.1% were newly diagnosed. Cirrhosis etiology was metabolic in 50.2%, alcoholic in 42.7%, autoimmune in 4.3%, HCV in 1.6%, and HBV in 1.1%. At admission, 80.8% had no ascites and 97.3% had no hepatic encephalopathy. he causes of GI hemorrhage were 86.1% esophageal varices, 3.2% gastric varices, 9.1% gastric ulcers, and 1.6% esophagitis.
Non-survivors had significantly lower systolic blood pressure (93.90 ± 16.3 mmHg vs. 107.92 ± 17.4 mmHg; p = 0.002) and mean arterial pressure (69.50 ± 14.5 mmHg vs. 79.67 ± 11.7 mmHg; p = 0.005) compared to survivors. Non-survivors exhibited significantly higher INR (1.79 ± 0.56 vs. 1.52 ± 0.41; p = 0.026) and total bilirubin (5.85 ± 8.73 mg/dL vs. 2.02 ± 2.82 mg/dL; p = 0.031), and lower serum albumin levels (2.40 ± 0.43 g/dL vs. 3.10 ± 0.54 g/dL; p < 0.001).

Prognostic scores were significantly higher among non-survivors: MELD (19.25 ± 10.09 vs. 13.57 ± 5.47; p = 0.002), MELD-Na (20.35 ± 9.76 vs. 14.44 ± 6.42; p = 0.002), Child-Pugh (9.15 ± 2.21 vs. 7.18 ± 1.90; p < 0.001), and ALBI score (-0.96 ± 0.51 vs. -1.76 ± 0.58; p < 0.001). Additionally, the length of hospital stay was significantly shorter among non-survivors (3.90 ± 3.82 days) compared to survivors (6.59 ± 5.58 days; p = 0.001).

• Higher ALBI score was significantly associated with mortality (Risk Ratio 25.80; 95% CI: 6.75–98.67; p < 0.001),
• Hospital stay <5 days (RR 9.91; 95% CI: 2.07–47.47; p = 0.004),
• Endoscopy performed within 12 hours (RR 7.53; 95% CI: 2.01–28.15; p = 0.003).

Conclusion

The ALBI score outperforms CP and MELD scores in predicting short-term mortality (in-hospital, 4 weeks, and 6 weeks) in cirrhotic patients with GI hemorrhage. Observed mortality was 10% in-hospital, 13% at 4 weeks, and 16% at 6 weeks.

Introduction

The urea breath test (UBT) is the clinic's most popular and accurate non-invasive diagnostic method for H. pylori infection. Yet, it is time-consuming and unavailable to some individuals. The oral rapid urease test (RUT) is an emerging non-invasive convenience method but lacks clinical data support.

Aims & Methods

A double-center, double-blind, methodological comparative design experiment is invited to evaluate the consistency of the oral RUT with UBT. 247 participants were enrolled. Their Dental plaque and tongue coating samples were collected, blind and tested with RUT.

Results

The significant association between the RUT and UBT was analyzed.A total of 247 participants were included in the study. The oral RUT showed a high level of agreement with the UBT. The sensitivity of the test reagent was 98.63% (95% CI: 92.64%, 99.76%), and the specificity was 96.34% (95% CI: 92.25%, 98.31%). The overall conformity rate was 97.05% (95% CI: 94.03%, 98.56%). The positive predictive value was 92.31%, and the negative predictive value was 99.37%. The positive likelihood ratio was 26.96, and the negative likelihood ratio was 0.01. The Kappa value was 0.97.

Conclusion

The efficacy of oral RUT for Helicobacter pylori infection diagnosis is extremely consistent with the UBT.

Introduction

Colorectal cancer (CRC) is the most common cancer in Spain, with an estimated 44,573 new cases in 2025. The standard CRC screening strategy involves the immunological faecal occult blood test (FIT), followed by colonoscopy in positive cases. However, the low specificity of FIT results in a significant number of unnecessary colonoscopies, placing a high burden on healthcare systems. There is a growing need to explore alternative screening strategies that offer better cost-effectiveness ratios. The gut microbiota plays a key role in CRC carcinogenesis, and several bacterial species involved in this process have been identified. A diagnostic tool based on the combination of FIT (cut-off 100 ng/mL – FIT100) and a bacterial signature has been designed to detect CRC and advanced lesions (AL, defined as ≥1 cm and/or high-grade dysplasia and/or a hairy component). This tool uses qPCR to analyse the relative abundance of specific bacteria in the same stool sample used for FIT testing. Previous studies, including a proof-of-concept (N=172), confirmatory study (N=327), and clinical performance study (N=2,481), have validated the tool.

Aims & Methods

This study aims to evaluate the diagnostic performance of the bacterial signature applied to FIT100 positive participants and its potential to reduce unnecessary colonoscopies in the CRC screening program in Catalonia.
A prospective observational study was conducted in a multicentre cohort across five hospitals, including participants from the CRC screening program with a positive FIT100. Blinding was applied to the FIT, bacterial signature, colonoscopy, and biopsy. Colonoscopy-biopsy was used as the reference standard. The study included 1,453 participants, of which 48 were excluded from the analysis mainly because of poor sample conditions, resulting in a final sample of 1,405 participants. Sensitivity was defined as the proportion of true positives detected by the FIT that the bacterial signature also identifies as positive. Specificity was defined as the proportion of false positives of FIT that the bacterial signature correctly identifies as true negatives.

Results

From the 1,405 analysed cases, 44 were CRC, 472 AL, and 889 without AL. For CRC detection, the sensitivity was 95.5%, with a specificity of 18.4%. The reduction in false positives was 18.4%. For AL and CRC combined, the sensitivity was 82.6%, with a specificity of 18.4%.

Conclusion

The bacterial signature applied to FIT100 positive participants demonstrates high sensitivity for CRC detection while reducing unnecessary colonoscopies by minimizing false positives. Its implementation in the CRC screening protocol could improve the overall efficiency of the screening process. Future studies should focus on cost minimization and assess the tool's cost-effectiveness to ensure a favourable risk-benefit ratio for broader implementation.

Introduction

Global rise in primary Helicobacter pylori (H. pylori) antibiotic resistance has led to a decrease in the treatment efficacy. Understanding the rates of clarithromycin (ClaR), metronidazole (MetR) and levofloxacin (LevR) resistance in H. pylori management is essential for determining the optimal eradication therapy and achieving successful clinical outcomes.

Aims & Methods

To evaluate the prevalence and geographical distribution of H. pylori primary ClaR, MetR and LevR in Europe. Bibliographical searches were conducted in PubMed until March 2024, with no language restrictions. Studies focused on children only or non-European countries were excluded.

Results

A total of 218 studies published since 1990 were included, of which 188 provided information on ClaR, 138 on MetR, and 77 on LevR (Table 1). The average ClaR in Europe, considering all studies and years, was 17%, showing an increase from 7.3% in the 1990s to 26% in the period 2010–2019, with a slight decrease to 22% in the period 2020–2024. The highest values were reported in Switzerland (66%), Ireland (50%), and Israel (44%). Southern European countries presented higher resistance rates (over 15–20%) compared to those in the north (under 10–15%). MetR remained consistently high (with a European average of 34%), particularly in Poland (66%), Turkey (67%), and Switzerland (60%). As for LevR, it was low in the 1990s but experienced a progressive increase over time, reaching approximately 15% during 2010–2019, and fluctuating between 20% and 25% in recent years.

Conclusion

In Europe, since the 1990s, primary ClaR has fluctuated but always remaining above 15%; MetR has remained consistently high; and LevR has shown a progressive increase throughout the study periods. These data highlight the urgent need for region-specific antibiotic stewardship and updated treatment guidelines to ensure H. pylori eradication success.

Disclosure

Javier P. Gisbert has served as speaker, consultant, and advisory member for or has received research funding from: Mayoly, Allergan/Abbvie, Diasorin, Richen, Juvisé and Biocodex.
Olga P. Nyssen received research funding from: Mayoly, Allergan/Abbvie, Richen, Juvisé and Biocodex.

Introduction

Differences in endoscopic response and biological features across ileal, ileocolonic, and colonic Crohn’s disease (CD) suggest distinct mechanisms for healing. We developed an endoscopic clustering method using segmental intestinal endoscopic scores in patients with moderately to severely active CD to investigate the potential influence of regional mucosal heterogeneity on treatment effect. We then evaluated endoscopic outcomes across subtypes between placebo (PBO), guselkumab (GUS), and ustekinumab (UST) in the Phase 3 GALAXI 2 and 3 studies.

Aims & Methods

Endoscopic clustering was established using baseline segment Simple Endoscopic Score for CD (SES-CD) values from terminal ileum, right colon, transverse colon, left/sigmoid colon, and rectum from cohort 1 (1233 patients, GALAXI 1, GALAXI 2, GRAVITI trials) and cohort 2 (525 patients, GALAXI 3). Patient clusters were identified using consensus hierarchical clustering, and a machine learning classification model was developed for patient cluster assignment of cohort 2. GALAXI 2 and GALAXI 3 patients were combined to evaluate Week (WK) 12 and WK48 endoscopic outcomes between PBO, GUS, and UST.

Results

We identified 7 CD endoscopic subtypes (ileum only, ileum dominant, right colon dominant, mid-colon, colonic, ileocolonic, rectum dominant), highlighting heterogeneity within Montreal classification. In total, GUS showed higher endoscopic remission rates than UST at WK12 and at WK48. Patient clusters were used with baseline stricturing data (SES-CD narrowing > 0) to consolidate groups with differential treatment effects: Group 1 (62% of patients, mixed ileocolonic/colonic) showed similar endoscopic remission rates at WK12 between GUS (26%) and UST (27%) with higher rates for GUS at WK48 (39-44% GUS, 30% UST); Group 2 (ileum only) and Group 3 (characterized by strictured right colon), totaling 38% of patients, showed higher endoscopic remission rates with GUS at WK12 (19%, 20%), where UST showed placebo-like efficacy (7%, 2%), with higher rates with GUS at WK48 (Group 2: 20-26% GUS, 18% UST; Group 3: 28-30% GUS, 12% UST). Endoscopic responders to GUS, and not UST, at WK12 in Group 2 and 3 patients with baseline stricturing showed greater reduction in narrowing than non-responders, contributing to 21% vs 5% reduction in total SES-CD.

Conclusion

Endoscopic patient clustering provides higher resolution of CD subtypes to delineate differential treatment effects. GUS demonstrated endoscopic efficacy across all patients at WK12, where UST showed placebo-like efficacy in 38% of patients, supporting superior endoscopic efficacy over UST across all patients by WK48. Reductions in narrowing with GUS proposes a role of GUS in affecting stricture biology in addition to broader segment-specific molecular treatment effects that will be explored in future research.

Disclosure

Dylan Richards, Loqmane Seridi, Klebea Sohn, Brad Mcrae, Natalie A. Terry, Marion Vetter, Daniel Cua, Patrick Branigan are employees of Janssen and may hold stock in Johnson & Johnson.
Walter Reinisch reports serving as a speaker for AbbVie, Celltrion, Ferring, Janssen, Galapagos Medice, MSD, Roche, Pfizer, Sobi, Takeda; serving as a consultant for AbbVie, Amgen, AOP Orphan, Boehringer Ingelheim, Bristol Myers Squibb, Calyx, Celltrion, Eli Lilly, Galapagos, Gilead, Index Pharma, Janssen, Medahead, Microbiotica, Pfizer, and Takeda; serving as an advisory board member for AbbVie, Amgen, Boehringer Ingelheim, Bristol Myers Squibb, Celltrion, Galapagos, Janssen, and Pfizer; and receiving research funding from AbbVie, Janssen, Sandoz, Sanofi, and Takeda.
Raja Atreya has served as a speaker or consultant, or received research grants from AbbVie, Amgen, Arena Pharmaceuticals, AstraZeneca, Biogen, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Celltrion Healthcare, DrFalk Pharma, Galapagos, Gilead, InDex Pharmaceuticals, Janssen-Cilag, Lilly, Merck Sharp & Dohme, Novartis, Pandion Therapeutics, Pfizer, Roche, Samsung Bioepis, Takeda, and Viatris.

Introduction

Europe’s Beating Cancer Plan identified the urgent need for a gastric cancer screening strategy. In response, the TOGAS consortium (TOwards GAstric cancer Screening in the European Union) was established to evaluate different methods for gastric cancer prevention and detection within Europe(1). One such approach involves population-based screening of young adults for Helicobacter pylori (H.pylori) as a primary preventative strategy.

Aims & Methods

The pilot study aimed to assess the feasibility of screening asymptomatic 30-34 year olds for H.pylori. Key outcome measures included:
1) Response rate
2) Seropositivity
3) Treatment acceptance rate
4) Treatment effectiveness
Methods: Individuals aged 30-34 years were invited to participate in free screening via GP practices or occupational-based screening programmes in the period January 2024- March 2025. Invitations were distributed through email or text message at the discretion of the recruitment stream. Exclusion criteria included prior history of treatment of H. pylori or gastrectomy. Those who tested positive on serology (BIOHIT H. pylori IgG antibody, antibody titer >30 IU/ml) were offered confirmatory 13-C urea breath testing (Richen IR Force 200). Positive participants were offered treatment with a 10-day regimen of single capsule combination therapy (Bismuth subcitrate 140mg/Metronidazole 125mg/Tetracycline 125mg, three tablets, QDS; PYLERA, Juvise pharmaceuticals) + Esomeprazole 40mg BD. Eradication confirmation was offered a minimum of 6 weeks post-treatment. Demographics, risk factors, and treatment effectiveness were recorded.
The calculated sample size for statistical significance at a 95% confidence interval with a presumed prevalence rate of 30% was 323. The Mann-Whitney U-test was used for comparison of continuous variables, and the Chi² test for categorical variables (significance set at p<0.05).

Results

3030 invites were distributed (80% GP practices, 20% occupation-based). 20%(n=604) of recipients expressed interest in participating. Among these; 5%(n=31) were excluded and 18%(n=109) refused or ceased responding. 464 consented to and completed the study. The median age of participants was 32, 48%(n=223) were male. 15% (n=75) of those who underwent serology testing were seropositive. 97% agreed to have a confirmatory 13-C UBT, of which 50/73 (66%) tested positive. The median titre in this dual positivity group was 109 IU/mL [range 40-142], compared to 37 IU/mL [range 32-148 IU/ml] in the 13-C UT negative group. Overall, the true ‘positivity’ rate among those who agreed to screening was 11%. 96%(48/50) of positive participants agreed to treatment, a further 2 were excluded due to pregnancy. Among those treated, 96% (44/46) reported >90% adherence. 1^st line eradication rates, confirmed by a 13-C UBT, were 97%(36/37) in the per-protocol group and 89%(33/37) in the intention-to-treat group. Side effects were reported by 24%, the majority of which were GI. 4 patients required 2^nd line therapy due to early discontinuation or poor compliance, 1 failed 2^nd line therapy on follow-up eradication confirmation.

Conclusion

These interim results indicate that a population-based H.pylori screening approach is feasible within an Irish population. Despite a decreasing worldwide prevalence, infection remains a persistent issue. Although initial response rates to screening are modest, this is a novel pilot programme and reflects trends seen in the early phases of other national screening programmes, such as the colorectal cancer screening. As public awareness increases, higher engagement rates are anticipated.

References

1. Commission E. TOGAS - Towards Gastric Cancer Screening Implementation in the European Union: European Commission; 2023 [Available from: https://health.ec.europa.eu/non-communicable-diseases/cancer/europes-beating-cancer-plan-eu4health-financed-projects/projects/togas_en.

Disclosure

Dr. Deane reports receipt of research funding support from EU4 Health grant GA number: 101101252