Introduction

Inflammatory Bowel Diseases (IBD) are chronic conditions whose etiology remains elusive. Several hypotheses, including a potential association with Helicobacter pylori (HP), have been proposed, as evidenced by declining prevalence due to eradication protocols. However, literature data exhibit considerable variability. Our study aims to determine the prevalence of HP infection in a population of IBD patients based on gastric biopsy results, alongside predictive factors for HP infection in this population, integrating epidemiological, endoscopic, and histological analyses.

Aims & Methods

This retrospective descriptive study spanned four and a half years from January 2019 to July 2023, encompassing all IBD patients who underwent gastroscopy with biopsy. Patients with fewer than four gastric biopsies were excluded. Data were collected from medical records, and statistical analysis was performed using SPSS software version 21.0.

Results

150 patients were included, with a median age of 39.9 years [range: 18-71 years; ±13.49], including 80 females (53.3%) and a sex - ratio of 0.8. All patients reported tea consumption (100%), while 25 patients (16.66%) were smokers, and 18 (12%) reported alcohol use. NSAID use was noted in 17 patients (11.3%), and proton pump inhibitor (PPI) use in 5 patients (3.3%). Additionally, 15 patients reported herbal therapy. All patients underwent gastroscopy with at least 3 antral and 2 fundic biopsies. 93.3% of patients underwent systematic gastroscopy. Among participants, 66 tested positive for HP (HP+) , including 61 asymptomatic individuals. Symptomatically, 4 patients experienced epigastric pain, and one case of gastroesophageal reflux disease (GERD) was observed. HP prevalence in our sample was 44%, with a higher prevalence among females (56% vs. 44% males). HP infection was more common among individuals aged 21-45 and over 60, peaking between 30 and 40. Endoscopic findings in HP+ patients included esophagitis in 6 patients (9%), erythematous and erosive gastritis in 4 patients (6%), hiatal hernia in 3 patients (4.5%), and micronodular antritis in 1 patient (1.5%). Duodenal and bulbar aphthoid ulcers were observed in 5 patients (7.5%). Notably, gastroscopy was normal in 112 patients. Epidemiological data analysis revealed that chronic NSAID use (P=0.01), herbal therapy (P=0.05), tea consumption (P=0.03), history of digestive cancer (P=0.01), young age (<37 years; P=0.05), and patients with ulcerative colitis (P=0.001) were significant risk factors for HP infection.

Conclusion

In our study, the prevalence of Helicobacter pylori infection was 44%. Ulcerative colitis was a significant risk factor for HP infection in our sample, with a highly significant P value of 0.0001. Therefore, should all IBD patients be systematically screened for HP infection?

Disclosure

No there is no Conflict of Interest into the text field below.

Introduction

Celiac disease (CD) is an immune-mediated enteropathy triggered by gluten ingestion in genetically predisposed individuals, characterized by small intestinal inflammation and villous atrophy. Microbial agents such as Helicobacter pylori (H. pylori) may influence autoimmune disorders, including CD, through immune modulation. However, the relationship remains controversial.This study aimed to assess the association between CD and H. pylori infection by comparing the prevalence of H. pylori in patients with and without CD.

Aims & Methods

We conducted a retrospective study from January 2019 to December 2024. Two groups were analyzed: patients with biopsy-confirmed CD and controls without CD who underwent upper endoscopy for dyspeptic or non-specific gastrointestinal symptoms. Exclusion criteria included prior H. pylori eradication, recent use of PPIs, antibiotics, or bismuth compounds, other autoimmune disorders, and incomplete data.

Results

A total of 231 patients were included: 103 with CD (19.4% male, mean age 28.8 ± 12.6 years) and 128 controls (28.1% male, mean age 33.9 ± 11.9 years).
No significant differences were observed in age (p = 0.73) or sex distribution (p = 0.167) between groups.
H. pylori was detected in 67% of CD patients and 50% of controls, with a significantly higher prevalence in the CD group (p = 0.014).

Conclusion

Contrary to some previous reports suggesting a protective effect, this study found a significantly higher prevalence of H. pylori in patients with CD compared to controls.
These findings highlight the need for further investigations into the potential impact of H. pylori on the clinical presentation and management of celiac disease.

Introduction

Helicobacter pylori (H. pylori) remains a significant global pathogen, implicated in chronic gastritis, peptic ulcer disease, and gastric cancer. Over the past two decades, escalating resistance to key antibiotics—particularly clarithromycin, levofloxacin, and metronidazole—has reduced the effectiveness of standard triple therapies, with eradication rates falling below 70%. Refractory H. pylori infection, defined in this study as persistent infection after three or more failed eradication regimens, presents a growing therapeutic challenge. The absence of standardised rescue protocols and limited access to antibiotic susceptibility testing in many regions further complicates treatment. Innovative empirical strategies, especially those using agents with low resistance profiles, are urgently needed.

Aims & Methods

This real-world, prospective observational study aimed to evaluate the efficacy of a Modified Concomitant Therapy (MCT) regimen for the eradication of refractory H. pylori. Adults aged ≥18 years with confirmed H. pylori infection persisting after at least three previous treatment attempts were recruited from a gastroenterology centre in Bogotá, Colombia, between January and November 2023.

The MCT protocol included:

• Esomeprazole 40 mg, twice daily (before breakfast and dinner)
• Furazolidone 100 mg, every 8 hours
• Amoxicillin 875 mg every 8 hours (in patients <70 kg) or 1 g every 8 hours (in ≥70 kg)
• Tetracycline 500 mg, every 6 hours

Patients were counselled about the therapeutic difficulty and potential adverse effects. The treatment duration was 14 days. Eradication was assessed 6–8 weeks post-therapy using histological evaluation with haematoxylin-eosin and Giemsa staining. This choice was based on prior discordance between breath test results (often negative) and biopsy (positive). Effectiveness was analysed both by modified intention-to-treat (mITT) and per-protocol (PP) methods.

Results

A total of 30 patients were enrolled (mean age: 45 ± 6 years; range: 28–63).

• mITT eradication rate: 27/30 (90%, 95% CI: 72.3–97.4)
• PP eradication rate: 25/27 (92.5%, 95% CI: 76.3–97.9)

Adverse events were reported in 8 patients:

• Nausea (30%)
• Headache (33%)
• Diarrhoea (16%)
• Constipation (10%)

Three patients discontinued treatment prematurely between days 10 and 12. No severe adverse events or hospitalisations occurred. The major limiting factor for broader enrolment was intermittent availability of tetracycline.

Conclusion

This study demonstrates that Modified Concomitant Therapy represents a promising and effective option for the eradication of refractory H. pylori infection in real-world settings. With an eradication rate exceeding 90% and manageable adverse effects, MCT using furazolidone, amoxicillin, tetracycline, and high-dose PPI constitutes a rational empirical rescue strategy in regions where antibiotic resistance testing is unavailable and first-line therapies have failed. Further multicentre studies with larger cohorts are warranted to confirm these findings and assess long-term outcomes. The development of accessible tetracycline formulations would enhance implementation.

References

1. Malfertheiner P, Megraud F, Rokkas T, Gisbert JP, Liou JM, Schulz C, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. Gut. 2022 Jan;71(1):172–95. doi:10.1136/gutjnl-2021-325210.
2. Graham DY, Lee YC, Wu MS. Rational Helicobacter pylori therapy: evidence-based medicine rather than medicine-based evidence. Clin Gastroenterol Hepatol. 2014 Feb;12(2):177–86.e3. doi:10.1016/j.cgh.2013.06.020.
3. Liou JM, Chen CC, Chang CY, Chen MJ, Fang YJ, Lee JY, et al. Sequential versus triple therapy for the first-line treatment of Helicobacter pylori: a multicentre, open-label, randomised trial. Lancet. 2013 Feb 16;381(9862):205–13. doi:10.1016/S0140-6736(12)61455-0.

Introduction

Previous epidemiological studies have examined the association between Helicobacter pylori and gastroesophageal reflux disease (GERD) but the findings were inconsistent This study aimed to explore the causal relation between Helicobacter pylori IgG and six specific antibody levels and risk of GERD using mendelian randomization analysis.

Aims & Methods

We used summary-level data from two large genome-wide association studies (GWAS), i.e. the FinnGen research project and the UK biobank cohort. Eighteen single nucleotide polymorphisms (SNPs) associated with levels of IgG and six Helicobacter pylori specific antibodies (UreA, CagA, VacA, Catalase, OMP, and GroEL) were used as instrument variables to predict levels of these markers for Helicobacter pylori infection. Associations between these SNPs and GERD risk were examined primarily using the inverse variance weighted method, and secondly using MR-Egger, weighted median, simple mode, and weighted mode methods. We further conducted multivariable mendelian randomization analysis on the association between levels of the six specific antibodies and risk of GERD.

Results

Genetically predicted Helicobacter pylori lgG antibody levels were not associated with risk of GERD in either FinnGen (odds ratio [OR]=0.992, 95% confidence interval [CI] 0.961-1.025) or UK Biobank (OR=0.999, 95%CI 0.998-1.001). Genetically predicted levels of the six Helicobacter pylori specific antibodies were not associated with risk of GERD, except for UreA antibody levels in MR-Egger method only (OR=1.138; 95%CI 1.005-1.289) for which pleiotropy was indicated (MR-Egger intercept -0.029, P=0.048). Multivariate MR also found no associations between levels of Helicobacter pylori specific antibodies and risk of GERD.

Conclusion

This Mendelian randomization study found no evidence for a causal relation between Helicobacter pylori infection and the risk of GERD.