You are currently viewing a new version of our website. To view the old version click .
MDPIMDPI
Search all articles
Journal of Clinical Medicine
Download PDF
  • Review
  • Open Access

28 August 2025

The Controversies in the Relationship Between Helicobacter pylori Infection and Inflammatory Bowel Disease: Narrative Review

and
1
Department of Internal Medicine, Division of Gastroenterology, University Hospital of Split, Spinciceva 1, 21000 Split, Croatia
2
Department of Internal Medicine, School of Medicine, University of Split, Soltanska 2, 21000 Split, Croatia
3
Faculty of Health Sciences, University of Split, Rudjera Boskovica 35, 21000 Split, Croatia
*
Author to whom correspondence should be addressed.
J. Clin. Med.2025, 14(17), 6083;https://doi.org/10.3390/jcm14176083
This article belongs to the Special Issue Clinical Advances in Gastrointestinal Inflammation
Version Notes
Order Reprints

Abstract

Background/Objective: The relationship between Helicobacter pylori (H. pylori) infection and inflammatory bowel disease (IBD) remains controversial. While H. pylori is a well-established pathogen in gastroduodenal diseases, emerging evidence suggests it may exert immunomodulatory effects that influence the pathogenesis and clinical course of IBD. This review aims to explore the association between H. pylori infection and IBD, focusing on infection prevalence among IBD patients, the potential protective or harmful roles of H. pylori, and the impact of eradication therapy on IBD onset and activity. Methods: A comprehensive literature search was conducted using PubMed up to, including clinical studies, meta-analyses, systematic reviews, and observational data. A total of 40 studies met the inclusion criteria and were critically reviewed. Results: The majority of studies indicate a significantly lower prevalence of H. pylori infection among patients with IBD compared to the general population. Several meta-analyses support a potential protective effect, particularly in Crohn’s disease and among CagA-positive H. pylori strains. However, data on the impact of eradication therapy on IBD progression remain inconclusive. Some studies suggest a higher relapse risk post-eradication, while others report no change in disease activity. Variability in outcomes may be influenced by geographic, demographic, and methodological differences, as well as disease activity at the time of eradication. Conclusions: Although numerous studies support an inverse association between H. pylori infection and IBD, the nature and direction of this relationship remain unclear. Given the complex interplay between host immunity, gut microbiota, and antibiotic exposure, the decision to eradicate H. pylori in IBD patients should be individualized. Further prospective studies are needed to clarify the immunological and microbiological mechanisms underlying this association and to inform clinical guidelines.

1. Introduction

Helicobacter pylori (H. pylori) has co-evolved with humans for over 60,000 years [1] and was first successfully isolated from a gastric biopsy in 1983 by Marshall and Warren [2]. This spiral-shaped, microaerophilic, Gram-negative bacterium infects more than 50% of the global population [3]. Its prevalence correlates with advancing age and lower socioeconomic status, although substantial geographic and demographic variations exist [4]. Early-life conditions, particularly poor hygiene and overcrowding during childhood, are key risk factors for acquisition [5,6].
H. pylori is primarily transmitted via oral–oral and fecal–oral routes, with contaminated water also recognized as a potential source [7]. Infection typically occurs in childhood and, without treatment, persists throughout life [8].
Clinically, H. pylori is associated with a wide spectrum of gastrointestinal and extra-gastrointestinal diseases, including peptic ulcer disease, autoimmune gastritis, gastric malignancies such as MALT lymphoma and adenocarcinoma, and extra-digestive conditions like iron deficiency anemia, vitamin B12 deficiency, and idiopathic thrombocytopenic purpura (ITP) [9,10]. Several studies have also noted a higher prevalence of H. pylori in patients with autoimmune conditions such as Hashimoto’s thyroiditis, Graves’ disease, systemic lupus erythematosus, rheumatoid arthritis, and primary Sjögren’s syndrome [11].
Interestingly, some studies have reported an inverse association between H. pylori colonization and autoimmune diseases, particularly inflammatory bowel diseases (IBD) like Crohn’s disease (CD) and ulcerative colitis (UC), suggesting a possible protective role [12]. While the exact nature of this relationship is unclear, these findings highlight the need for further investigation into potential causality and the clinical relevance of H. pylori in autoimmune settings.
IBD is a chronic, relapsing-remitting inflammatory disorder of the gastrointestinal tract, encompassing CD, UC, and related entities [13]. Mucosal inflammation manifests with abdominal pain, diarrhea, rectal bleeding, and weight loss, driven by infiltration of neutrophils and macrophages that release pro-inflammatory mediators [13,14]. The pathogenesis involves a complex interplay of genetic predisposition, environmental triggers (e.g., Westernized diet, smoking, and antibiotic exposure), and immune dysregulation. IBD often includes extraintestinal manifestations such as arthritis, dermatologic disorders, and hepatobiliary involvement [15].
Since the mid-20th century, IBD incidence has increased globally, particularly in industrializing regions of Asia, Africa, and South America, despite stabilization in Western countries [16,17,18]. Prevalence rates are highest in Europe and North America [18], and the burden among the elderly is projected to rise by 2051, posing major public health challenges [19].
Crohn’s disease most often involves the terminal ileum, cecum, and colon in a discontinuous pattern, while ulcerative colitis affects the rectum and extends proximally in a continuous fashion [15,20,21]. CD shows transmural inflammation, fissuring ulcers, and granulomas, while UC is limited to mucosa and submucosa, with features such as cryptitis and crypt abscesses [15,21,22].
The coexistence of H. pylori infection and IBD raises important clinical questions. Epidemiological data consistently report lower H. pylori prevalence among IBD patients [23], possibly due to antibiotic use, immune dysregulation, or altered gut microbiota. However, the impact of H. pylori eradication on IBD remains unclear. Some studies suggest increased relapse risk, while others report no significant effect [23,24,25,26].
Despite ongoing research, the implications of H. pylori eradication in IBD are not yet fully understood. Some have proposed that eradication may act as an environmental trigger in genetically susceptible individuals, warranting caution in treatment decisions and highlighting the need for prospective controlled studies. This review explores the complexity of H. pylori infection in IBD patients, focusing on prevalence, clinical outcomes, and therapeutic challenges, with the aim of identifying gaps in current knowledge and guiding future research.

2. Materials and Methods

2.1. Information Source and Search Strategies

The aim of this review was to explore (1) the association between Helicobacter pylori (H. pylori) infection and inflammatory bowel disease (IBD); (2) the prevalence of H. pylori infection in patients with ulcerative colitis and Crohn’s disease; (3) the impact of H. pylori eradication therapy on the onset or exacerbation of IBD; and (4) the potential cause-and-effect relationship between these two chronic gastrointestinal conditions. A comprehensive literature search was conducted using the PubMed electronic database from inception to 25 May 2025. PubMed was selected due to its broad coverage of biomedical and clinical research, which aligns with the focus of this review. We acknowledge this as a limitation and note that additional databases, such as Scopus or Web of Science, may contain relevant publications not captured in our search. The search strategy included the use of Medical Subject Headings (MeSH) terms: “Helicobacter pylori,” “inflammatory bowel disease,” “eradication,” and “association.” Initially, all terms were combined using the Boolean operator “AND,” but due to limited results, alternative combinations were applied: “Helicobacter pylori” AND “inflammatory bowel disease” AND “eradication,” and “Helicobacter pylori” AND “inflammatory bowel disease” AND “association.” The reference lists of included studies were also manually screened for additional relevant articles.
Only publications in English and with free full-text access were included. Eligible study types encompassed clinical studies, clinical trials, controlled clinical trials, meta-analyses, multicenter studies, observational studies, randomized controlled trials, reviews, and systematic reviews involving both adult and pediatric populations, as well as animal studies when relevant. Studies were excluded if they met any of the following criteria: (1) primary endpoints not aligned with the aims of this review; (2) case reports, case series, commentaries, letters, preprints, or book chapters; (3) in vitro studies; (4) articles in languages other than English; or (5) publications without full-text availability. All included studies were critically reviewed. A detailed overview of the selected publications is provided in the Results section in tabular format.

2.2. Eligibility Criteria

Specific inclusion criteria involved human studies with adult and pediatric study populations and animal studies, too. Clinical studies, clinical trials, controlled clinical trials, meta-analyses, multicenter studies, observational studies, randomized controlled trials, reviews, and systematic reviews written in English with free full text availability are included in our review.
Exclusion criteria for this review were delineated as follows: (1) studies with primary endpoints not aligned with the scope of this review; (2) books and documents, letter, commentaries, preprint, case reports, and case series; (3) in vitro studies; (4) studies published in languages other than English; and (5) articles without full-text availability.

3. Results

Using MeSH terms “Helicobacter pylori” AND “inflammatory bowel disease” AND “eradication”, the article search identified twenty-six relevant full-text articles from the PubMed electronic database, of which sixteen articles met the full inclusion criteria [12,23,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41]. By searching the electronic database PubMed using MeSH terms “Helicobacter pylori” AND “inflammatory bowel disease” AND “association”, we have identified seventy-six full-text articles. After elimination of duplicate articles with the first search and identification of additional manuscripts, twenty-four studies that met the full inclusion criteria for this article were retrieved and fully reviewed [11,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65].
A total of 40 articles were selected for review, including 18 review articles, 9 meta-analyses, 4 systematic reviews, 1 umbrella review of meta-analyses, 2 bibliometric analyses, 3 multicenter studies, and 3 observational studies. The results are presented in Table 1, Table 2 and Table 3.
Table 1. List of studies/research on the topic of the association/eradication between H. pylori infection and inflammatory bowel diseases in adult study population.
Table 2. List of studies/research on the topic of the association/eradication between H. pylori infection and inflammatory bowel diseases in pediatric study population.
Table 3. List of studies/research on the topic of the association/eradication between H. pylori infection and inflammatory bowel diseases in pediatric and adult study populations.
Research into the relationship between Helicobacter pylori infection and inflammatory bowel disease (IBD) began to take shape around 2009 and has gained momentum over the years. Since then, interest in this topic has grown steadily, with a marked increase in studies exploring possible protective, immunological, and microbial mechanisms. Importantly, many of these studies are based on high levels of evidence, including numerous systematic reviews and meta-analyses. These consistently show a lower prevalence of H. pylori infection in IBD patients across various populations and settings. The fact that such findings are replicated across different study designs and regions strengthens the validity of this association. Together, the accumulated evidence points to a meaningful biological link that warrants further investigation.

4. Discussion

The coexistence of Helicobacter pylori infection and Inflammatory Bowel Disease (IBD) presents a unique set of challenges that complicate both diagnosis and management. While H. pylori is a recognized pathogen implicated in significant gastric morbidity, its relationship with IBD remains controversial. The lower prevalence of H. pylori in IBD patients, consistently reported across multiple studies, raises questions about potential protective roles or interactions between the bacterium and host immunity [11,12,23,31,33,34,35,37,38,39,43,44,46,47,48,49,50,51,52,55,56,57,58,59,60,61,62,63]. This phenomenon has been attributed to several factors, including extensive antibiotic use in IBD management, immune modulation associated with chronic inflammation, and dysbiosis of the gut microbiota. The frequent use of antibiotics, particularly broad-spectrum agents during IBD flares or for perioperative prophylaxis in Crohn’s disease, likely contributes to the observed lower colonization rates. However, this reduced prevalence may not uniformly translate into clinical benefit, as it introduces unique diagnostic and therapeutic challenges.
From a diagnostic perspective, the accuracy of non-invasive tests for H. pylori, such as the urea breath test (UBT) and stool antigen test, is diminished in IBD patients due to confounding factors such as active intestinal inflammation and the use of proton pump inhibitors (PPIs). These medications, commonly prescribed for upper GI symptoms in IBD patients, suppress bacterial load and gastric acidity, leading to false-negative test results. Endoscopic biopsy remains the gold standard for diagnosis, offering the opportunity for histological examination and culture, but the invasive nature of this procedure poses risks for IBD patients, particularly during active disease. Moreover, in patients with Crohn’s disease involving the upper GI tract, the differentiation between H. pylori-related gastritis and Crohn’s disease-associated gastroduodenitis adds an additional layer of complexity.
Therapeutically, H. pylori eradication in IBD patients necessitates a nuanced approach, balancing the benefits of eradication against the potential risks of exacerbating IBD symptoms. Therapy consisting of a PPI, clarithromycin, and amoxicillin achieves eradication rates of approximately 70–80% in the general population. However, rising rates of antibiotic resistance, particularly to clarithromycin and metronidazole, reduce the efficacy of these regimens in IBD patients, many of whom have been exposed to antibiotics for disease management [64]. Bismuth-containing quadruple therapy or regimens tailored based on antibiotic susceptibility testing may be required in these cases.
A critical concern in IBD patients undergoing H. pylori eradication therapy is the potential for antibiotic-induced gut microbiota disruption. Dysbiosis, a hallmark of IBD, may be exacerbated by the broad-spectrum antibiotics used in eradication therapy, leading to disease flares or worsening symptoms. Oral supplementation with a narrow spectrum of Gram-positive bacteria has shown clinical improvement in H. pylori-related symptoms, yet microbiota alterations may predispose individuals to intestinal or systemic diseases later in life. Emerging evidence suggests that using multi-strain probiotics or paraprobiotics, rather than single-strain formulations, may help reduce the incidence of metabolic disturbances associated with dysbiosis [65].
Considering the diverse effects of different bacterial strains, high-throughput sequencing technologies are essential for characterizing microbiota changes at the strain level and personalizing probiotic interventions. Furthermore, next-generation probiotics and genetically modified microorganisms are being explored to enhance clinical outcomes, either by restoring disease-specific bacterial taxa or by producing therapeutic compounds such as antimicrobial peptides. Innovations such as microencapsulation and nanotechnology are also being developed to optimize probiotic delivery and minimize adverse metabolic effects. These advances may offer promising adjuncts in managing H. pylori eradication in the context of IBD [66]. Additionally, PPIs, an essential component of H. pylori therapy, may interact with immunosuppressive agents such as azathioprine, methotrexate, or biologics, potentially altering their pharmacokinetics and efficacy. The impact of H. pylori eradication on IBD activity remains debated. Some articles suggest that H. pylori colonization may exert an immunomodulatory effect by reducing pro-inflammatory cytokine production and promoting regulatory T-cell activity [67,68]. Consequently, eradication might remove this protective mechanism and exacerbate IBD symptoms. Conversely, H. pylori may aggravate upper GI symptoms in IBD patients, including dyspepsia or gastric ulceration, thereby impairing quality of life and complicating disease management.
In light of these complexities, a tailored approach to managing H. pylori infection in IBD patients is essential. Routine screening may not be justified in asymptomatic individuals, but targeted testing should be performed in patients with upper GI symptoms, a history of peptic ulcer disease, or those requiring long-term PPI use. Whenever possible, eradication therapy should be timed during IBD remission to minimize the risk of flares. A multidisciplinary approach involving gastroenterologists, microbiologists, and clinical pharmacologists is recommended to optimize outcomes and mitigate risks.
Future research should focus on the long-term impact of H. pylori eradication on IBD progression, microbiota composition, and patient quality of life. Large-scale studies using germ-free mice colonized with human microbiota, and clinical trials combining broad-spectrum antibiotic regimens with targeted probiotic interventions, are needed to better understand the role of microbiome modulation in this population. The integration of novel diagnostic tools and personalized medicine strategies holds the potential to transform the management of H. pylori in the context of IBD and improve clinical outcomes for this unique patient group.
A limitation of this review is the exclusive reliance on the PubMed database for literature retrieval, without inclusion of other major electronic databases such as Web of Science, Scopus, and Cochrane, which may have resulted in the omission of pertinent studies. This limitation underscores the need for future high-quality systematic reviews or meta-analyses based on comprehensive multi-database searches and standardized methodological frameworks to ensure a more exhaustive evaluation of the available evidence.

5. Conclusions

While Helicobacter pylori eradication offers clear oncological benefits—most notably in the prevention of gastric cancer—it presents distinct challenges in patients with IBD. A key concern is the potential to trigger de novo IBD or exacerbate existing disease following eradication therapy. Although observational studies suggest a possible association, the causal mechanisms remain poorly defined. Current international guidelines lack specific recommendations for H. pylori management in IBD patients, underscoring a notable gap in clinical guidance. An often overlooked factor is the disease stage at the time of eradication. Patients in remission may respond differently to microbiota-altering antibiotics than those with active inflammation. The degree of mucosal integrity, immune activity, and dysbiosis likely influences outcomes, making timing critical. Similarly, a patient’s immunosuppressive regimen, prior eradication attempts, and antibiotic resistance patterns may affect therapeutic response and recurrence risk. These factors emphasize the need for an individualized, patient-centered approach rather than standardized treatment strategies. Future studies should stratify patients by disease activity, phenotype, immunosuppressive therapy, and eradication history. Prospective trials with validated clinical, endoscopic, and biochemical endpoints are essential to optimize treatment decisions. In countries with population-wide H. pylori screening, guidelines must incorporate considerations specific to IBD—particularly immunological and microbiome-related risks. Clinicians need tools to distinguish true IBD flares from expected post-eradication changes, and decisions to withhold or delay therapy should be based on individualized risk–benefit assessments. Ultimately, managing H. pylori in IBD requires a multidisciplinary perspective—integrating gastroenterology, microbiology, and immunology—to support evidence-based, personalized care. This evolving field offers important opportunities to improve patient outcomes and deepen our understanding of host–microbiome interactions in immune-mediated disease.

6. Future Directions

Future research should aim to clarify the causal mechanisms underlying the inverse association between Helicobacter pylori infection and inflammatory bowel disease, with particular focus on the immunological and microbiome-related pathways involved. It remains important to determine whether the observed relationship reflects a true biological interaction or is influenced by confounding factors such as antibiotic use, disease severity, or treatment history. Further investigation into the role of specific H. pylori strains, host genetics, and environmental exposures could provide deeper insight into the variability seen among patients. Additionally, studies assessing the impact of H. pylori eradication on IBD activity, therapeutic response, and gut microbial balance will be essential for informed clinical management. Incorporating microbiome analysis, immune profiling, and precision medicine strategies may help identify patient subgroups that could benefit from personalized approaches. A clearer understanding of this complex interplay could ultimately refine both diagnostic and therapeutic practices in IBD care.

Author Contributions

Conceptualization, methodology, formal analysis, resources, writing—original draft preparation, writing—review and editing, J.V. and I.J. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

References

  1. Moodley, Y.; Linz, B.; Bond, R.P.; Nieuwoudt, M.; Soodyall, H.; Schlebusch, C.M.; Bernhöft, S.; Hale, J.; Suerbaum, S.; Mugisha, L.; et al. Age of the association between Helicobacter pylori and man. PLoS Pathog. 2012, 8, e1002693. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  2. Warren, J.R.; Marshall, B. Unidentified curved bacilli on gastric epithelium in active chronic gastritis. Lancet 1983, 1, 1273–1275. [Google Scholar] [CrossRef] [PubMed]
  3. Hooi, J.K.Y.; Lai, W.Y.; Ng, W.K.; Suen, M.M.Y.; Underwood, F.E.; Tanyingoh, D.; Malfertheiner, P.; Graham, D.Y.; Wong, V.W.S.; Wu, J.C.Y.; et al. Global Prevalence of Helicobacter pylori Infection: Systematic Review and Meta-Analysis. Gastroenterology 2017, 153, 420–429. [Google Scholar] [CrossRef] [PubMed]
  4. Azevedo, N.F.; Huntington, J.; Goodman, K.J. The epidemiology of Helicobacter pylori and public health implications. Helicobacter 2009, 14 (Suppl. S1), 1–7. [Google Scholar] [CrossRef] [PubMed]
  5. Eusebi, L.H.; Zagari, R.M.; Bazzoli, F. Epidemiology of Helicobacter pylori infection. Helicobacter 2014, 19 (Suppl. S1), 1–5. [Google Scholar] [CrossRef] [PubMed]
  6. Nguyen, J.; Kotilea, K.; Bontems, P.; Miendje Deyi, V.Y. Helicobacter pylori Infections in Children. Antibiotics 2023, 12, 1440. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  7. Brown, L.M. Helicobacter pylori: Epidemiology and routes of transmission. Epidemiol. Rev. 2000, 22, 283–297. [Google Scholar] [CrossRef] [PubMed]
  8. Wroblewski, L.E.; Peek, R.M., Jr. Helicobacter pylori: A stealth assassin. Trends Cancer 2021, 7, 807–808. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  9. Wong, F.; Rayner-Hartley, E.; Byrne, M.F. Extraintestinal manifestations of Helicobacter pylori: A concise review. World J. Gastroenterol. 2014, 20, 11950–11961. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  10. Malfertheiner, P.; Megraud, F.; O’Morain, C.A.; Atherton, J.; Axon, A.T.; Bazzoli, F.; Gensini, G.F.; Gisbert, J.P.; Graham, D.Y.; Rokkas, T.; et al. European Helicobacter Study Group. Management of Helicobacter pylori infection—The Maastricht IV/ Florence Consensus Report. Gut 2012, 61, 646–664. [Google Scholar] [CrossRef] [PubMed]
  11. Wang, L.; Cao, Z.M.; Zhang, L.L.; Dai, X.C.; Liu, Z.J.; Zeng, Y.; Li, X.Y.; Wu, Q.J.; Lv, W.L. Helicobacter Pylori and Autoimmune Diseases: Involving Multiple Systems. Front. Immunol. 2022, 13, 833424. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  12. Luther, J.; Dave, M.; Higgins, P.D.; Kao, J.Y. Association between Helicobacter pylori infection and inflammatory bowel disease: A meta-analysis and systematic review of the literature. Inflamm. Bowel Dis. 2010, 16, 1077–1084. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  13. Szigethy, E.; McLafferty, L.; Goyal, A. Inflammatory bowel disease. Child Adolesc. Psychiatr. Clin. N. Am. 2010, 19, 301–318. [Google Scholar] [CrossRef] [PubMed]
  14. Stokkers, P.C.; Hommes, D.W. New cytokine therapeutics for inflammatory bowel disease. Cytokine 2004, 28, 167–173. [Google Scholar] [CrossRef] [PubMed]
  15. Khor, B.; Gardet, A.; Xavier, R.J. Genetics and pathogenesis of inflammatory bowel disease. Nature 2011, 474, 307–317. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  16. Korzenik, J.R.; Podolsky, D.K. Evolving knowledge and therapy of inflammatory bowel disease. Nat. Rev. Drug Discov. 2006, 5, 197–209. [Google Scholar] [CrossRef] [PubMed]
  17. Hanauer, S.B. Inflammatory bowel disease: Epidemiology, pathogenesis, and therapeutic opportunities. Inflamm. Bowel Dis. 2006, 12 (Suppl. S1), S3–S9. [Google Scholar] [CrossRef] [PubMed]
  18. Ng, S.C.; Shi, H.Y.; Hamidi, N.; Underwood, F.E.; Tang, W.; Benchimol, E.I.; Panaccione, R.; Ghosh, S.; Wu, J.C.Y.; Chan, F.K.L.; et al. Worldwide incidence and prevalence of inflammatory bowel disease in the 21st century: A systematic review of population-based studies. Lancet 2017, 390, 2769–2778. [Google Scholar] [CrossRef] [PubMed]
  19. Liu, Y.; Li, J.; Yang, G.; Meng, D.; Long, X.; Wang, K. Global burden of inflammatory bowel disease in the elderly: Trends from 1990 to 2021 and projections to 2051. Front. Aging 2024, 5, 1479928. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  20. Yamamoto, S.; Ma, X. Role of Nod2 in the development of Crohn’s disease. Microbes Infect. 2009, 11, 912–918. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  21. Abraham, C.; Cho, J.H.; Cho, J.H. Inflammatory bowel disease. N. Engl. J. Med. 2009, 361, 2066–2078. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  22. Gajendran, M.; Loganathan, P.; Catinella, A.P.; Hashash, J.G. A comprehensive review and update on Crohn’s disease. Dis. Mon. 2018, 64, 20–57. [Google Scholar] [CrossRef] [PubMed]
  23. Zhong, Y.; Zhang, Z.; Lin, Y.; Wu, L. The Relationship Between Helicobacter Pylori and Inflammatory Bowel Disease. Arch. Iran. Med. 2021, 24, 317–325. [Google Scholar] [CrossRef] [PubMed]
  24. Rosania, R.; Von Arnim, U.; Link, A.; Rajilic-Stojanovic, M.; Franck, C.; Canbay, A.; Malfertheiner, P.; Venerito, M. Helicobacter Pylori Eradication Therapy Is Not Associated with the Onset of Inflammatory Bowel Diseases. A Case-Control Study. J. Gastrointestin Liver Dis. 2018, 27, 119–125. [Google Scholar] [CrossRef] [PubMed]
  25. Shinzaki, S.; Fujii, T.; Bamba, S.; Ogawa, M.; Kobayashi, T.; Oshita, M.; Tanaka, H.; Ozeki, K.; Takahashi, S.; Kitamoto, H.; et al. Seven Days Triple Therapy for Eradication of Helicobacter Pylori Does Not Alter the Disease Activity of Patients with Inflammatory Bowel Disease. Intest. Res. 2018, 16, 609–618. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  26. Lahat, A.; Kopylov, U.; Neuman, S.; Levhar, N.; Yablecovitch, D.; Avidan, B.; Weiss, B.; Ben-Horin, S.; Eliakim, R.; on behalf of the Israeli IBD research Network (IIRN). Helicobacter Pylori Prevalence and Clinical Significance in Patients with Quiescent Crohn’s Disease. BMC Gastroenterol. 2017, 17, 27. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  27. Gravina, A.G.; Pellegrino, R.; Iascone, V.; Palladino, G.; Federico, A.; Zagari, R.M. Impact of Helicobacter pylori Eradication on Inflammatory Bowel Disease Onset and Disease Activity: To Eradicate or Not to Eradicate? Diseases 2024, 12, 179. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  28. Dilaghi, E.; Felici, E.; Lahner, E.; Pilozzi, E.; Furio, S.; Lucchini, L.; Quatrale, G.; Piccirillo, M.; Parisi, P.; Curto, S.; et al. Helicobacter Pylori infection in children with inflammatory bowel disease: A prospective multicenter study. BMC Pediatr. 2024, 24, 417. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  29. Kotilea, K.; Romano, C.; Miele, E.; Kindermann, A.; Dolstra, Y.; Misak, Z.; Urbonas, V.; Sykora, J.; Urruzuno, P.; Krauthammer, A.; et al. ESPGHAN H. pylori special interest group. Helicobacter pylori infection found during upper endoscopy performed for the diagnosis of celiac, inflammatory bowel diseases, and eosinophilic esophagitis: A multicenter pediatric European study. Helicobacter 2024, 29, e13092. [Google Scholar] [CrossRef] [PubMed]
  30. Bretto, E.; Frara, S.; Armandi, A.; Caviglia, G.P.; Saracco, G.M.; Bugianesi, E.; Pitoni, D.; Ribaldone, D.G. Helicobacter pylori in Inflammatory Bowel Diseases: Active Protagonist or Innocent Bystander? Antibiotics 2024, 13, 267. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  31. Ravikumara, M. Helicobacter pylori in children: Think before you kill the bug! Therap. Adv. Gastroenterol. 2023, 16, 17562848231177610. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  32. Murad, H.; Rafeeq, M.; Mosli, M.; Gari, M.; Basheikh, M. Effect of sequential eradication therapy on serum osteoprotegerin levels in patients with Helicobacter pylori infection and co-existing inflammatory bowel disease. J. Int. Med. Res. 2021, 49, 3000605211060648. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  33. Reshetnyak, V.I.; Burmistrov, A.I.; Maev, I.V. Helicobacter pylori: Commensal, symbiont or pathogen? World J. Gastroenterol. 2021, 27, 545–560. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  34. Aguilera Matos, I.; Diaz Oliva, S.E.; Escobedo, A.A.; Villa Jiménez, O.M.; Velazco Villaurrutia, Y.D.C. Helicobacter pylori infection in children. BMJ Paediatr. Open. 2020, 4, e000679. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  35. Yu, Y.; Zhu, S.; Li, P.; Min, L.; Zhang, S. Helicobacter pylori infection and inflammatory bowel disease: A crosstalk between upper and lower digestive tract. Cell Death Dis. 2018, 9, 961. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  36. Murad, H.A. Does Helicobacter pylori eradication therapy trigger or protect against Crohn’s disease? Acta Gastroenterol. Belg. 2016, 79, 349–354. [Google Scholar] [PubMed]
  37. Arnold, I.C.; Müller, A. Helicobacter pylori: Does Gastritis Prevent Colitis? Inflamm. Intest. Dis. 2016, 1, 102–112. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  38. Robinson, K. Helicobacter pylori-Mediated Protection against Extra-Gastric Immune and Inflammatory Disorders: The Evidence and Controversies. Diseases 2015, 3, 34–55. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  39. Ierardi, E.; Goni, E.; Losurdo, G.; Di Mario, F. Helicobacter pylori and nonmalignant diseases. Helicobacter 2014, 19 (Suppl. S1), 27–31. [Google Scholar] [CrossRef] [PubMed]
  40. Wang, Z.; Zhao, S.; Zhong, X.; Su, Y.; Song, Y.; Li, J.; Shi, Y. Debate on the relationship between Helicobacter pylori infection and inflammatory bowel disease: A bibliometric analysis. Front. Microbiol. 2024, 15, 1479941. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  41. Li, Y.; Li, L.; Yin, W.; Wan, J.; Zhong, X. Bibliometric analysis of the correlation between H. pylori and inflammatory bowel disease. JGH Open 2024, 8, e70014. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  42. Kong, G.; Liu, Z.; Lu, Y.; Li, M.; Guo, H. The association between Helicobacter pylori infection and inflammatory bowel disease in children: A systematic review with meta-analysis. Medicine 2023, 102, e34882. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  43. Feilstrecker Balani, G.; Dos Santos Cortez, M.; Picasky da Silveira Freitas, J.E.; Freire de Melo, F.; Zarpelon-Schutz, A.C.; Teixeira, K.N. Immune response modulation in inflammatory bowel diseases by Helicobacter pylori infection. World J. Gastroenterol. 2023, 29, 4604–4615. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  44. He, J.; Liu, Y.; Ouyang, Q.; Li, R.; Li, J.; Chen, W.; Hu, W.; He, L.; Bao, Q.; Li, P.; et al. Helicobacter pylori and unignorable extragastric diseases: Mechanism and implications. Front. Microbiol. 2022, 13, 972777. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  45. Abd El-Wahab, E.W.; Youssef, E.I.; Hassouna, E. Helicobacter pylori infection in patients with inflammatory bowel diseases: A single-centre, prospective, observational study in Egypt. BMJ Open 2022, 12, e057214. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  46. Axelrad, J.E.; Cadwell, K.H.; Colombel, J.F.; Shah, S.C. The role of gastrointestinal pathogens in inflammatory bowel disease: A systematic review. Therap. Adv. Gastroenterol. 2021, 14, 17562848211004493. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  47. Gravina, A.G.; Priadko, K.; Ciamarra, P.; Granata, L.; Facchiano, A.; Miranda, A.; Dallio, M.; Federico, A.; Romano, M. Extra-Gastric Manifestations of Helicobacter pylori Infection. J. Clin. Med. 2020, 9, 3887. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  48. Santos, M.L.C.; de Brito, B.B.; da Silva, F.A.F.; Sampaio, M.M.; Marques, H.S.; Oliveira E Silva, N.; de Magalhães Queiroz, D.M.; de Melo, F.F. Helicobacter pylori infection: Beyond gastric manifestations. World. J. Gastroenterol. 2020, 26, 4076–4093. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  49. Axelrad, J.E.; Cadwell, K.H.; Colombel, J.F.; Shah, S.C. Systematic review: Gastrointestinal infection and incident inflammatory bowel disease. Aliment. Pharmacol. Ther. 2020, 51, 1222–1232. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  50. Tepler, A.; Narula, N.; Peek, R.M., Jr.; Patel, A.; Edelson, C.; Colombel, J.F.; Shah, S.C. Systematic review with meta-analysis: Association between Helicobacter pylori CagA seropositivity and odds of inflammatory bowel disease. Aliment. Pharmacol. Ther. 2019, 50, 121–131. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  51. Wang, W.L.; Xu, X.J. Correlation Between Helicobacter Pylori Infection and Crohn’s Disease: A Meta-Analysis. Eur. Rev. Med. Pharmacol. Sci. 2019, 23, 10509–10516. [Google Scholar] [CrossRef] [PubMed]
  52. Kayali, S.; Gaiani, F.; Manfredi, M.; Minelli, R.; Nervi, G.; Nouvenne, A.; Leandro, G.; Di Mario, F.; De’ Angelis, G.L. Inverse association between Helicobacter pylori and inflammatory bowel disease: Myth or fact? Acta Biomed. 2018, 89, 81–86. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  53. Yu, Q.; Zhang, S.; Li, L.; Xiong, L.; Chao, K.; Zhong, B.; Li, Y.; Wang, H.; Chen, M. Enterohepatic Helicobacter Species as a Potential Causative Factor in Inflammatory Bowel Disease: A Meta-Analysis. Medicine 2015, 94, e1773. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  54. Papamichael, K.; Konstantopoulos, P.; Mantzaris, G.J. Helicobacter pylori infection and inflammatory bowel disease: Is there a link? World J. Gastroenterol. 2014, 20, 6374–6385. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  55. Owyang, S.Y.; Luther, J.; Owyang, C.C.; Zhang, M.; Kao, J.Y. Helicobacter pylori DNA’s anti-inflammatory effect on experimental colitis. Gut Microbes 2012, 3, 168–171. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  56. Song, M.J.; Park, D.I.; Hwang, S.J.; Kim, E.R.; Kim, Y.H.; Jang, B.I.; Lee, S.H.; Ji, J.S.; Shin, S.J. The prevalence of Helicobacter pylori infection in Korean patients with inflammatory bowel disease, a multicenter study. Korean J. Gastroenterol. 2009, 53, 341–347. [Google Scholar] [CrossRef] [PubMed]
  57. Xiang, Z.; Chen, Y.P.; Ye, Y.F.; Ma, K.F.; Chen, S.H.; Zheng, L.; Yang, Y.D.; Jin, X. Helicobacter pylori and Crohn’s disease: A retrospective single-center study from China. World J. Gastroenterol. 2013, 19, 4576–4581. [Google Scholar] [CrossRef] [PubMed]
  58. Imawana, R.A.; Smith, D.R.; Goodson, M.L. The relationship between inflammatory bowel disease and Helicobacter pylori across East Asian, European and Mediterranean countries: A meta-analysis. Ann. Gastroenterol. 2020, 33, 485–494. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  59. Pellicano, R.; Ianiro, G.; Fagoonee, S.; Settanni, C.R.; Gasbarrini, A. Review: Extragastric diseases and Helicobacter pylori. Helicobacter 2020, 25 (Suppl. S1), e12741. [Google Scholar] [CrossRef] [PubMed]
  60. Wu, X.-W.; Ji, H.-Z.; Yang, M.-F.; Wu, L.; Wang, F.Y. Helicobacter pylori infection and inflammatory bowel disease in Asians: A meta-analysis. World J. Gastroenterol. 2015, 21, 4750–4756. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  61. Rokkas, T.; Gisbert, J.P.; Niv, Y.; O’Morain, C. The association between Helicobacter pylori infection and inflammatory bowel disease based on meta-analysis. United Eur. Gastroenterol. J. 2015, 3, 539–550. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  62. Castaño-Rodríguez, N.; Kaakoush, N.O.; Lee, W.S.; Mitchell, H.M. Dual role of Helicobacter and Campylobacter species in IBD: A systematic review and meta-analysis. Gut 2017, 66, 235–249. [Google Scholar] [CrossRef] [PubMed]
  63. Piovani, D.; Danese, S.; Peyrin-Biroulet, L.; Nikolopoulos, G.K.; Lytras, T.; Bonovas, S. Environmental Risk Factors for Inflammatory Bowel Diseases: An Umbrella Review of Meta-analyses. Gastroenterology 2019, 157, 647–659.e4. [Google Scholar] [CrossRef] [PubMed]
  64. Matsumoto, H.; Shiotani, A.; Graham, D.Y. Current and Future Treatment of Helicobacter Pylori Infections. Adv. Exp. Med. Biol. 2019, 1149, 211–225. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  65. Nabavi-Rad, A.; Sadeghi, A.; Asadzadeh Aghdaei, H.; Yadegar, A.; Smith, S.M.; Zali, M.R. The double-edged sword of probiotic supplementation on gut microbiota structure in Helicobacter pylori management. Gut Microbes 2022, 14, 2108655. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  66. Aijun, X.; Mengge, G.; Haishun, D.; Xuejun, P. Next-generation probiotics delivery: Innovations and applications of single-cell encapsulation. Curr. Opin. Food Sci. 2024, 61, 101234. [Google Scholar] [CrossRef]
  67. Bartels, L.E.; Dahlerup, J.F. Association of Helicobacter pylori and Crohn’s Disease Incidence: An Inversion Reaction? Dig. Dis. Sci. 2017, 62, 2217–2219. [Google Scholar] [CrossRef] [PubMed]
  68. Alotaibi, A.D.; Al-Abdulwahab, A.A.; Ismail, M.H.; AlElyani, J.M.; Alamri, T.A.; Alsulaiman, R.M.; Alhafid, I.A.; Alzahrani, I.M.; AlSulaiman, R.S.; Althubaity, A.; et al. Prevalence of H. Pylori in inflammatory bowel disease patients and its association with severity. BMC Gastroenterol. 2025, 25, 317. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Article Metrics

Citations

Article Access Statistics

Journal Statistics
Multiple requests from the same IP address are counted as one view.
Download PDF
Perioperative Myocardial Injury and Acute Kidney Injury in Patients Undergoing Hepatic Resection: Incidence, Risk Factors, and Effects on Outcomes
Previous
Investigation of the Medium- and Long-Term Results of a Pioneering Method in the Treatment of Geriatric Intertrochanteric Femur Fractures: Osteosynthesis Using the WALANT Technique
Next