Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (912 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Inflammation of the duodenum section of the small intestine (intestine, small). Erosive duodenitis may cause bleeding in the upper GI tract and peptic ulcer.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Erosive Duodenitis; Duodenitis, Erosive.
Where it fits in the MeSH classification
- Broader topics
- Enteritis; Duodenal Diseases
Related concepts
- Duodenum
- Intestines
- Small
- Upper
- Tract
- Peptic Ulcer
Research landscape
PubMed indexes 1,668 records tagged with the MeSH heading “Duodenitis” (counts retrieved 2026-11-04). 96 of them (5.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,099 records.
Reviews account for 132 records (7.9%) and meta-analyses for 0. Randomized controlled trials number 34 (2.0%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,099 |
| 2000-2009 | 235 |
| 2010-2019 | 238 |
| 2020 onward | 96 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 132 | 7.9% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 34 | 2.0% |
Method: PubMed query "Duodenitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in digestive system and liver
Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The global, regional, and national patterns of change in the burden of nonmalignant upper gastrointestinal diseases from 1990 to 2019 and the forecast for the next decade | 2025 | Research article Design not recorded in structured metadata | 91 | cc by PMID 38959095 · DOI · PMC11745775 |
| Immune checkpoint inhibitor-associated celiac disease | 2020 | Research article Design not recorded in structured metadata | 55 | cc by PMID 32581063 · DOI · PMC7319774 |
| Dupilumab Can Induce Remission of Eosinophilic Gastritis and Duodenitis: A Retrospective Case Series | 2024 | Research article Design not recorded in structured metadata | 23 | cc by PMID 37753954 · DOI · PMC10811686 |
The global, regional, and national patterns of change in the burden of nonmalignant upper gastrointestinal diseases from 1990 to 2019 and the forecast for the next decade [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundNonmalignant upper gastrointestinal diseases, including peptic ulcer disease (PUD), gastritis and duodenitis (GD), and gastroesophageal reflux disease (GERD), significantly challenge global healthcare.
- Closing excerpt
- This targeted approach is essential for effectively mitigating the disease burden.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (320 words)
BackgroundNonmalignant upper gastrointestinal diseases, including peptic ulcer disease (PUD), gastritis and duodenitis (GD), and gastroesophageal reflux disease (GERD), significantly challenge global healthcare. These conditions not only impact patient health but also highlight socioeconomic development issues and healthcare system accessibility and efficiency. Utilizing the Global Burden of Disease database, this study aims to comprehensively assess the global burden of PUD, GD, and GERD, examining their association with the sociodemographic index (SDI).MethodsEmploying data from the Global Burden of Disease 2019 database, this study analyzed the disability-adjusted life years for PUD, GD, and GERD. We integrated the SDI with the inequality slope index and concentration index for an international health inequality analysis, assessing disparities in the burden of these nonmalignant upper gastrointestinal diseases. Decomposition analysis was conducted to determine the effects of population growth, aging, and epidemiological change on disease burden. Frontier analysis was performed to identify potential improvement areas and disparities among countries by development status. Disease time trends were depicted using a Joinpoint regression model, and the Bayesian age-period-cohort model projected the disease burden up to 2030.ResultsBetween 1990 and 2019, the age-standardized disability-adjusted life years rates for nonmalignant upper gastrointestinal diseases declined. However, global geographic heterogeneity remained evident and closely linked to the SDI. Notably, low-SDI countries experienced higher disease burdens. Population growth and aging emerged as principal contributors to the increasing disease burden. Despite development levels, many countries have considerable potential for reducing the burden of these diseases. Furthermore, significant variations in the time trends of nonmalignant upper gastrointestinal diseases were observed among countries and regions with different SDI levels, a pattern expected to continue through 2030.ConclusionNonmalignant upper gastrointestinal diseases demonstrate notable heterogeneity across age, sex, and geography, with the disparities most marked in underdeveloped regions or countries. Consequently, it is imperative to focus research on policy development and to enact prevention and treatment strategies tailored to high-risk groups. This targeted approach is essential for effectively mitigating the disease burden.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 38959095 · DOI · PMC11745775
Immune checkpoint inhibitor-associated celiac disease [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundRare cases of immune checkpoint inhibitor (ICI)-associated celiac disease (ICI-CeD) have been reported, suggesting that disruption of tolerance mechanisms by ICIs can unmask celiac disease (CeD).
- Closing excerpt
- We conclude that ICI-CeD is biologically similar to ICI-Duo and is likely a variant of ICI-Duo, but treatment strategies differ, with ICI-CeD often improving with GFD alone, whereas ICI-Duo requires systemic immunosuppression.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (345 words)
BackgroundRare cases of immune checkpoint inhibitor (ICI)-associated celiac disease (ICI-CeD) have been reported, suggesting that disruption of tolerance mechanisms by ICIs can unmask celiac disease (CeD). This study aims to characterize the clinicopathological and immunophenotypic features of ICI-CeD in comparison to ICI-associated duodenitis (ICI-Duo) and usual CeD.MethodsA medical and pathological records search between 2015 and 2019 identified eight cases of ICI-CeD, confirmed by tTG-IgA. Nine cases of ICI-Duo, 28 cases of moderate CeD, as well as 5 normal controls were used as comparison groups. Clinical information was collected from the electronic medical records. Immunohistochemistry for CD3, CD8, T-cell receptor gamma/delta (γδ), programmed death ligand 1 (PD-L1), and programmed death 1 (PD-1) were performed, with quantification of intraepithelial lymphocyte (IEL) subsets in three well-oriented villi. CD68, PD-L1, and PD-1 were assessed as a percentage of lamina propria surface area infiltrated by positive cells. Statistical significance was calculated by the Student's t-test and Fisher's exact test.ResultsThe eight patients with ICI-CeD (F:M=1:3) and nine patients with ICI-Duo (F:M=5:4) presented similarly with diarrhea (13/17) and abdominal pain (11/17) after a median of 1.6 months on ICI therapy. In patients with ICI-CeD, tTG-IgA ranged from 104 to >300 IU/mL. Histological findings in ICI-CeD and ICI-Duo were similar and included expansion of the lamina propria, active neutrophilic duodenitis, variably increased IELs, and villous blunting. Immunohistochemistry showed that the average number of IELs per 100 enterocytes is comparable between ICI-CeD and ICI-Duo, with increased CD3+ CD8+ T cells compared with normal duodenum but decreased γδ T cells compared with CeD. Average PD-L1 percentage was 9% in ICI-CeD and 18% in ICI-Duo, in comparison to ConclusionsICI-CeD resembles ICI-Duo clinically and histologically but shares the serological features and response to gluten withdrawal with classic CeD. Immunophenotyping of IELs in ICI-CeD and ICI-Duo also shows similar CD3, CD8, γδ T cell subsets, and PD-L1 populations, all of which differed quantitatively from usual CeD. We conclude that ICI-CeD is biologically similar to ICI-Duo and is likely a variant of ICI-Duo, but treatment strategies differ, with ICI-CeD often improving with GFD alone, whereas ICI-Duo requires systemic immunosuppression.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32581063 · DOI · PMC7319774
Dupilumab Can Induce Remission of Eosinophilic Gastritis and Duodenitis: A Retrospective Case Series [3]
Abstract reading summary — source excerpts
- Opening excerpt
- IntroductionNoneosinophilic esophagitis eosinophilic gastrointestinal disorders (non-EoE-EGIDs) have limited treatment options to induce histologic and clinical remission.
- Closing excerpt
- DiscussionIn this retrospective case series, we showed preliminary evidence that dupilumab may be effective in inducing histologic and symptomatic remission in patients with non-EoE-EGIDs.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (247 words)
IntroductionNoneosinophilic esophagitis eosinophilic gastrointestinal disorders (non-EoE-EGIDs) have limited treatment options to induce histologic and clinical remission. Dupilumab is a human monoclonal antibody against the interleukin-4 receptor ɑ subunit, which has been reported to induce improvement in pediatric patients with non-EoE-EGIDs.MethodsWe conducted a retrospective chart review to identify if patients with eosinophilic gastritis (EoG) and/or eosinophilic duodenitis (EoD) experience clinical and histologic remission with dupilumab.ResultsTwelve patients were included (2 patients with EoG and EoD, 3 patients with EoG only, and 7 patients with EoD only). All patients experienced improvement of at least 1 symptom on dupilumab, 3 patients (25%) had no change in severity of 1 or more of their symptoms, and no patients had worsening symptoms. On dupilumab, 2 patients with EoG (40%) and 3 patients with EoD (33.3%) were completely asymptomatic. Histologic changes were investigated in a subanalysis including 8 patients (2 patients with EoG and EoD, 2 patients with EoG only, and 4 patients with EoD only). Median peak gastric eosinophil counts in patients with EoG reduced from 80.5 eos/hpf (min-max 32-150, Q1-Q3 45.5-111) to 7.5 eos/hpf (min-max 0-28, Q1-Q3 1.5-16.8). Median peak duodenal eosinophil counts in patients with EoD reduced from 39 eos/hpf (min-max 30-50, Q1-Q3 37.3-46.3) to 16.5 eos/hpf (min-max 0-50, Q1-Q3 8-38.5). All 4 patients (100%) with EoG and 4 patients (66.6%) with EoD had histologic remission on dupilumab.DiscussionIn this retrospective case series, we showed preliminary evidence that dupilumab may be effective in inducing histologic and symptomatic remission in patients with non-EoE-EGIDs.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37753954 · DOI · PMC10811686
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Kyoto global consensus report on Helicobacter pylori gastritis [4]
- Research article Helicobacter pylori and the pathogenesis of gastroduodenal inflammation [5]
- Research article Helicobacter pylori and gastroduodenal disease [6]
- Research article The Sydney System: endoscopic division. Endoscopic appearances in gastritis/duodenitis [7]
- Research article Duodenal ulcer, Campylobacter pylori, and the "leaking roof" concept [8]
- Research article Duodenal inflammation: an emerging target for functional dyspepsia? [9]
References
- Bai Z, Wang H, Shen C, An J, Yang Z, Mo X. The global, regional, and national patterns of change in the burden of nonmalignant upper gastrointestinal diseases from 1990 to 2019 and the forecast for the next decade. . 2025. PMID 38959095 · DOI · PMC11745775
- Badran YR, Shih A, Leet D, Mooradian MJ, Coromilas A, Chen J, et al.. Immune checkpoint inhibitor-associated celiac disease. . 2020. PMID 32581063 · DOI · PMC7319774
- Sia T, Bacchus L, Tanaka R, Khuda R, Mallik S, Leung J. Dupilumab Can Induce Remission of Eosinophilic Gastritis and Duodenitis: A Retrospective Case Series. . 2024. PMID 37753954 · DOI · PMC10811686
- Sugano K, Tack J, Kuipers EJ, Graham DY, El-Omar EM, Miura S, et al.. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015. PMID 26187502 · DOI · PMC4552923
- Blaser MJ. Helicobacter pylori and the pathogenesis of gastroduodenal inflammation. J Infect Dis. 1990. PMID 2181029 · DOI
- Cover TL, Blaser MJ. Helicobacter pylori and gastroduodenal disease. Annu Rev Med. 1992. PMID 1580578 · DOI
- Tytgat GN. The Sydney System: endoscopic division. Endoscopic appearances in gastritis/duodenitis. J Gastroenterol Hepatol. 1991. PMID 1912432 · DOI
- Goodwin CS. Duodenal ulcer, Campylobacter pylori, and the "leaking roof" concept. Lancet. 1988. PMID 2904580 · DOI
- Wauters L, Burns G, Ceulemans M, Walker MM, Vanuytsel T, Keely S, et al.. Duodenal inflammation: an emerging target for functional dyspepsia?. Expert Opin Ther Targets. 2020. PMID 32249629 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.