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Celiac Disease

Digestive System and Liver · NLM MeSH · updated 2026-11-04 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 5 min read

A malabsorption syndrome that is precipitated by the ingestion of foods containing gluten, such as wheat, rye, and barley.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. Full-text reviews7. References8. About this article

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: 4 complete abstracts (868 words), 10 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

A malabsorption syndrome that is precipitated by the ingestion of foods containing gluten, such as wheat, rye, and barley. It is characterized by inflammation of the small intestine, loss of microvilli structure, failed intestinal absorption, and malnutrition.

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: Disease, Celiac; Gluten Enteropathy; Enteropathies, Gluten; Enteropathy, Gluten; Gluten Enteropathies; Gluten-Sensitive Enteropathy; Enteropathies, Gluten-Sensitive; Enteropathy, Gluten-Sensitive.

Where it fits in the MeSH classification

Broader topics
Malabsorption Syndromes
See also
Sprue, Tropical; Wheat Hypersensitivity; Enteropathy-Associated T-Cell Lymphoma

Related concepts

  • Gluten
  • Inflammation
  • Small Intestine
  • Microvilli
  • Intestinal Absorption
  • Malnutrition

Research landscape

PubMed indexes 23,401 records tagged with the MeSH heading “Celiac Disease” (counts retrieved 2026-10-31). 3,440 of them (14.7%) were published from 2020 onward, and the busiest period so far is through 1999 with 9,283 records.

Reviews account for 3,408 records (14.6%) and meta-analyses for 207. Randomized controlled trials number 239 (1.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 9,283 records; 2000-2009: 4,690 records; 2010-2019: 5,988 records; 2020 onward: 3,440 records9,283through 19994,6902000-20095,9882010-20193,4402020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19999,283
2000-20094,690
2010-20195,988
2020 onward3,440
Share of records by publication typeReviews: 14.6 percent; Meta-analyses: 0.9 percent; Randomized controlled trials: 1.0 percentReviews14.6% (3,408)Meta-analyses0.9% (207)Randomized controlled trials1.0% (239)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 23,401 PubMed records
TypeRecordsShare
Reviews3,40814.6%
Meta-analyses2070.9%
Randomized controlled trials2391.0%

Method: PubMed query "Celiac Disease"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.

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 comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
Immune-epithelial-stromal networks define the cellular ecosystem of the small intestine in celiac disease
FitzPatrick MEB, Antanaviciute A, Dunstan M, Künnapuu K, Trzupek D, Provine NM, et al.
2025Research article
Design not recorded in structured metadata
21cc by
PMID 40328997 · DOI · PMC12133578
Gluten-free diet management and well-being in children with celiac disease: A qualitative study
Maddison-Roberts H, Jones C, Satherley RM
2025Research article
Design not recorded in structured metadata
10cc by
PMID 40099805 · DOI · PMC11916637
FODMAP Diet in Celiac Disease and Gluten-Related Disorders
Usai Satta P, Mocci G, Lai M
2024Review article
Design not recorded in structured metadata
10cc by
PMID 39683583 · DOI · PMC11644508
Ultra-short celiac disease in children: histological and autoimmune features
Demir AM, Hızal G, Ateş BB, Akbaba B, Kırsaçlıoğlu CT, Hızlı Ş, et al.
2026Research article
Design not recorded in structured metadata
2cc by
PMID 41518458 · DOI · PMC12790501

Immune-epithelial-stromal networks define the cellular ecosystem of the small intestine in celiac disease [1]

Research article FitzPatrick MEB, Antanaviciute A, Dunstan M, Künnapuu K, Trzupek D, Provine NM, et al. · · 2025 · cited 21 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The immune-epithelial-stromal interactions underpinning intestinal damage in celiac disease (CD) are incompletely understood.
Closing excerpt
Receptor-ligand spatial analyses integrated with disease susceptibility gene expression defined networks of altered chemokine and morphogen signaling, and provide potential therapeutic targets for CD prevention and treatment.
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 (154 words)

The immune-epithelial-stromal interactions underpinning intestinal damage in celiac disease (CD) are incompletely understood. To address this, we performed single-cell transcriptomics (RNA sequencing; 86,442 immune, parenchymal and epithelial cells; 35 participants) and spatial transcriptomics (20 participants) on CD intestinal biopsy samples. Here we show that in CD, epithelial populations shifted toward a progenitor state, with interferon-driven transcriptional responses, and perturbation of secretory and enteroendocrine populations. Mucosal T cells showed numeric and functional changes in regulatory and follicular helper-like CD4+ T cells, intraepithelial lymphocytes, CD8+ and γδ T cell subsets, with skewed T cell antigen receptor repertoires. Mucosal changes remained detectable despite treatment, representing a persistent immune-epithelial 'scar'. Spatial transcriptomics defined transcriptional niches beyond those captured in conventional histological scores, including CD-specific lymphoid aggregates containing T cell-B cell interactions. Receptor-ligand spatial analyses integrated with disease susceptibility gene expression defined networks of altered chemokine and morphogen signaling, and provide potential therapeutic targets for CD prevention and treatment.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40328997 · DOI · PMC12133578

Gluten-free diet management and well-being in children with celiac disease: A qualitative study [2]

Research article Maddison-Roberts H, Jones C, Satherley RM · · 2025 · cited 10 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundManagement of celiac disease (CD) requires adherence to a strict gluten-free diet (GFD).
Closing excerpt
To better support children with CD, holistic support may target anxiety to support well-being alongside GFD management.
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 (199 words)

BackgroundManagement of celiac disease (CD) requires adherence to a strict gluten-free diet (GFD). However, little is known about how children with CD manage the GFD. This qualitative study sought to gain a comprehensive understanding of how children with CD experience and navigate the GFD, focusing on their dietary preferences, perceptions, and challenges, as well as the impact of these experiences.MethodsFifteen children with CD, aged 8-13 years, who had been following the GFD for a minimum of one year, were interviewed with their parents about their management of the GFD. Reflexive thematic analysis was used to analyze the data.ResultsChildren described a range of strategies for managing the GFD. While some adopt problem-focused strategies such as planning ahead and carrying gluten-free foods on their person, others exhibit heightened anxiety and persistent doubts, indicating the need for tailored healthcare support. Importantly, the study uncovers socioecological influences, including social roles, communication patterns, and environmental factors, which shape children's beliefs and coping strategies.ConclusionsThe study underscores the importance of monitoring gluten-related distress, beliefs, and behaviors in children with CD, as well as the broader context of children's lives. To better support children with CD, holistic support may target anxiety to support well-being alongside GFD management.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40099805 · DOI · PMC11916637

FODMAP Diet in Celiac Disease and Gluten-Related Disorders [3]

Review article Usai Satta P, Mocci G, Lai M · · 2024 · cited 10 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
BackgroundIndividuals with celiac disease (CD) often report the persistence of gastrointestinal symptoms despite adherence to a gluten-free diet (GFD).
Closing excerpt
ConclusionsRecent evidence supports the role of FODMAP restriction in CD patients with persistent symptoms on a GFD and in decreasing gastrointestinal disturbances in NCGS, although the GFD still represents the first-line therapy.
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 (201 words)

BackgroundIndividuals with celiac disease (CD) often report the persistence of gastrointestinal symptoms despite adherence to a gluten-free diet (GFD). A diet rich in fermentable oligo-, di-, and monosaccharides and polyols (FODMAPs) could cause symptoms in CD on a GFD, and conversely a low-FODMAP diet could positively influence the therapeutic management of CD and non-celiac gluten sensitivity (NCGS). The aim of this review was to explore the hypothetical impact of the FODMAD diet and the low-FODMAP diet (LFD) in CD and gluten-related disorders.MethodsA complete online search for FODMAP related to CD, NCGS, and the GFD was carried out using the Pubmed, Medline, and Cochrane databases.ResultsIndeed, an LFD could successfully provide symptom relief in GFD-treated CD patients. Fructans, typical components of FODMAPs, have been associated with digestive symptoms in NCGS, and an LFD could improve the clinical picture. According to some evidence, an LFD could also improve the psychological status both in celiac patients on a GFD and in NCGS. However, an LFD should not have a significant impact on gut microbiota.ConclusionsRecent evidence supports the role of FODMAP restriction in CD patients with persistent symptoms on a GFD and in decreasing gastrointestinal disturbances in NCGS, although the GFD still represents the first-line therapy.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39683583 · DOI · PMC11644508

Ultra-short celiac disease in children: histological and autoimmune features [4]

Research article Demir AM, Hızal G, Ateş BB, Akbaba B, Kırsaçlıoğlu CT, Hızlı Ş, et al. · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Ultra-short celiac disease (USCD) represents a histopathological variant with selective involvement of the duodenal bulb.
Closing excerpt
• Isolated duodenal bulb involvement may be sufficient to initiate systemic autoimmunity in celiac disease, despite mild clinical and serological features.
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 (314 words)

Ultra-short celiac disease (USCD) represents a histopathological variant with selective involvement of the duodenal bulb. The mechanisms underlying the sparing of the second duodenal portion remain unclear. The histopathological progression of USCD under continued gluten exposure is not yet defined and represents a significant gap in current understanding. This retrospective study assessed histological changes in the duodenal bulb and second portion of the duodenum in pediatric patients who maintained gluten consumption until a definitive USCD diagnosis. Inclusion criteria required persistent dietary gluten intake, initial diagnosis confirmed by Marsh-Oberhuber classification, and elevated tissue transglutaminase (tTG) antibody levels. Fifteen out of 35 patients with USCD underwent repeat endoscopies. Villous atrophy was consistently confined to the first portion of the duodenum, with preservation of the second portion despite gluten exposure. Extensive celiac disease (ECD), characterized by involvement of the second portion of the duodenum, was associated with a significantly increased prevalence of short stature (p < 0.001) and iron deficiency anemia (p = 0.010), as well as substantially higher titers of tTG antibodies (p < 0.001). Both the USCD and ECD groups had similar rates of additional autoimmune diseases. Conclusion: In children, USCD presents with a distinct and localized duodenal response to gluten. Although USCD presents with a milder clinical and serological profile, the comparable autoimmune burden underscores the necessity for accurate diagnosis and timely treatment. What is Known: • Patients with USCD typically demonstrate milder clinical symptoms and lower serological markers compared to those with more extensive small-intestinal involvement. • The histopathological response to ongoing gluten exposure in USCD has not been characterized to date. What is New: • USCD remains histologically confined to the duodenal bulb, with no progression to the second portion of the duodenum observed over time, even with continued gluten intake. • Isolated duodenal bulb involvement may be sufficient to initiate systemic autoimmunity in celiac disease, despite mild clinical and serological features.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41518458 · DOI · PMC12790501

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 Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis [5]
    Singh P, Arora A, Strand TA, Leffler DA, Catassi C, Green PH, et al. · Clin Gastroenterol Hepatol · 2018 · cited 1,072 times (Europe PMC)
  • Research article Incidence of Celiac Disease Is Increasing Over Time: A Systematic Review and Meta-analysis [6]
    King JA, Jeong J, Underwood FE, Quan J, Panaccione N, Windsor JW, et al. · Am J Gastroenterol · 2020 · cited 308 times (Europe PMC)
  • Research article Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-HLA shared loci [7]
    Zhernakova A, Stahl EA, Trynka G, Raychaudhuri S, Festen EA, Franke L, et al. · PLoS Genet · 2011 · cited 294 times (Europe PMC)
  • Research article Systematic review with meta-analysis: associations between coeliac disease and type 1 diabetes [8]
    Elfström P, Sundström J, Ludvigsson JF · Aliment Pharmacol Ther · 2014 · cited 143 times (Europe PMC)
  • Research article The Immunobiology and Pathogenesis of Celiac Disease [9]
    Iversen R, Sollid LM · Annu Rev Pathol · 2023 · cited 139 times (Europe PMC)
  • Research article Celiac disease [10]
    Rostom A, Dubé C, Cranney A, Saloojee N, Sy R, Garritty C, et al. · Evid Rep Technol Assess (Summ) · 2004 · cited 136 times (Europe PMC)

Full-text reviews on EvidenceLib

Open-access review articles about this topic, reproduced in full with authors, licence and references.

  • Narrative Review: Nutrient Deficiencies in Adults and Children with Treated and Untreated Celiac Disease

    Johanna M Kreutz, Marlou P M Adriaanse, Elisabeth M C van der Ploeg et al. · Nutrients 2020 · CC BY 4.0

  • Celiac Disease, Gluten-Free Diet, and Metabolic and Liver Disorders

    Marco Valvano, Salvatore Longo, Gianpiero Stefanelli et al. · Nutrients 2020 · CC BY 4.0

References

  1. FitzPatrick MEB, Antanaviciute A, Dunstan M, Künnapuu K, Trzupek D, Provine NM, et al.. Immune-epithelial-stromal networks define the cellular ecosystem of the small intestine in celiac disease. . 2025. PMID 40328997 · DOI · PMC12133578
  2. Maddison-Roberts H, Jones C, Satherley RM. Gluten-free diet management and well-being in children with celiac disease: A qualitative study. . 2025. PMID 40099805 · DOI · PMC11916637
  3. Usai Satta P, Mocci G, Lai M. FODMAP Diet in Celiac Disease and Gluten-Related Disorders. . 2024. PMID 39683583 · DOI · PMC11644508
  4. Demir AM, Hızal G, Ateş BB, Akbaba B, Kırsaçlıoğlu CT, Hızlı Ş, et al.. Ultra-short celiac disease in children: histological and autoimmune features. . 2026. PMID 41518458 · DOI · PMC12790501
  5. Singh P, Arora A, Strand TA, Leffler DA, Catassi C, Green PH, et al.. Global Prevalence of Celiac Disease: Systematic Review and Meta-analysis. Clin Gastroenterol Hepatol. 2018. PMID 29551598 · DOI
  6. King JA, Jeong J, Underwood FE, Quan J, Panaccione N, Windsor JW, et al.. Incidence of Celiac Disease Is Increasing Over Time: A Systematic Review and Meta-analysis. Am J Gastroenterol. 2020. PMID 32022718 · DOI
  7. Zhernakova A, Stahl EA, Trynka G, Raychaudhuri S, Festen EA, Franke L, et al.. Meta-analysis of genome-wide association studies in celiac disease and rheumatoid arthritis identifies fourteen non-HLA shared loci. PLoS Genet. 2011. PMID 21383967 · DOI · PMC3044685
  8. Elfström P, Sundström J, Ludvigsson JF. Systematic review with meta-analysis: associations between coeliac disease and type 1 diabetes. Aliment Pharmacol Ther. 2014. PMID 25270960 · DOI
  9. Iversen R, Sollid LM. The Immunobiology and Pathogenesis of Celiac Disease. Annu Rev Pathol. 2023. PMID 36067801 · DOI
  10. Rostom A, Dubé C, Cranney A, Saloojee N, Sy R, Garritty C, et al.. Celiac disease. Evid Rep Technol Assess (Summ). 2004. PMID 15346868

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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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.

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At a glance

23,401
PubMed records on this heading
15%
published since 2020
3,408
review articles
239
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-31; they show how much has been written, not how strong the evidence is.

Related topics See all →

  • Malabsorption SyndromesDigestive System and Liver
  • SteatorrheaDigestive System and Liver
  • Lactose IntoleranceRare and Inherited Diseases
  • Short Bowel SyndromeDigestive System and Liver
  • EnterocolitisDigestive System and Liver

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