Patients with serum IgA endomysial antibodies and intact duodenal villi: Clinical characteristics and management options

Dickey, William; Hughes, D.; McMillan, S A

doi:10.1080/00365520510023747

Cited by 41 publications

(38 citation statements)

References 20 publications

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“…It is suggested that many undiagnosed celiac patients accept a state of chronic vague ill health as a normal condition, but are able to recognize this only after they have been placed on a GFD. 47,[52][53][54] A recent randomized study also shows that apparently asymptomatic EMA-positive subjects seem to benefit from their serological screening and subsequent GFD, 55 thereby supporting earlier evidence from Dickey et al; 56 however, some authors have suggested that EMA positivity in individuals with normal mucosa constitutes a separate entity (potential CD), different from CD. 57 A strict GFD sets major limitations on daily life and it is expensive and difficult to maintain.…”

Section: The Gfd: ''That a Treatment Is Available''mentioning

confidence: 60%

Screening for celiac disease in the general population and in high‐risk groups

et al. 2015

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Background: Celiac disease (CD) occurs in approximately 1% of the Western population. It is a lifelong disorder that is associated with impaired quality of life (QOL) and an excessive risk of comorbidity and death. Objectives: To review the literature on screening for CD in relation to the current World Health Organization (WHO) criteria for mass screening. Methods: We performed a PubMed search to identify indexed papers on CD screening with a publication date from 1900 until 1 June 2014. When we deemed an abstract relevant, we read the corresponding paper in detail. Results: CD fulfills several WHO criteria for mass screening (high prevalence, available treatment and difficult clinical detection), but it has not yet been established that treatment of asymptomatic CD may reduce the excessive risk of severe complications, leading to higher QOL nor that it is cost-effective. Conclusions: Current evidence is not sufficient to support mass screening for CD, but active case-finding may be appropriate, as we recognize that most patients with CD will still be missed by this strategy. Although proof of benefit is still lacking, screening for CD may be appropriate in high-risk groups.

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Section: The Gfd: ''That a Treatment Is Available''mentioning

confidence: 60%

Screening for celiac disease in the general population and in high‐risk groups

et al. 2015

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“…In all previous studies in other areas of the world (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20), the prevalences of biopsy-positive patients are nearly the same (1-5%). It has been demonstrated recently that all patients with elevated serum tTG IgA and intact duodenal villi will develop CD (28). In another study, serology found at the diagnosis of DM1 was predictive of future development of CD (29).…”

Section: Discussionmentioning

confidence: 97%

Prevalence of celiac disease in patients with type 1 diabetes mellitus in the south of Iran

Honar

Karamizadeh²,

Saki³

2013

Turk J Gastroenterol

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“…In human CD, enteropathy probably evolves gradually from intraepithelial lymphocytosis to subtotal villous atrophy, and in clinical practice serum tTG IgA may precede intestinal damage (37,38). Autoantibodies specific for tTG typically appear in serum for the first time between the ages of 1 and 7 years, but can be transient or even reappear later in childhood (39).…”

Section: Discussionmentioning

confidence: 99%

Resistance to Celiac Disease in Humanized HLA-DR3-DQ2-Transgenic Mice Expressing Specific Anti-Gliadin CD4+ T Cells

Kauwe

Chen

Anderson

et al. 2009

The Journal of Immunology

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Celiac disease is a chronic inflammatory enteropathy caused by cellular immunity to dietary gluten. More than 90% of patients carry HLA-DQ2 encoded by HLA-DQA1*05 and DQB1*02, and gluten-specific CD4+ T cells from intestinal biopsies of these patients are HLA-DQ2-restricted, produce Th1 cytokines and preferentially recognize gluten peptides deamidated by tissue transglutaminase. We generated mice lacking murine MHC class II genes that are transgenic for human CD4 and the autoimmunity and celiac disease-associated HLA-DR3-DQ2 haplotype. Immunization with the α-gliadin 17-mer that incorporates the overlapping DQ2-α-I and DQ2-α-II epitopes immunodominant in human celiac disease generates peptide-specific HLA-DQ2-restricted CD4+ T cells. When exposed to dietary gluten, naive or gliadin-primed mice do not develop pathology. Coincident introduction of dietary gluten and intestinal inflammation resulted in low-penetrance enteropathy and tissue transglutaminase-specific IgA. Two further strains of transgenic mice expressing HLA-DR3-DQ2 and human CD4, one with a NOD background and another TCR transgenic having over 90% of CD4+ T cells specific for the DQ2-α-II epitope with a Th1 phenotype, were also healthy when consuming gluten. These humanized mouse models indicate that gluten ingestion can be tolerated without intestinal pathology even when HLA-DQ2-restricted CD4+ T cell immunity to gluten is established, thereby implicating additional factors in controlling the penetrance of celiac disease.

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Patients with serum IgA endomysial antibodies and intact duodenal villi: Clinical characteristics and management options

Cited by 41 publications

References 20 publications

Screening for celiac disease in the general population and in high‐risk groups

Screening for celiac disease in the general population and in high‐risk groups

Prevalence of celiac disease in patients with type 1 diabetes mellitus in the south of Iran

Resistance to Celiac Disease in Humanized HLA-DR3-DQ2-Transgenic Mice Expressing Specific Anti-Gliadin CD4+ T Cells

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