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Concept: Anti-gliadin antibodies

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Background: Intestinal exposure to gliadin leads to zonulin upregulation and consequent disassembly of intercellular tight junctions and increased intestinal permeability. We aimed to study response to gliadin exposure, in terms of barrier function and cytokine secretion, using intestinal biopsies obtained from four groups: celiac patients with active disease (ACD), celiac patients in remission (RCD), non-celiac patients with gluten sensitivity (GS) and non-celiac controls (NC). Methods: Ex-vivo human duodenal biopsies were mounted in microsnapwells and luminally incubated with either gliadin or media alone. Changes in transepithelial electrical resistance were monitored over 120 min. Media was subsequently collected and cytokines quantified. Results: Intestinal explants from all groups (ACD (n = 6), RCD (n = 6), GS (n = 6), and NC (n = 5)) demonstrated a greater increase in permeability when exposed to gliadin vs. media alone. The increase in permeability in the ACD group was greater than in the RCD and NC groups. There was a greater increase in permeability in the GS group compared to the RCD group. There was no difference in permeability between the ACD and GS groups, between the RCD and NC groups, or between the NC and GS groups. IL-10 was significantly greater in the media of the NC group compared to the RCD and GS groups. Conclusions: Increased intestinal permeability after gliadin exposure occurs in all individuals. Following gliadin exposure, both patients with gluten sensitivity and those with active celiac disease demonstrate a greater increase in intestinal permeability than celiacs in disease remission. A higher concentration of IL-10 was measured in the media exposed to control explants compared to celiac disease in remission or gluten sensitivity.

Concepts: Wheat, Coeliac disease, Gluten, Wheat allergy, Gliadin, Anti-gliadin antibodies, Triticeae glutens, Zonulin

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Until recently gluten intolerance has been believed to be typical of celiac disease (CD) and wheat allergy (WA). In the last few years, however, several study results have been published that have proved that gluten intolerance can also affect people who do not suffer from any of the above mentioned diseases. The new syndrome has been named non-celiac gluten sensitivity (NCGS) or gluten sensitivity (GS). It has been included in the new list of gluten-related disorders published in 2012. Researchers believe that NCGS is the most common syndrome of gluten intolerance. This review discusses many aspects of NCGS epidemiology, pathophysiology, clinical spectrum, and treatment and current tools to identify patients suffering from CD, WA, and NCGS.

Concepts: Wheat, Coeliac disease, Gluten, Gluten-free diet, Dermatitis herpetiformis, Wheat allergy, Gliadin, Anti-gliadin antibodies

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The avoidance of wheat- and gluten-containing products is a worldwide phenomenon. While celiac disease is a well-established entity, the evidence base for gluten as a trigger of symptoms in patients without celiac disease (so-called ‘non-celiac gluten sensitivity’ or NCGS) is limited. The problems lie in the complexity of wheat and the ability of its carbohydrate as well as protein components to trigger gastrointestinal symptoms, the potentially false assumption that response to a gluten-free diet equates to an effect of gluten withdrawal, and diagnostic criteria for coeliac disease. Recent randomized controlled re-challenge trials have suggested that gluten may worsen gastrointestinal symptoms, but failed to confirm patients with self-perceived NCGS have specific gluten sensitivity. Furthermore, mechanisms by which gluten triggers symptoms have yet to be identified. This review discusses the most recent scientific evidence and our current understanding of NCGS.

Concepts: Wheat, Coeliac disease, Gluten, Gluten-free diet, Dermatitis herpetiformis, Wheat allergy, Gliadin, Anti-gliadin antibodies

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Noncoeliac gluten sensitivity (NCGS) is a controversial emerging disorder. Despite reported symptoms related to the ingestion of gluten, NCGS remains a diagnosis based on the exclusion of coeliac disease, given the absence of reliable biomarkers.

Concepts: Wheat, Coeliac disease, Gluten, Gluten-free diet, Dermatitis herpetiformis, Wheat allergy, Gliadin, Anti-gliadin antibodies

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Reports suggest that gluten sensitivity (GS) exists in the absence of coeliac disease (CD). This clinical entity has been termed noncoeliac gluten sensitivity (NCGS).

Concepts: Medical statistics, Wheat, Prevalence, Coeliac disease, Gluten, Gluten-free diet, Wheat allergy, Anti-gliadin antibodies

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Celiac disease (CD) is an intestinal inflammatory condition that develops in genetically susceptible individuals after exposure to dietary wheat gliadin. The role of post-translational modifications of gliadin catalyzed by tissue transglutaminase (tTG) seems to play a crucial role in CD. However, it remains to be established how and where tTG is activated in vivo. We have investigated whether gliadin peptides modulate intracellular Ca(2+) homeostasis and tTG activity.

Concepts: Protein, Amino acid, Histone, Cell biology, Coeliac disease, Tissue transglutaminase, Gliadin, Anti-gliadin antibodies

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One of the challenges in coeliac disease is the significant under-diagnosis despite the increasing prevalence and international guidelines for serological screening in appropriate patient cohorts. Several point-of-care tests for coeliac disease have been developed over the past decade with the aim of improving case detection using rapid and convenient testing. Most point-of-care tests, such as Biocard, detect anti-tissue transglutaminase (tTG) IgA antibodies, whereas Simtomax uniquely detects anti-deamidated gliadin peptide (DGP) IgA/IgG antibodies. A recent head-to-head trial in adults comparing two tTG-based point-of-care tests (Biocard and Celiac Quick Test) and Simtomax found that Simtomax was superior to Biocard and Celiac Quick Test, with sensitivities of 92.7%, 72.2% and 77.8%, respectively.

Concepts: Antibody, Wheat, Coeliac disease, Gluten, Tissue transglutaminase, Gliadin, Anti-gliadin antibodies, Prolamin

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Tight junction (TJ) injuries induced by pepsin-trypsin-resistant gliadin (PT-G) play an important role in the pathogenesis of celiac disease. Previously, 1,25-dihydroxy vitamin D3 (VD3) was reported to be a TJ regulator that attenuates lipopolysaccharide- and alcohol-induced TJ injuries. However, whether VD3 can attenuate PT-G-induced TJ injuries is unknown.

Concepts: Vitamin D, Attenuation, Coeliac disease, Play, Gliadin, Anti-gliadin antibodies

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The onset of coeliac disease (CD) in the first year of life is uncommon and the diagnosis can be challenging due to the suboptimal sensitivity of tissue transglutaminase antibodies (tTG) at this age and the many other possible causes of malabsorption in infants. Antibodies to deamidated gliadin peptides (anti-DGPs), especially IgG, may appear earlier than IgA anti-tTG in very young children with CD.

Concepts: Immune system, Coeliac disease, Gluten, Malabsorption, Anti-transglutaminase antibodies, Tissue transglutaminase, Gliadin, Anti-gliadin antibodies

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Staple gluten-free (GF) foods have been available on prescription to patients diagnosed with gluten sensitivity enteropathies, such as coeliac disease, since the late 1960s.

Concepts: Wheat, Maize, Coeliac disease, Gluten, Gluten-free diet, Dermatitis herpetiformis, Wheat allergy, Anti-gliadin antibodies