Celiac sprue: a unique autoimmune disorder

Rashtak, Shadi; Marietta, Eric; Murray, Joseph A.

doi:10.1586/eci.09.30

Cited by 18 publications

(15 citation statements)

References 162 publications

(187 reference statements)

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“…Certainly there was evidence that she had common variable immunodeficiency (CVID) with immunoglobulin deficiencies and poor responses to immunization per her treating rheumatologist. One may argue whether she had celiac sprue at all, however, classic antibodies may be absent in CVID [4,5]. Also, she responded well with decreased stools, weight gain and nutritional improvement of Vitamin K and D. She clearly had osteomalcia with secondary hyperparathyroidism.…”

Section: Discussionmentioning

confidence: 99%

A Polyglandular Autoimmune Syndrome of a Different Type: A Case Report

Mt¹

2013

MCR

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IntroductionPatients may present with autoimmune conditions abruptly or, more commonly, slowly over time requiring increased vigilance on part of their physician. Though many combinations have been previously described and linked to genetic etiologies, most physicians deal with one problem at a time until there is a realization that a polyglandular process is ongoing. Obviously, one of the most feared autoimmune syndromes is adrenal insufficiency, since unrecognized, it can lead to death. A question that is commonly asked on board exams for primary care providers. We present a case of a patient with a variety of autoimmune diseases presenting over time and on occasion with a complete surprise.

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Section: Discussionmentioning

confidence: 99%

A Polyglandular Autoimmune Syndrome of a Different Type: A Case Report

Mt¹

2013

MCR

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“…Transglutaminase antibodies are characteristic in DH; however a study with immunodeficient mice that received sera from DH patients suggested that circulating antibodies are not pathogenic alone . Using a transgenic mouse model of DH, other authors found similar results , proposing that transglutaminase antibodies may not be sufficient by themselves for the pathology to occur.…”

Section: Extradigestive Manifestations In CD and Ncgs: Linking Diseasmentioning

confidence: 97%

“…The current immunogenetic model for CD does not clarify many of the extradigestive disorders related to CD and NCGS . HLA‐DQ2 and HLA‐DQ8 are the main contributors to CD.…”

Section: Introductionmentioning

confidence: 99%

Extraintestinal manifestations of celiac disease: 33‐mer gliadin binding to glutamate receptor GRINA as a new explanation

García-Quintanilla

Miranzo-Navarro

2016

BioEssays

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We propose a biochemical mechanism for celiac disease and non-celiac gluten sensitivity that may rationalize many of the extradigestive disorders not explained by the current immunogenetic model. Our hypothesis is based on the homology between the 33-mer gliadin peptide and a component of the NMDA glutamate receptor ion channel - the human GRINA protein - using BLASTP software. Based on this homology the 33-mer may act as a natural antagonist interfering with the normal interactions of GRINA and its partners. The theory is supported by numerous independent data from the literature, and provides a mechanistic link with otherwise unrelated disorders, such as cleft lip and palate, thyroid dysfunction, restless legs syndrome, depression, ataxia, hearing loss, fibromyalgia, dermatitis herpetiformis, schizophrenia, toxoplasmosis, anemia, osteopenia, Fabry disease, Barret's adenocarcinoma, neuroblastoma, urinary incontinence, recurrent miscarriage, cardiac anomalies, reduced risk of breast cancer, stiff person syndrome, etc. The hypothesis also anticipates better animal models, and has the potential to open new avenues of research.

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“…Because CD is associated with other autoimmune diseases [33], it is likely that genes that contribute toward the development of autoimmunity are required for the development of the gluten-sensitive diseases; this theory is supported by the finding that DQ2 and DQ8 only provide 30% to 35% of the familial risk for developing CD [34]. Many of the non-HLA candidate genes that have been identified in a Genomic Wide Association Study (GWAS) are involved in immune function, with some specifically associated with T-cell development of the thymus and other autoimmune diseases, such as type 1 diabetes (T1D) [35].…”

Section: Genetic Predisposition Toward Autoimmunitymentioning

confidence: 99%

Animal models to study gluten sensitivity

Marietta

Murray

2012

Semin Immunopathol

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The initial development and maintenance of tolerance to dietary antigens is a complex process that, when prevented or interrupted, can lead to human disease. Understanding the mechanisms by which tolerance to specific dietary antigens is attained and maintained is crucial to our understanding of the pathogenesis of diseases related to intolerance of specific dietary antigens. Two diseases that are the result of intolerance to a dietary antigen are celiac disease (CD) and dermatitis herpetiformis (DH). Both of these diseases are dependent upon the ingestion of gluten (the protein fraction of wheat, rye, and barley) and manifest in the gastrointestinal tract and skin, respectively. These gluten-sensitive diseases are two examples of how devastating abnormal immune responses to a ubiquitous food can be. The well-recognized risk genotype for both is conferred by either of the HLA class II molecules DQ2 or DQ8. However, only a minority of individuals who carry these molecules will develop either disease. Also of interest is that the age at diagnosis can range from infancy to 70–80 years of age. This would indicate that intolerance to gluten may potentially be the result of two different phenomena. The first would be that, for various reasons, tolerance to gluten never developed in certain individuals, but that for other individuals, prior tolerance to gluten was lost at some point after childhood. Of recent interest is the concept of non-celiac gluten sensitivity, which manifests as chronic digestive or neurologic symptoms due to gluten, but through mechanisms that remain to be elucidated. This review will address how animal models of gluten-sensitive disorders have substantially contributed to a better understanding of how gluten intolerance can arise and cause disease.

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Celiac sprue: a unique autoimmune disorder

Cited by 18 publications

References 162 publications

A Polyglandular Autoimmune Syndrome of a Different Type: A Case Report

A Polyglandular Autoimmune Syndrome of a Different Type: A Case Report

Extraintestinal manifestations of celiac disease: 33‐mer gliadin binding to glutamate receptor GRINA as a new explanation

Animal models to study gluten sensitivity

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