The Significance of Coeliac Disease Antibodies in Patients with Ankylosing Spondylitis: A Case-Controlled Study

Toğrol, Erdem; Nalbant, Selim; Solmazgül, Emrullah; Özyurt, Mustafa; Kaplan, Mustafa; Kıralp, Mehmet Zeki; Dinçer, Ümit; Şahan, Burak

doi:10.1177/147323000903700127

Cited by 14 publications

(18 citation statements)

References 27 publications

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“…Our study confirms prior findings of elevated CD-associated antibodies in patients with SpA [4–7], extending these observations for the first time to pediatric SpA. We also confirm prior observations of elevated total serum IgA levels in SpA patients [15].…”

Section: Discussionsupporting

confidence: 92%

“…However, there is contradictory data with respect to the presence of antibodies associated with CD in patients with pediatric or adult arthritis. Several studies have identified increased anti-gliadin IgA or anti-tissue transglutaminase (TTG) IgA antibodies in adults with psoriatic arthritis (PsA) or ankylosing spondylitis (AS) [4–7], while others found no differences in antibody titers [8, 9]. Similar data exist in children, and several studies have shown increased frequency of CD-associated antibodies in patients with JIA [10–13], although none of the studies evaluated children with SpA.…”

Section: Introductionmentioning

confidence: 99%

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IgA Transglutaminase Levels in Children with Juvenile Idiopathic Arthritis

Stoll¹,

Patel²,

Christadoss³

et al. 2012

Ann Paediatr Rheum

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Objectives Several studies have indicated that adult patients with spondyloarthritis (SpA) have elevated levels of antibodies associated with celiac disease (CD). This has not been studied in children, and none of the studies corrected for total IgA levels. Methods We measured total IgA and IgA against tissue transglutaminase (TTG) levels in 42 children with Juvenile Idiopathic Arthritis (JIA), of whom 11 had SpA, along with 10 non-inflammatory control subjects. Results Median (IQR) TTG IgA levels were elevated among children with ERA (8.8, 4.6 – 21) compared to ‘JIA controls’ (JIA subgroups other than ERA) (2.8, 1.5 – 5.9) and a healthy non-inflammatory control group (1.5, 0.82 – 12), p = 0.017, Kruskal-Wallis. There was no correlation between TTG IgA levels and measures of disease activity or with medicine use. None of the children were diagnosed endoscopically with celiac disease. Patients with ERA likewise had elevated total IgA level compared to the other groups (p = 0.001), and total IgA levels correlated highly with TTG IgA (r = 0.599, p<0.001). Conclusion These findings suggest that elevations in TTG IgA may reflect increased polyclonal IgA production, rather than a specific intestinal inflammatory process.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

IgA Transglutaminase Levels in Children with Juvenile Idiopathic Arthritis

Stoll¹,

Patel²,

Christadoss³

et al. 2012

Ann Paediatr Rheum

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“…Also, no association could be demonstrated with the occurrence of peripheral arthritis or uveitis. Also, no relationship of CeD and the presence of EmAIgA could be found agreeing with the findings of Riente et al [6] but contrary to Togrol et al [7]. Such discrepancy could be explained by the fact that CeD is a very common disease (affecting 1:300 to 1:500 of the general population) [14] and a coincidence of these two diseases can be due to a false positive caused by the small sample number studied rather than to a true association.…”

Section: Discussioncontrasting

confidence: 66%

“…Riente et al [6] found no increased prevalence of anti-tissue transglutaminase (tTG) in ankylosing spondylitis and psoriatic arthritis patients, but Togrol et al [7] found a prevalence of 10% of anti-endomysial (EmA) positivity. EmA-IgA as well as anti-tTG has allowed evaluating the potential risk for CeD in individuals with suggestive symptoms and in high-risk populations.…”

Section: Introductionmentioning

confidence: 99%

Anti-Saccharomyces cerevisiae (ASCA) and anti-endomysial antibodies in spondyloarthritis

Andretta

Vieira

Nishiara³

et al. 2011

Rheumatol Int

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Spondyloarthritis (SpA) are diseases with increased gut inflammation. To search for (anti-Saccharomyces cerevisiae) ASCA IgA, ASCA IgG, and anti-endomysial antibodies (EmA-IgA) in a cohort of 70 patients with SpA, we found 18.6% (13/70) positive for IgA-ASCA in the SpA group and 3/57 (5.2%) in the control group (P = 0.031). ASCA IgG and EmA-IgA were found at the same frequency in SpA and controls. No relationship of ASCA IgA positivity could be established with disease activity (measured by ESR, C-reactive protein, and BASDAI), presence of uveitis, or peripheral arthritis neither with functional status measured by BASFI. SpA patients present an increase in the IgA-ASCA positivity without any relationship to disease activity, functional index, clinical profile or the presence of HLA-B27. There is no evidence of higher prevalence of EmA-IgA in SpA patients in the studied sample.

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“…Detection of anti-gliadin antibodies (AGA) has been abandoned as a test for CD diagnosis due to their poor specificity for the disease. However, AGA of the class IgG has been previously reported as a possible biomarker of increased intestinal permeability [10], [11].…”

Section: Introductionmentioning

confidence: 99%

Proof of Concept of Microbiome-Metabolome Analysis and Delayed Gluten Exposure on Celiac Disease Autoimmunity in Genetically At-Risk Infants

et al. 2012

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Celiac disease (CD) is a unique autoimmune disorder in which the genetic factors (DQ2/DQ8) and the environmental trigger (gluten) are known and necessary but not sufficient for its development. Other environmental components contributing to CD are poorly understood. Studies suggest that aspects of gluten intake might influence the risk of CD occurrence and timing of its onset, i.e., the amount and quality of ingested gluten, together with the pattern of infant feeding and the age at which gluten is introduced in the diet. In this study, we hypothesize that the intestinal microbiota as a whole rather than specific infections dictates the switch from tolerance to immune response in genetically susceptible individuals. Using a sample of infants genetically at risk of CD, we characterized the longitudinal changes in the microbial communities that colonize infants from birth to 24 months and the impact of two patterns of gluten introduction (early vs. late) on the gut microbiota and metabolome, and the switch from gluten tolerance to immune response, including onset of CD autoimmunity. We show that infants genetically susceptible to CD who are exposed to gluten early mount an immune response against gluten and develop CD autoimmunity more frequently than at-risk infants in which gluten exposure is delayed until 12 months of age. The data, while derived from a relatively small number of subjects, suggest differences between the developing microbiota of infants with genetic predisposition for CD and the microbiota from infants with a non-selected genetic background, with an overall lack of bacteria of the phylum Bacteriodetes along with a high abundance of Firmicutes and microbiota that do not resemble that of adults even at 2 years of age. Furthermore, metabolomics analysis reveals potential biomarkers for the prediction of CD. This study constitutes a definite proof-of-principle that these combined genomic and metabolomic approaches will be key to deciphering the role of the gut microbiota on CD onset.

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The Significance of Coeliac Disease Antibodies in Patients with Ankylosing Spondylitis: A Case-Controlled Study

Cited by 14 publications

References 27 publications

IgA Transglutaminase Levels in Children with Juvenile Idiopathic Arthritis

IgA Transglutaminase Levels in Children with Juvenile Idiopathic Arthritis

Anti-Saccharomyces cerevisiae (ASCA) and anti-endomysial antibodies in spondyloarthritis

Proof of Concept of Microbiome-Metabolome Analysis and Delayed Gluten Exposure on Celiac Disease Autoimmunity in Genetically At-Risk Infants

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