57 research outputs found
Sa1350 Intraepithelial Lymphocyte Phenotype and Clonality Provide Differential Prognostic Information in Refractory Celiac Disease
M2046 Clonality Assessment Is a Better Determinant of Celiac Disease Outcome Compared to Detection of Phenotypic Aberrations of Intra-Epithelial Lymphocytes
Commentary: refractory coeliac disease - rigorous management revealing, or resulting in, rarity?
S2054 Hemolysis Induces Tissue Transglutaminase, but Not Deamidated Gliadin Peptide, False Negative Results in Celiac Disease Patients With Low Antibody Levels
Sa1344 Celiac Disease-Associated Antibodies in the Phenotypic Spectrum of Alopecia Areata
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Lack of serologic evidence to link IgA nephropathy with celiac disease or immune reactivity to gluten.
IgA nephropathy is the most common form of primary glomerulonephritis worldwide. Mucosal infections and food antigens, including wheat gluten, have been proposed as potential contributing environmental factors. Increased immune reactivity to gluten and/or association with celiac disease, an autoimmune disorder triggered by ingestion of gluten, have been reported in IgA nephropathy. However, studies are inconsistent about this association. We aimed to evaluate the proposed link between IgA nephropathy and celiac disease or immune reactivity to gluten by conducting a comprehensive analysis of associated serologic markers in cohorts of well-characterized patients and controls. Study participants included patients with biopsy-proven IgA nephropathy (n = 99), unaffected controls of similar age, gender, and race (n = 96), and patients with biopsy-proven celiac disease (n = 30). All serum specimens were tested for IgG and IgA antibodies to native gliadin and deamidated gliadin, as well as IgA antibody to transglutaminase 2 (TG2). Anti-TG2 antibody-positive nephropathy patients and unaffected controls were subsequently tested for IgA anti-endomysial antibody and genotyped for celiac disease-associated HLA-DQ2 and -DQ8 alleles. In comparison to unaffected controls, there was not a statistically significant increase in IgA or IgG antibody reactivity to gliadin in individuals with IgA nephropathy. In addition, the levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between IgA nephropathy patients and unaffected controls. Results of the additional anti-endomysial antibody testing and HLA genotyping were corroborative. The data from this case-control study do not reveal any evidence to suggest a significant role for celiac disease or immune reactivity to gluten in IgA nephropathy
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