Celiac disease-specific and inflammatory bowel disease-related antibodies in patients with recurrent aphthous stomatitis.


Journal

Immunobiology
ISSN: 1878-3279
Titre abrégé: Immunobiology
Pays: Netherlands
ID NLM: 8002742

Informations de publication

Date de publication:
01 2019
Historique:
received: 31 05 2018
revised: 23 10 2018
accepted: 30 10 2018
pubmed: 18 11 2018
medline: 18 12 2019
entrez: 18 11 2018
Statut: ppublish

Résumé

The etiology of recurrent aphthous stomatitis (RAS) remains unknown. RAS can be presented as primary, idiopathic condition and as a secondary RAS, which is associated with a systemic disease. The aim of our study was to evaluate the presence and concentrations of antibodies specific for celiac disease (CeD) and antibodies related to inflammatory bowel diseases (IBD) in patients with RAS without gastrointestinal symptoms. Antibodies against tissue transglutaminase (anti-tTG), deaminated gliadin peptides (DGP), deaminated gliadin-analogous fragments (anti-GAF-3X) and Saccharomyces cerevisiae (ASCA) were determined by ELISA and antineutrophil cytoplasmic antibodies (ANCA) by indirect immunoflurescence (IIF) in 57 patients with RAS and 60 control subjects. The prevalence of CeD specific antibodies did not differ between RAS patients and controls. However, the concentrations of IgA anti-tTG, IgA anti-GAF-3X antibodies in patients with RAS were significantly higher compared to controls (p = 0.002 and p = 0.04 respectively). Histological changes consistent with CeD were confirmed by duodenal biopsy in one RAS patient with highly positive IgA anti-tTG, anti-GAF-3X and anti-DGP antibodies. Higher prevalence along with higher concentrations of IgG ASCA were found in RAS patients compared to controls (p < 0.01). Patients with positive IgG ASCA in the absence of clinical symptoms decided not to pursue any further testing. Dysfunction of oral mucosa and the exposure to various antigens might be a reason for the loss of tolerance resulting in increased production of autoantibodies. It seems likely that antibodies are markers of aberrant immune response, rather than key effectors involved in the pathogenesis of the disease.

Identifiants

pubmed: 30446336
pii: S0171-2985(18)30176-1
doi: 10.1016/j.imbio.2018.10.006
pii:
doi:

Substances chimiques

Antibodies, Antineutrophil Cytoplasmic 0
Biomarkers 0
Immunoglobulin A 0
Gliadin 9007-90-3
Protein Glutamine gamma Glutamyltransferase 2 EC 2.3.2.13
Transglutaminases EC 2.3.2.13
GTP-Binding Proteins EC 3.6.1.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

75-79

Informations de copyright

Copyright © 2018 Elsevier GmbH. All rights reserved.

Auteurs

Borivoj Bijelić (B)

School of Dental Medicine, University of Belgrade, dr Subotica 4, Belgrade 11000, Serbia. Electronic address: borivojbijelic@yahoo.com.

Ivana Z Matić (IZ)

Institute of Oncology and Radiology of Serbia, Pasterova 14, Belgrade 11000, Serbia.

Irina Besu (I)

Institute of Oncology and Radiology of Serbia, Pasterova 14, Belgrade 11000, Serbia.

Ljiljana Janković (L)

School of Dental Medicine, University of Belgrade, dr Subotica 4, Belgrade 11000, Serbia.

Zorica Juranić (Z)

Institute of Oncology and Radiology of Serbia, Pasterova 14, Belgrade 11000, Serbia.

Senka Marušić (S)

Clinic of Gastroenterohepatology, Clinical Center of Serbia, Koste Todorovica 2, Belgrade 11000, Serbia.

Sladjana Andrejević (S)

Clinic of Allergy and Clinical Immunology, Clinical Center of Serbia, Koste Todorovica 2, Belgrade 11000, Serbia.

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Classifications MeSH