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Licensed Unlicensed Requires Authentication Published by De Gruyter November 20, 2014

Evidence of Crohn’s disease-related anti-glycoprotein 2 antibodies in patients with celiac disease

  • Dirk Roggenbuck EMAIL logo , Severine Vermeire , Ilse Hoffman , Dirk Reinhold , Peter Schierack , Alexander Goihl , Ulrike von Arnim , Gert De Hertogh , Dimitrios Polymeros , Dimitrios P. Bogdanos and Xavier Bossuyt

Abstract

Background: Autoantibodies to exocrine-pancreatic glycoprotein 2 (anti-GP2) are Crohn’s disease (CD) markers. However, CD-specific antibodies have also been found in celiac-disease (CeD) patients, in which type 1 diabetes-specific autoantibodies against endocrine pancreatic targets can be present. We investigated whether anti-GP2 are also present in CeD, a disease like CD which is also characterised by intestinal mucosal inflammation with barrier impairment.

Methods: Antibodies against GP2, tissue transglutaminase (tTG), deamidated gliadin (dGD), glutamic decarboxylase (GAD), and islet antigen-2 (IA2) were tested in sera from 73 CD patients, 90 blood donors (BD), and 79 (58 de novo) CeD patients (2 consecutive sera were available from 40 patients).

Results: IgA and/or IgG anti-GP2 were found in 15/79 (19.0%) CeD patients on at least one occasion, in 25/73 (34.2%) CD patients, and in 4/90 (4.4%) BD (CeD vs. CD, p=0.042; BD vs. CeD and CD, p<0.001, respectively). Amongst the 58 de novo CeD patients, anti-GP2 IgA and/or IgG were present in 11 (19.0%). Anti-GP2 IgA was significantly less prevalent in CeD compared with CD (p=0.004). Anti-GP2 IgA and IgG in CD patients demonstrated a significantly higher median level compared to patients with CeD (p<0.001, p=0.008, respectively). IgA anti-GP2 levels correlated significantly with IgA anti-tTG and anti-dGD levels in CeD Spearman’s coefficient of rank correlation (ρ)=0.42, confidence interval (CI): 0.26–0.56, p<0.001; ρ=0.54, CI 0.39–0.65, p<0.001, respectively.

Conclusions: The presence of anti-GP2 in CeD patients supports the notion that loss of tolerance to GP2 can probably be a manifestation of an autoinflammatory process in this intestinal disorder.


Corresponding author: Prof. Dr. Dirk Roggenbuck, MD PhD, Faculty of Natural Sciences, Brandenburg Technical University Cottbus-Senftenberg, Grossenhainer Str. 57, 01968 Senftenberg, Germany, Phone: +49 33708 441716, Fax: +49 33708 441725, E-mail: ; and Medipan GmbH, Dahlewitz/Berlin, Germany
aDimitrios P. Bogdanos and Xavier Bossuyt share senior authorship.

Acknowledgments

We thank Doreen Dillaerts for expert technical assistance.

Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

Financial support: None declared.

Employment or leadership: Dirk Roggenbuck is a shareholder of GA Generic Assays GmbH and Medipan GmbH. The remaining authors declare that they have no competing financial interests.

Honorarium: None declared.

Competing interests: The funding organisation(s) played no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the report for publication.

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Received: 2014-3-4
Accepted: 2014-10-3
Published Online: 2014-11-20
Published in Print: 2015-8-1

©2015 by De Gruyter

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