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Autoimmune Diseases
Volume 2014 (2014), Article ID 237107, 8 pages
http://dx.doi.org/10.1155/2014/237107
Research Article

Anti-Transglutaminase 6 Antibodies in Children and Young Adults with Cerebral Palsy

1Department of Pediatrics, Centre for Rehabilitation Research and Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, 70185 Örebro, Sweden
2Department of Neurology and Department of Neuroradiology, The Royal Hallamshire Hospital, Sheffield S10 2JF, UK
3Matrix Biology & Tissue Repair Research Unit, College of Biomedical and Life Sciences, School of Dentistry, Cardiff University, Cardiff CF14 4XY, UK

Received 18 November 2013; Revised 10 February 2014; Accepted 17 February 2014; Published 2 April 2014

Academic Editor: Kalle Kurppa

Copyright © 2014 Reidun Stenberg et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objectives. We have previously reported a high prevalence of gluten-related serological markers (GRSM) in children and young adults with cerebral palsy (CP). The majority had no enteropathy to suggest coeliac disease (CD). Antibodies against transglutaminase 6 (anti-TG6) represent a new marker associated with gluten-related neurological dysfunction. The aim of this study was to investigate the prevalence of anti-TG6 antibodies in this group of individuals with an early neurological injury resulting in CP. Materials and Methods. Sera from 96 patients with CP and 36 controls were analysed for IgA/IgG class anti-TG6 by ELISA. Results. Anti-TG6 antibodies were found in 12/96 (13%) of patients with CP compared to 2/36 (6%) in controls. The tetraplegic subgroup of CP had a significantly higher prevalence of anti-TG6 antibodies 6/17 (35%) compared to the other subgroups and controls. There was no correlation of anti-TG6 autoantibodies with seropositivity to food proteins including gliadin. Conclusions. An early brain insult and associated inflammation may predispose to future development of TG6 autoimmunity.