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Ataxia and the Role of Antigliadin Antibodies

Published online by Cambridge University Press:  02 December 2014

D. Wong ,
M. Dwinnel ,
M. Schulzer ,
M. Nimmo ,
B. R. Leavitt  and
S. D. Spacey
D. Wong
Affiliation:
Division of Neurology, Department of Medicine, The Centre for Molecular Medicine and Therapeutics, BC
M. Dwinnel
Affiliation:
Michael Smith Laboratory, The Centre for Molecular Medicine and Therapeutics, BC
M. Schulzer
Affiliation:
Pacific Parkinson's Research Centre, The Centre for Molecular Medicine and Therapeutics, BC
M. Nimmo
Affiliation:
Department of Pathology, The Centre for Molecular Medicine and Therapeutics, BC
B. R. Leavitt
Affiliation:
Division of Neurology, Department of Medicine, The Centre for Molecular Medicine and Therapeutics, BC
S. D. Spacey
Affiliation:
Division of Neurology, Department of Medicine, The Centre for Molecular Medicine and Therapeutics, BC
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Abstract

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Background:

Although it is acknowledged that patients with celiac disease can develop neurological complications such as ataxia, the association of antigliadin antibodies in the etiology of sporadic ataxia and the usefulness of this testing in diagnosis of ataxia is controversial.

Methods:

We investigated this association by testing for the presence of IgG and IgA antigliadin antibodies in 56 ataxic patients and 59 controls. The ataxia patients were subsequently classified into three groups: sporadic, hereditary and MSA.

Results:

Of the total ataxic patients, 6/56 (11%) were positive for either IgG or IGA antigliadin antibodies compared to the controls of which 5/59 (8%) were positive (p = 0.68). In a subgroup analysis, 4/29 (14%) of the samples in the sporadic ataxic subgroup were positive for antigliadin antibodies (IgG or IgA) compared to control (p = 0.44). Similar negative results were found in the remaining subgroup analyses.

Conclusions:

These results do not support an association between antigliadin antibodies and sporadic ataxias.

Résumé:

RÉSUMÉ:Contexte:

Bien qu'il soit connu que les patients atteints de la maladie c?liaque peuvent présenter des complications neurologiques comme de l'ataxie, le rôle des anticorps antigliadine dans l'étiologie de l'ataxie sporadique et l'utilité de ce test dans le diagnostic de l'ataxie demeurent controversés.

Méthodes :

Nous avons étudié cette association chez 56 sujets ataxiques et 59 témoins chez qui nous avons vérifié la présence d'anticorps antigliadine IgG et IgA. Les patients ataxiques ont ensuite été répartis en trois groupes, selon qu'ils étaient atteints d'ataxie sporadique, héréditaire ou d'atrophie multisystémique.

Résultats :

Six des 56 patients ataxiques (11%) et 5 des 59 témoins (8%) avaient des anticorps antigliadine IgG ou IgA (p = 0,68). Une analyse de sous-groupes a montré que 4 des 29 patients atteints d'ataxie sporadique avaient des anticorps antigliadine (IgG ou IgA) par rapport aux témoins, p = 0,44. Des résultats négatifs ont également été obtenus lors de l'analyse des données des autres sous-groupes.

Conclusions :

Ces résultats ne sont pas en faveur d'une association entre les anticorps antigliadine et les ataxies sporadiques.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 34 , Issue 2 , May 2007 , pp. 193 - 196
Copyright
Copyright © The Canadian Journal of Neurological 2007

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