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Neurological dysfunction in coeliac disease and non-coeliac gluten sensitivity

Hadjivassiliou, Marios, Rao, Dasappaiah G., Grünewald, Richard A., Sarrigiannis, Ptolemaios G., Aeschlimann, Daniel P., Hoggard, Nigel, Aeschlimann, Pascale, Mooney, Peter D. and Sanders, David D. 2016. Neurological dysfunction in coeliac disease and non-coeliac gluten sensitivity. The American Journal of Gastroenterology 111 (4) , pp. 561-567. 10.1038/ajg.2015.434

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Abstract

Objectives: Non-coeliac gluten sensitivity (NCGS) refers to patients with primarily gastrointestinal symptoms without enteropathy that symptomatically benefit from gluten-free diet (GFD). Little is known about its pathophysiology, propensity to neurological manifestations and if these differ from patients with coeliac disease (CD). We investigated the clinical and immunological characteristics of patients presenting with neurological manifestations with CD and those with NCGS. Methods: We compared clinical, neurophysiological and imaging data of patients with CD and NCGS presenting with neurological dysfunction assessed and followed up regularly over a period of 20 years. Results: 562 out of 700 patients were included. Exclusion criteria included no bowel biopsy to confirm CD, no HLA type available and failure to adhere to GFD. All patients presented with neurological dysfunction and had circulating anti-gliadin antibodies. Out of 562 patients, 228 (41%) had evidence of enteropathy (Group 1, CD), and 334 (59%) did not (Group 2, NCGS). The commonest neurological manifestations were cerebellar ataxia, peripheral neuropathy and encephalopathy. The severity of ataxia and response to GFD did not differ between the 2 groups. Patients in Group 1 had more severe neuropathy. TG2 antibodies were found in 91% in Group 1 and in 29% in group 2. Comparison between those patients in Group 2 with HLA DQ2/DQ8 and those without, as well as those with positive TG2 compared with those with negative TG2 antibodies identified no differences within these subgroups. Serological positivity for TG6 antibodies was similar in the 2 groups (67% and 60%). Conclusions: The neurological manifestations of CD and NCGS are similar and equally responsive to a GFD suggestive of common pathophysiological mechanisms.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Dentistry
Subjects: R Medicine > R Medicine (General)
R Medicine > RC Internal medicine > RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry
R Medicine > RZ Other systems of medicine
Publisher: Nature Publishing Group
ISSN: 0002-9270
Date of First Compliant Deposit: 30 March 2016
Date of Acceptance: 17 December 2015
Last Modified: 28 May 2019 12:35
URI: http://orca.cf.ac.uk/id/eprint/84156

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