ORIGINAL CONTRIBUTIONS: SMALL BOWEL

Neurological Dysfunction in Coeliac Disease and Non-Coeliac Gluten Sensitivity

Hadjivassiliou, Marios MD1; Rao, Dasappaiah G MD1; Grìnewald, Richard A DPhil1; Aeschlimann, Daniel P PhD2; Sarrigiannis, Ptolemaios G MD1; Hoggard, Nigel MD3; Aeschlimann, Pascale BSc3; Mooney, Peter D MD4; Sanders, David S MD4

Author Information

1Academic Department of Neurosciences, Royal Hallamshire Hospital, Sheffield, UK

2Matrix Biology and Tissue Repair Research Unit, College of Biomedical and Life Sciences, School of Dentistry, Cardiff University, Cardiff, Wales, UK

3Academic Department of Neuroradiology, Royal Hallamshire Hospital, Sheffield, UK

4Department of Gastroenterology, Royal Hallamshire Hospital, Sheffield, UK

Correspondence: Marios Hadjivassiliou, MD, Academic Department of Neurosciences, Royal Hallamshire Hospital, Glossop Road, Sheffield S10 2JF, UK. E-mail: [email protected]

Received 13 October 2015; accepted 17 December 2015

Guarantor of the article: Marios Hadjivassiliou, MD.

Specific author contributions: Marios Hadjivassiliou, Richard A. Grìnewald, and David S. Sanders collected the data over the past 20 years. Marios Hadjivassiliou analyzed the data and produced the first draft. Dasappaiah G. Rao and Ptolemaios G. Sarrigiannis reviewed the neurophysiologal assessments. Nigel Hoggard reviewed all the brain imaging. Peter D. Mooney and David S. Sanders performed all the gastroscopies and biopsies. Daniel P. Aeschlimann and Pascale Aeschlimann performed all the TG6 assays. Richard A. Grìnewald was responsible for all the statistical analysis. All authors read and critically revised the manuscript and approved the final version.

Financial support: This work was funded by BRET, Coeliac UK, Ataxia UK.

Potential competing interests: None.

American Journal of Gastroenterology 111(4):p 561-567, April 2016. | DOI: 10.1038/ajg.2015.434

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: 

Out of 700 patients, 562 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 most common neurological manifestations were cerebellar ataxia, peripheral neuropathy, and encephalopathy. There was a greater proportion of patients with encephalopathy in Group 1 and with a greater proportion of neuropathy in Group 2. The severity of ataxia did not differ between the two groups. Patients in Group 1 had more severe neuropathy. All patients from both groups responded to gluten-free diet. Anti-tissue transglutaminase (TG2) antibodies were found in 91% of patients in Group 1 and in 29% of patients 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 two 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.

© The American College of Gastroenterology 2016. All Rights Reserved.

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