Brain, Vol. 126, No. 9, E4,
September 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg214
Letters to the Editor |
Gluten ataxia ‘in perspective’
1 Department of Neurology, Queens Medical Centre, Nottingham and 2 Department of Immunology, Southmead Hospital, Bristol, UK
Correspondence to: Adrian J. Wills. E-mail: adewills61{at}hotmail.com
The interesting concept of a gluten sensitive ataxia remains unproven (Hadjivassiliou et al., 2003
). We agree that the concept is worthy of consideration, but suggest more critical review of the data. Reasoning that antigliadin antibodies (AGA) seropositivity per se justifies the term ‘gluten sensitive’ is like regarding all VDRL-positive cases as having a spirochaete related neurosyphilis. ‘Gluten sensitivity’ should be reserved for cases where gluten withdrawal is followed by unequivocal, objective evidence of benefit (as is true in coeliac disease, and Dermatitis Herpetiformis). Thus far, a single abstract from an Association of British Neurologists meeting poster (describing a subjective non-blinded study) is offered to support the argument (Hadjivassiliou et al., 2002).
The authors own data shows that AGAs are very non-specific with up to 12% of normal healthy controls exhibiting AGA seropositivity (Hadjivassiliou et al., 2003). Hence, in any hospital clinic, AGA seropositives will be found in 
10% or more patients. It would be ill advised to, for example, screen patients with idiopathic lung fibrosis, labelling the AGA seropositive cases (who also happen to be HLA DQ2) as having ‘gluten lung syndrome’. Remember, HLA DQ2 is a very common HLA allele which is present in approximately one-third of UK Caucasians (as well as 72% of the ataxic group). Control studies to address whether AGA titres are simply higher in all DQ2 individuals are awaited.
Gluten enteropathy is found in 1% of the population (Cook et al., 2000), and an accepted higher incidence of 5% is found in other related conditions including type 1 insulin-dependant diabetes mellitus (IDDM). (Incidentally, this does not suggest that IDDM is directly caused by gluten sensitivity.) The claim here of gluten enteropathy in around one-quarter (12 of 54) of the seropositives with sporadic ataxia is astounding (Hadjivassiliou et al., 2003). From the original Sheffield group of ataxic cases, this equates to a prevalence for enteropathy of at least 9%, i.e. amongst the highest prevalence rates for gluten enteropathy yet reported.
Clearly, controlled studies by other groups are needed to ascertain whether the suprisingly high prevalence of gluten enteropathy reported here is confirmed in an unselected group of ataxic patients elsewhere. At the same time, studies can be conducted to determine whether AGA seropositivity reflects carriage of DQ2 in any study group or whether this is peculiar to ‘gluten ataxia’.
References
Cook HB, Burt MJ, Collett JA, Whitehead MR, Frampton CM, Chapman BA. Adult coeliac disease: prevalence and clinical significance. J Gastroenterol Hepatol 2000; 15: 1032–6.[CrossRef][Web of Science][Medline]
Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Kandler RH, Jarratt JA, Davies-Jones GA. Gluten ataxia and gluten neuropathy: the effect of a gluten-free diet [abstract]. J Neurol Neurosurg Psychiatry 2002; 72: 139.
Hadjivassiliou M, Grunewald R, Sharrack B, Sanders D, Lobo A, Williamson C, et al. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Brain 2003; 126: 685–91.
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