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• W1984920803 abstract "We read with interest the Personal View by Hadjivassiliou and colleagues,1Hadjivassiliou M Sanders DA Grunewald RA Woodroofe N Boscolo S Aeschlimann D Gluten sensitivity: from gut to brain.Lancet Neurol. 2010; 9: 318-330Summary Full Text Full Text PDF PubMed Scopus (287) Google Scholar which focuses on neurological manifestations of gluten sensitivity. The article discusses the serological tests that can be used to help diagnose such manifestations. The authors emphasise the association between serum anti-transglutaminase-6 (TG6) antibodies and gluten ataxia,2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar an apparently sporadic ataxia with positive serological markers for gluten sensitivity.3Hadjivassiliou M Gibson A Davies-Jones GAB Lobo A Stephenson TJ Milford-Ward A Is cryptic gluten sensitivity an important cause of neurological illness?.Lancet. 1996; 347: 369-371Summary PubMed Scopus (300) Google ScholarIn our coeliac disease centre we have assessed about 650 patients, none of whom had gluten ataxia and, in our neurological institute, no case of sporadic ataxia has been ascribed to gluten sensitivity. However, we recently reported subclinical cerebellar, mostly ocular motor, signs in 16 of 42 patients with coeliac disease (as proven by a biopsy sample) who were on a gluten-free diet.4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar These patients did not, and still do not, have any cerebellar clinical symptoms. Cerebellar signs were not associated with patients' age or diet duration or compliance, and none of the sera samples collected at disease onset, when the patients were on gluten-containing diets, showed antibody reactivity against primate cerebellar tissue.4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google ScholarTo test whether antibodies to TG6 were associated with subclinical cerebellar involvement, we measured serum concentrations of both anti-TG6 IgG and IgA antibodies in these patients (the same sera of the previous study),4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar and in age-matched healthy controls. Mean (±SE) serum anti-TG6 IgG antibody concentrations in the whole group of patients with coeliac disease (39·9±9·5 U/mL) were higher than in healthy controls (16·2±2·1 U/mL; Mann-Whitney test, p=0·0016), but were not significantly different between patients with coeliac disease who had cerebellar signs (35·1±5·5 U/mL) and patients with coeliac disease without such signs (42·8±15·1 U/mL). These two groups of coeliac disease patients with or without cerebellar signs also showed similar frequency of positivity for anti-TG6 IgG antibodies (χ2 test, p=0·55), whereas this frequency in the whole group of patients with coeliac disease was higher than in healthy controls (Fisher test, p=0·001). Both mean values of serum anti-TG6 IgA antibody concentrations and the frequency of positivity for anti-TG6 IgA antibodies did not significantly differ in patients with coeliac disease with or without cerebellar signs and in healthy controls.These findings are in contrast to those of Hadjivassiliou and colleagues,1Hadjivassiliou M Sanders DA Grunewald RA Woodroofe N Boscolo S Aeschlimann D Gluten sensitivity: from gut to brain.Lancet Neurol. 2010; 9: 318-330Summary Full Text Full Text PDF PubMed Scopus (287) Google Scholar, 2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar who concluded that, in addition to HLA typing, anti-gliadin, and anti-TG2 antibodies, antibodies to TG6 might be useful markers to identify a subgroup of patients with gluten sensitivity who are likely to develop neurological manifestations. The main bias of our data, which prevents a thorough comparison with the findings from Hadjivassiliou and colleagues,2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar is the absence of gluten-sensitive neurological syndromes in our series. Nevertheless, our previously published findings support the much debated perception5Freeman HJ Neurological disorders in adult celiac disease.Can J Gastroenterol. 2008; 22: 909-911Crossref PubMed Scopus (53) Google Scholar that gluten sensitivity might affect cerebellar function,4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar albeit subclinically and with a possibly higher frequency than that of full gluten ataxia, while we suggest that anti-TG6 IgG antibodies, but not anti-TG6 IgA antibodies, could be used as markers of coeliac disease when the other autoantibodies usually associated with the disease are negative.We have no conflicts of interest. We read with interest the Personal View by Hadjivassiliou and colleagues,1Hadjivassiliou M Sanders DA Grunewald RA Woodroofe N Boscolo S Aeschlimann D Gluten sensitivity: from gut to brain.Lancet Neurol. 2010; 9: 318-330Summary Full Text Full Text PDF PubMed Scopus (287) Google Scholar which focuses on neurological manifestations of gluten sensitivity. The article discusses the serological tests that can be used to help diagnose such manifestations. The authors emphasise the association between serum anti-transglutaminase-6 (TG6) antibodies and gluten ataxia,2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar an apparently sporadic ataxia with positive serological markers for gluten sensitivity.3Hadjivassiliou M Gibson A Davies-Jones GAB Lobo A Stephenson TJ Milford-Ward A Is cryptic gluten sensitivity an important cause of neurological illness?.Lancet. 1996; 347: 369-371Summary PubMed Scopus (300) Google Scholar In our coeliac disease centre we have assessed about 650 patients, none of whom had gluten ataxia and, in our neurological institute, no case of sporadic ataxia has been ascribed to gluten sensitivity. However, we recently reported subclinical cerebellar, mostly ocular motor, signs in 16 of 42 patients with coeliac disease (as proven by a biopsy sample) who were on a gluten-free diet.4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar These patients did not, and still do not, have any cerebellar clinical symptoms. Cerebellar signs were not associated with patients' age or diet duration or compliance, and none of the sera samples collected at disease onset, when the patients were on gluten-containing diets, showed antibody reactivity against primate cerebellar tissue.4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar To test whether antibodies to TG6 were associated with subclinical cerebellar involvement, we measured serum concentrations of both anti-TG6 IgG and IgA antibodies in these patients (the same sera of the previous study),4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar and in age-matched healthy controls. Mean (±SE) serum anti-TG6 IgG antibody concentrations in the whole group of patients with coeliac disease (39·9±9·5 U/mL) were higher than in healthy controls (16·2±2·1 U/mL; Mann-Whitney test, p=0·0016), but were not significantly different between patients with coeliac disease who had cerebellar signs (35·1±5·5 U/mL) and patients with coeliac disease without such signs (42·8±15·1 U/mL). These two groups of coeliac disease patients with or without cerebellar signs also showed similar frequency of positivity for anti-TG6 IgG antibodies (χ2 test, p=0·55), whereas this frequency in the whole group of patients with coeliac disease was higher than in healthy controls (Fisher test, p=0·001). Both mean values of serum anti-TG6 IgA antibody concentrations and the frequency of positivity for anti-TG6 IgA antibodies did not significantly differ in patients with coeliac disease with or without cerebellar signs and in healthy controls. These findings are in contrast to those of Hadjivassiliou and colleagues,1Hadjivassiliou M Sanders DA Grunewald RA Woodroofe N Boscolo S Aeschlimann D Gluten sensitivity: from gut to brain.Lancet Neurol. 2010; 9: 318-330Summary Full Text Full Text PDF PubMed Scopus (287) Google Scholar, 2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar who concluded that, in addition to HLA typing, anti-gliadin, and anti-TG2 antibodies, antibodies to TG6 might be useful markers to identify a subgroup of patients with gluten sensitivity who are likely to develop neurological manifestations. The main bias of our data, which prevents a thorough comparison with the findings from Hadjivassiliou and colleagues,2Hadjivassiliou M Aeschlimann P Strigun A et al.Autoantibodies in gluten ataxia recognize a novel neuronal transglutaminase.Ann Neurol. 2008; 64: 332-343Crossref PubMed Scopus (205) Google Scholar is the absence of gluten-sensitive neurological syndromes in our series. Nevertheless, our previously published findings support the much debated perception5Freeman HJ Neurological disorders in adult celiac disease.Can J Gastroenterol. 2008; 22: 909-911Crossref PubMed Scopus (53) Google Scholar that gluten sensitivity might affect cerebellar function,4Versino M Franciotta D Colnaghi S et al.Cerebellar signs in celiac patients.Neurology. 2009; 72: 2046-2048Crossref PubMed Scopus (12) Google Scholar albeit subclinically and with a possibly higher frequency than that of full gluten ataxia, while we suggest that anti-TG6 IgG antibodies, but not anti-TG6 IgA antibodies, could be used as markers of coeliac disease when the other autoantibodies usually associated with the disease are negative. We have no conflicts of interest. Gluten sensitivity and the CNS: diagnosis and treatment – Authors' replyWe thank Versino and colleagues for their comments. They state that they regularly follow up patients in their coeliac disease centre but that none of them had gluten ataxia. This statement seems to be contrary to their publication1 reporting that, after detailed neurological examination in 42 of their patients with coeliac disease who were on a gluten-free diet, 16 (38%) had signs of cerebellar dysfunction. A gluten-free diet can improve or at least stabilise the ataxia and thus these patients, because of their gastrointestinal symptoms, might have been diagnosed with coeliac disease early and were probably treated before they developed symptomatic cerebellar dysfunction. Full-Text PDF" @default.
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