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BRIEF COMMUNICATIONS: M. Abele, L. Schöls, S. Schwartz, and T. Klockgether Prevalence of antigliadin antibodies in ataxia patients Neurology 2003; 60: 1674-1675 [Abstract] [Full text] [PDF]

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Prevalence of antigliadin antibodies in ataxia patients

Khalaf Bushara, Mark Hallett   (28 October 2003)

Reply to Bushara and Hallett

Thomas Klockgether, Michael Abele   (28 October 2003)

Prevalence of antigliadin antibodies in ataxia patients 28 October 2003
Khalaf Bushara, Minneapolis VA Medical center Neurology service (127), 1 Veterans Drive, MN 55417, Mark Hallett Send Correspondence to journal: Re: Prevalence of antigliadin antibodies in ataxia patients busha001{at}umn.edu Khalaf Bushara, et al.	We read with interest the article by Abele et al that reported no significant increase in antigliadin antibodies (AGA) in hereditary or sporadic cerebellar ataxia. [1] Although the study found that the prevalence of AGA positivity in both hereditary and sporadic cerebellar ataxia was about double that in normal controls, the difference was not statistically significant. Their results confirm our findings of generally equal prevalence of AGA in hereditary and sporadic ataxia. [2] The difference between Abele’s finding and ours can be explained by the type of patients screened. For example, they studied only two patients with SCA2, both were AGA-negative. We screened five patients with SCA 2 (from five different families) and all were AGA-positive. We have now screened more patients with SCA2. Thus far, 60 % (12 of 20) SCA2 patients were AGA-positive. This is significant when compared to 12% AGA positivity (4/33) in normal volunteers (CI= 95, X2=13.5, p<0.001) (unpublished results). Other groups found similar results in SCA2 (S. Boesch, personal communications). Hadjivassiou et al screened 268 ataxia patients and found a significantly high prevalence of AGA only in sporadic ataxia. [3] However, their sample of autosomal dominant ataxia contained only three patients with SCA2, two with SCA6 and one with SCA7. Thus, it is likely that only certain SCA types are associated with AGA positivity which makes the comparison between different studies difficult as different groups screened cohorts with different SCA types. Further studies of larger number of ataxia patients are needed to clarify the current discrepancies and to determine the prevalence of AGA in different SCA types. Molecularly diagnosed hereditary ataxias are likely to be the most revealing group to study. Sporadic ataxia cohorts are likely to contain a mixture of various ataxia types with negative family history including unlinked recessive hereditary ataxias, hereditary ataxias with de novo mutations including false paternity. [4] High IgG or IgA AGA in patients with sporadic ataxia should not be interpreted to indicate that these patients have a distinct disease entity or “gluten ataxia”. [3,5] The results of Abele and coworkers further show that AGA positivity does not distinguish “gluten ataxia” from other ataxia types including molecularly characterized hereditary ataxias. References 1. Abele M, Schols L, Schwartz S, Klockgether T. Prevalence of antigliadin antibodies in ataxia patients. Neurology 2003;60:1674- 1675. 2. Bushara KO, Goebel SU, Shill H, Goldfarb LG, Hallett M. Gluten sensitivity in sporadic and hereditary cerebellar ataxia. Ann Neurol 2001;49:540-543. 3. 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(Pt 3):685-691. 4. Moseley ML, Benzow KA, Schut LJ, Bird TD, Gomez CM, Barkhaus PE, et al. Incidence of dominant spinocerebellar and Friedreich triplet repeats among 361 ataxia families. Neurology 1998;51:1666-1671. 5. Hadjivassiliou M, Grunewald RA, Chattopadhyay AK, Davies-Jones GA, Gibson A, Jarratt JA, et al. Clinical, radiological, neurophysiological, and neuropathological characteristics of gluten ataxia. Lancet 1998;352:1582-1585.
Reply to Bushara and Hallett 28 October 2003
Thomas Klockgether, Department of Neurology, University Bonn Sigmund-Freud-Str. 25, 53105 Bonn, Germany, Michael Abele Send Correspondence to journal: Re: Reply to Bushara and Hallett klockgether{at}uni-bonn.de Thomas Klockgether, et al.	We appreciate Dr. Bushara and Dr. Hallett's comments. We agree that their data and our data show a roughly equal prevalence of antigliadin antibodies in hereditary and sporadic ataxia patients. However, their study did not include a control group which makes a meaningful interpretation of the data difficult. [2] Further studies of larger cohorts of patients with genetically defined ataxias might clarify existing discrepancies concerning the prevalence of antigliadin antibodies, but will probably not contribute very much to the understanding of these diseases.