Prevalence of antigliadin antibodies in ataxia patients

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_0.001 unpublished="unpublished" results.="results." p="p"/>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 ataxiaâ€�. [3,5]

The results of Abele and coworkers further show that AGA positivity does not distinguish “gluten ataxiaâ€� 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.