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Rheumatology Advance Access originally published online on February 8, 2006
Rheumatology 2006 45(5):646; doi:10.1093/rheumatology/kel034
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


LETTER TO THE EDITOR

ß2-Glycoprotein I IgA antibodies and ischaemic stroke: reply

T. Kahles, M. Humpich, M. Sitzer and E. Lindhoff-Last

University Hospital, Department of Neurology, JW Goethe University, Frankfurt/Main, Germany

Correspondence to: T. Kahles, University Hospital, Department of Neurology, JW Goethe University, Schleusenweg 2–16, ZNN, D-60528 Frankfurt/Main, Germany. E-mail: t.kahles{at}em.uni-frankfurt.de

SIR, We appreciate the interest of Staub et al. in our recent article [1] and welcome their comment. We apologize for not referring to their paper published in Arquivos de Neuropsyquiatria in 2003 [2], in which they analysed the frequency of different phospholipid antibodies and antibodies to heat-shock proteins in patients with ischaemic stroke. They reported significantly higher positive test results for heat-shock protein 65 IgG and anti-ß2-glycoprotein IgA in cases than in controls.

In accordance with our results, elevated titres of anti-ß2-glycoprotein IgA appear to be associated with ischaemic stroke. In our, study this was also the case after correction for multiple comparison. Additionally, we were able to show significantly higher titres of anti-phosphatidylserine IgG in patients with ischaemic stroke compared to healthy controls.

Moreover, we tested for an association of a broad panel of phospholipid antibodies within stroke subtypes with special regard to cryptogenic stroke. We found a trend for positivity for lupus anticoagulant and anti-phosphatidylinositol IgM in patients with cryptogenic stroke compared with those with a determined cause of stroke, which was not significant after modified Bonferroni correction for multiple comparison.

Establishing a causal link between cerebral ischaemia and elevated anti-ß2-glycoprotein IgA titres on the one hand and atheroma plaques containing ß-2-glycoprotein on the other hand requires at least the separation of strokes into their aetiological subtypes. Such a link remains to be elucidated.

However, we fully agree with Dr Staub and colleagues that anti-ß2-glycoprotein IgA is associated with ischaemic stroke. The results of our recent study may serve as the base for upcoming prospective studies, which should focus on the relevant phospholipid antibodies found to be associated.

The authors have declared no conflicts of interest.

References

  1. Kahles T, Humpich M, Steinmetz H, Sitzer M, Lindhoff-Last E. Phosphatidylserine IgG and beta-2-glycoprotein I IgA antibodies may be a risk factor for ischaemic stroke. Rheumatology 2005;44:1161–5.[Abstract/Free Full Text]
  2. Staub HL, Norman GL, Crowther T et al. Antibodies to the atherosclerotic plaque components beta-2-gycoprotein I and heat-shock proteins as risk factors for acute cerebral ischemia. Arq Neuropsyquiatr 2003;61:757–63.
Accepted 6 January 2006


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This Article
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