Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 2009;40:e24
Published online before print December 18, 2008, doi: 10.1161/STROKEAHA.108.540062
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
40/2/e24    most recent
STROKEAHA.108.540062v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Grond-Ginsbach, C.
Right arrow Articles by Reuner, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grond-Ginsbach, C.
Right arrow Articles by Reuner, K.

(Stroke. 2009;40:e24.)
© 2009 American Heart Association, Inc.


Letters to the Editor

No Association of the Plasma Glutathione Peroxidase (GPx-3) Gene With Cerebral Venous Thrombosis in the German Population

Caspar Grond-Ginsbach, PhD; Marie-Luise Arnold, PhD Christoph Lichy, MD

Deparment of Neurology, University of Heidelberg, Heidelberg, Germany

Armin Grau, MD

Department of Neurology, Klinikum der Stadt Ludwigshafen, Ludwigshafen, Germany

Karl Reuner, MD

Institut für Labormedizin, Kassel, Germany


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

To the Editor:

In a recent publication in Stroke, cerebral venous thrombosis (CVT) was found to be associated with a variant of the plasma glutathione peroxidase (GPx-3) gene (promoter haplotype H2).1 The observed association was strong (OR >10) and highly significant (P<0.0001). However, the number of analyzed patients was small (n=23) and the findings were not confirmed in an independent study population. We analyzed 79 patients with nonseptic CVT and 203 healthy control subjects and sought to confirm the association between GPx-3 and CVT. Our study groups were characterized in detail elsewhere.2 We tagged haplotype H2 with SNP rs1946235 (this is polymorphism –927 T/C in the study of Voetsch et al1) as described before.3 The C allele of rs1946235 identifies haplotype H2, as well as the rare (<1% in our population) haplotypes H7 and H8.

In our series of healthy control subjects, we found 3 homozygous and 52 heterozygous carriers of haplotype H2. The frequency of H2 in this control series is therefore 14.3%. In the patients group we found one homozygous and 17 heterozygous carriers of haplotype H2 (estimated frequency of H2=12.0%). Comparison of the H2 frequencies in the 2 study groups by {chi}2 testing revealed that the difference was not significant (P=0.48).

In an additional series of 500 healthy German control persons, we genotyped SNP rs1946235 and found 11 CC, 112 CT and 377 TT, which corresponds to an estimated H2 frequency of 13.4%.

Our findings . . . [Full Text of this Article]