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Journal of Neurology

, Volume 249, Issue 10, pp 1391–1397 | Cite as

Evaluation of the interactions of common genetic mutations in stroke subtypes

  • Zoltán Szolnoki
  • Ferenc Somogyvári
  • András Kondacs
  • Mihály Szabó
  • Lajos Fodor
ORIGINAL COMMUNICATION

Abstract.

Objective: Ischemic stroke is a frequent heterogeneous multifactorial disease that is affected by several genetic mutations and environmental factors. We hypothesised the clinical importance of the co-occurrence of common, unfavorable genetic mutations in the development of different stroke subtypes. Method and material: The Factor V Leiden G1691A (Leiden V), the prothrombin G20210A and the methylenetetrahydrofolate reductase C677T (MTHFR C677T) mutations and the angiotensin-converting enzyme I/D (ACE I/D) and apolipoprotein E (APOE) genotypes were examined by the PCR technique in 689 ischemic stroke patients and 652 stroke-free controls. Logistic regression models were used to estimate the relative risks of different stroke subtypes for different genotype combination patterns. Results: The ACE D/D genotype alone or in combination with the MTHFR 677T or the APOE 4 allele or with both was highly specific for small-vessel infarction. The Leiden V mutation alone or in different combination patterns with the ACE D, APOE 4 and MTHFR 677T alleles was specifically predisposed to large-vessel infarction. The APOE 4 allele alone was calculated to be a general, minor genetic risk factor for ischemic stroke. The MTHFR 677T allele alone was not a risk factor for any stroke subtype. In the different specific predisposition gene combinations, however, both the APOE 4 and MTHFR 677T alleles could increase the relative risk of the given stroke subgroup. Conclusions: Common mutations which alone are minor or non-significant risk factors for ischemic stroke can yield, in specific combination patterns, a highly significant, moderate genetic risk of specific stroke subtypes.

Key words stroke genetics risk factors genetic interactions 

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Copyright information

© Steinkopff Verlag 2002

Authors and Affiliations

  • Zoltán Szolnoki
    • 1
  • Ferenc Somogyvári
    • 2
  • András Kondacs
    • 3
  • Mihály Szabó
    • 3
  • Lajos Fodor
    • 2
  1. 1.H-5600 Békéscsaba, Pipacs köz 9, Hungary. szolnoki99@hotmail.comHU
  2. 2.Central Laboratory, Pándy Kálmán County Hospital, Gyula, HungaryHU
  3. 3.Department of Neurology and Neurophysiology, Pándy Kálmán County Hospital, H-5700 Gyula, Semmelweis 1, HungaryHU

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