Prof. Natan M. Bornstein, MD, Department of Neurology, Tel-Aviv Sourasky Medical Center, 6 Weizman Street, Tel Aviv 64239, Israel (tel.: +972-3-6973159; fax: +972-3-6973146; e-mail: [email protected]).

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Abstract

C-reactive protein (CRP) increases following an acute stroke/transient ischemic attack (TIA), but the increment level varies among patients. We analyzed CRP concentrations during an acute stroke/TIA in relation to the CRP gene −717A>G polymorphism. Six months following an acute ischemic stroke/TIA, basal concentrations of CRP were measured in 507 controls and 219 patients and were found to be unassociated with the CRP −717A>G polymorphism. However, during the acute phase of stroke/TIA, individuals with the AG/GG genotype had significantly elevated CRP concentrations as opposed to those with the AA genotype (2.02 ± 1.59 vs. 1.73 ± 1.69 mg/l, P = 0.027). In addition, significant 3.22-fold increments in CRP concentrations was noted in individuals carrying the −717G allele when comparing the acute phase with the basal state of each patient and averaging the results. CRP −717A>G polymorphism is associated with triggered CRP concentrations during acute stroke/TIA. These findings might shed more light on the mechanisms of CRP elevation in acute ischemic stroke/TIA.

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Volume14, Issue3

March 2007

Pages 315-320

Triggered C-reactive protein (CRP) concentrations and the CRP gene −717A>G polymorphism in acute stroke or transient ischemic attack

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Triggered C-reactive protein (CRP) concentrations and the CRP gene −717A>G polymorphism in acute stroke or transient ischemic attack

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