Article ID Journal Published Year Pages File Type
1967254 Clinica Chimica Acta 2008 5 Pages PDF
Abstract

BackgroundC-reactive protein, a proinflammatory factor, is involved in the development of atherosclerosis. The CRP 1059G>C polymorphism appeared to be a susceptive marker for atherosclerosis. We investigated the relationship of the distribution of cerebral atherosclerosis with triggered serum CRP concentrations following acute ischemic stroke/transient ischemic attack (IS/TIA) and CRP 1059G>C polymorphism.MethodsWe recruited 222 IS/TIA patients (122 with only intracranial atherosclerotic lesions and 100 with isolated extracranial atherosclerotic lesions) and 227 controls. Intra- and extracranial atherosclerotic lesions were determined by digital subtraction angiography. Serum CRP concentrations were measured by particle-enhanced immunonephelometry assay. CRP 1059G>C genotypes were obtained through PCR amplification and restriction enzyme digestion.ResultsCRP concentrations were significantly higher in intra- and extracranial groups than in controls. No significant difference was found in CRP concentrations between intra- and extracranial groups. The CRP 1059G>C single-nucleotide polymorphism did not influence CRP serum concentrations. CRP genotype and allele frequencies did not differ significantly between patients and controls. However, the frequencies of GC genotype and C allele were significantly higher in extracranial group than that in intracranial group. The GC individuals showed a higher risk of extracranial atherosclerosis compared with GG individuals (OR 3.41; 95%CI, 1.124–10.347; P = 0.030).ConclusionsSerum CRP is associated with cerebral atherosclerotic disease. CRP 1059G>C polymorphism is one possible genetic determinant for the difference between intra- and extracranial atherosclerosis.

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