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(Stroke. 2006;37:2018.)
© 2006 American Heart Association, Inc.

Original Contributions

Serum C-Reactive Protein Concentration and Genotype in Relation to Ischemic Stroke Subtype

Claes Ladenvall, MSc; Katarina Jood, MD, PhD; Christian Blomstrand, MD, PhD; Staffan Nilsson, PhD; Christina Jern, MD, PhD Per Ladenvall, MD, PhD

From the Institute of Neuroscience and Physiology (C.L., K.J., C.B., C.J.), Sahlgrenska Academy at Göteborg University, Göteborg; the Department of Clinical Genetics (C.L., C.J.), Sahlgrenska University Hospital/Östra; the Arvid Carlsson Institute for Neuroscience (C.B.), Sahlgrenska Academy at Göteborg University, Göteborg; the Department of Mathematical Statistics (S.N.), Chalmers University of Technology, Göteborg, Sweden; and the Clinical Experimental Research Laboratory (P.L.), Institute of Medicine, Sahlgrenska Academy at Göteborg University, Göteborg, Sweden.

Correspondence to Claes Ladenvall, Institute of Neuroscience and Physiology, Department of Neuroscience and Rehabilitation, Sahlgrenska Academy at Göteborg University, Guldhedsgatan 19, S-413 45 Göteborg, Sweden. E-mail claes.ladenvall{at}neuro.gu.se

Background and Purpose— C-reactive protein (CRP) has evolved as an inflammatory risk marker of cardiovascular disease. Several single-nucleotide polymorphisms at the CRP locus have been found to be associated with CRP levels. The aim of the present study was to investigate CRP levels and genetic variants in etiological subtypes of ischemic stroke.

Methods— The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) comprises 600 consecutive ischemic stroke cases (18 to 69 years) and 600 matched controls from western Sweden. Stroke subtypes were defined by the TOAST classification. Serum CRP levels were determined by a high-sensitivity immunometric assay.

Results— CRP levels were significantly higher for all ischemic stroke subtypes compared with controls, both in the acute phase and at the 3-month follow-up. After adjustment for traditional risk factors, CRP at follow-up was related to higher odds ratios (ORs) of overall ischemic stroke (OR, 1.25; 95% CI, 1.09 to 1.43) and large-vessel disease (OR, 1.48; 95% CI, 1.09 to 2.00). The CRP –286C>T>A, 1059G>C, and 1444C>T single-nucleotide polymorphisms showed significant associations with CRP levels. However, neither CRP genotypes nor haplotypes showed an association to overall ischemic stroke.

Conclusions— This is the first large study on CRP in different TOAST subtypes in a young ischemic stroke population. CRP levels differed between etiological subtypes of ischemic stroke both in the acute phase and at the 3-month follow-up. CRP at follow-up was associated with overall ischemic stroke and the large-vessel disease subtype. Genetic variants at the CRP locus were associated with CRP levels, but no association was detected for overall ischemic stroke.

Key Words: C-reactive protein • polymorphism • genetics • stroke, ischemic • stroke classification

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