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Serum C-reactive protein concentration and genotype in relation to ischemic stroke subtype

Journal article
Authors Claes Ladenvall
Katarina Jood
Christian Blomstrand
Staffan Nilsson
Christina Jern
Per Ladenvall
Published in Stroke
Volume 37
Issue 8
Pages 2018-23
ISSN 00392499
Publication year 2006
Published at Cardiovascular Institute
Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Department of Mathematical Sciences, Mathematical Statistics
Pages 2018-23
Language en
Keywords Adult, Aged, Brain Ischemia/*blood/complications/*genetics, C-Reactive Protein/*genetics/*metabolism, Case-Control Studies, Cerebral Infarction/blood/etiology/physiopathology, Cerebrovascular Accident/*blood/classification/*genetics, Genotype, Haplotypes, Humans, Middle Aged, Osmolar Concentration, *Variation (Genetics)
Subject categories Dermatology and Venereal Diseases


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.

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