Ladenvall Claes, Jood Katarina, Blomstrand Christian, Nilsson Staffan, Jern Christina, Ladenvall Per
Institute of Neuroscience and Physiology, Department of Neuroscience and Rehabilitation, Sahlgrenska Academy at Göteborg University, Guldhedsgatan 19, S-413 45 Göteborg, Sweden.
Stroke. 2006 Aug;37(8):2018-23. doi: 10.1161/01.STR.0000231872.86071.68. Epub 2006 Jun 29.
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.
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.
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.
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.
C反应蛋白(CRP)已成为心血管疾病的一种炎症风险标志物。已发现CRP基因座的几个单核苷酸多态性与CRP水平相关。本研究的目的是调查缺血性卒中病因亚型中的CRP水平和基因变异。
瑞典哥德堡大学医学院缺血性卒中研究(SAHLSIS)纳入了600例连续的缺血性卒中病例(年龄18至69岁)以及来自瑞典西部的600例匹配对照。卒中亚型通过TOAST分类进行定义。血清CRP水平通过高敏免疫比浊法测定。
在急性期和3个月随访时,所有缺血性卒中亚型的CRP水平均显著高于对照组。在对传统风险因素进行校正后,随访时的CRP与总体缺血性卒中(比值比[OR],1.25;95%置信区间[CI],1.09至1.43)和大血管疾病(OR,1.48;9%CI,1.09至2.00)的较高比值比相关。CRP -286C>T>A、1059G>C和1444C>T单核苷酸多态性与CRP水平显著相关。然而,CRP基因型和单倍型均与总体缺血性卒中无关联。
这是首次在年轻缺血性卒中人群中针对不同TOAST亚型的CRP进行的大型研究。缺血性卒中病因亚型在急性期和3个月随访时的CRP水平存在差异。随访时的CRP与总体缺血性卒中和大血管疾病亚型相关。CRP基因座的基因变异与CRP水平相关,但未检测到与总体缺血性卒中的关联。