Inflammatory Marker Expression and Its Implication in Korean Ischemic Stroke Patients.
10.3343/kjlm.2007.27.3.197
- Author:
Su Yon PARK
1
;
Meoung Hee KIM
;
So Young KANG
;
Jin Tae SUH
;
Woo In LEE
Author Information
1. Department of Laboratory Medicine, Kyunghee Medical Center, Kyunghee University, College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Ischemic stroke;
Inflammatory markers;
ApoE polymorphism
- MeSH:
Aged;
Apolipoproteins E/*genetics;
Biological Markers/blood;
Brain Ischemia/complications/*diagnosis;
C-Reactive Protein/analysis;
Carotid Artery Diseases/complications;
Female;
Genotype;
Humans;
Inflammation Mediators/*blood;
Korea;
Male;
Matrix Metalloproteinase 9/blood;
Middle Aged;
Polymorphism, Genetic;
Stroke/*diagnosis/etiology/immunology;
Tissue Inhibitor of Metalloproteinase-1/blood
- From:The Korean Journal of Laboratory Medicine
2007;27(3):197-204
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Ischemic stroke is a complex condition influenced by many factors. Previous studies have demonstrated that inflammatory markers might play a role in such vascular diseases. Therefore the purpose of this study was to compare the expression of inflammatory markers in Korean ischemic stroke patients and to investigate their relationship to APOE polymorphism. METHODS: The patient group consisted of 275 patients with large artery atherosclerosis (LAA, n=169) and small artery occlusion (SAO, n=106). One hundred and nineteen age matched healthy subjects were recruited as the control group. Serum levels of three inflammatory markers (matrix metalloproteinase, MMP-9; tissue inhibitor of metalloproteinase-1, TIMP-1; and high-sensitivity C-reactive protein, hs-CRP) were measured in each patient by using commercially available kits. Comparison of clinical risk factors, inflammatory marker levels, and APOE genotypes between the stroke patient group and control group and between the two patient subgroups was assessed. RESULTS: Comparison of the stroke group to control group showed significantly elevated levels of circulating MMP-9 (P<0.01) and hs-CRP (P=0.01). Comparison between the individual subgroups revealed a significantly higher level of only TIMP-1 in the LAA subgroup compared to the SAO subgroup (P<0.01). There was no significant difference in inflammatory marker levels among each allele carrier. CONCLUSIONS: The present study revealed the obvious tendency of increased circulating inflammatory markers in the patients with acute ischemic attack, especially MMP-9 and hs-CRP. Our observations suggest that measurement of serum MMP-9, TIMP-1, and hs-CRP levels may be useful in the diagnosis of ischemic stroke patients.
