The Relationship Between Serum Mannose-Binding Lectin Levels and Acute Ischemic Stroke Risk

被引:23
作者
Wang, Zhen-Yu [1 ,2 ]
Sun, Zhong-Ren [2 ]
Zhang, Li-Ming [1 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 1, Harbin, Heilongjiang, Peoples R China
[2] Heilongjiang Univ Chinese Med, Coll Acupuncture Moxibust & Massage, Harbin 150009, Heilongjiang, Peoples R China
关键词
Acute ischemic stroke; Mannose-binding lectin; Chinese; Risk; CORONARY-ARTERY-DISEASE; REPERFUSION INJURY; INFLAMMATORY RESPONSE; COMPLEMENT ACTIVATION; VARIANT ALLELES; ASSOCIATION; GENE; ATHEROSCLEROSIS; POLYMORPHISMS; WOMEN;
D O I
10.1007/s11064-013-1214-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Complement activation and inflammation have been suggested in the pathogenesis of stroke, mannose-binding lectin (MBL) were found to have roles during the process. The aim of this study was to investigate the relationship between acute ischemic stroke (AIS) and serum MBL levels in Chinese population. From January 1 to June 30 2013, all patients with first-ever AIS were recruited to participate in the study. Serum MBL levels and routine test were examined. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to MBL levels. During the inclusion period, 148 patients with AIS were registered and completed study. The results indicated that the serum MBL levels were significantly (p < 0.0001) higher in acutely ischemic stroke patients as compared to normal controls [1,332; interquartile range (IQR) 996-2,134 mu g/L and 897; IQR 678-1,100 mu g/L, respectively]. There was a correlation between serum levels of MBL and NIHSS score [r (spearman) = 0.608, p < 0.0001). In multivariate analysis, serum MBL as a continuous variable was associated with an increased risk of AIS, after adjustment for above possible confounders (OR 1.002, 95 % CI 1.001-1.008; p < 0.0001). These results indicated that elevated MBL levels could be considered as an independent stroke risk factor in Chinese population, suggesting a role of MBL and the lectin pathway of complement activation in the pathogenesis of stroke.
引用
收藏
页码:248 / 253
页数:6
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