[1]陈璟,熊小檍,王鹏飞,等.CD36促进脑出血患者血肿吸收及其临床意义[J].第三军医大学学报,2015,37(08 ):792-796.
 Chen Jing,Xiong Xiaoyi,Wang Pengfei,et al.CD36 promotes hematoma absorption in patients with intracerebral hemorrhage and its clinical significance[J].J Third Mil Med Univ,2015,37(08 ):792-796.
点击复制

CD36促进脑出血患者血肿吸收及其临床意义(/HTML )
分享到:

《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
37卷
期数:
2015年第08期
页码:
792-796
栏目:
论著
出版日期:
2015-04-30

文章信息/Info

Title:
CD36 promotes hematoma absorption in patients with intracerebral hemorrhage and its clinical significance
作者:
陈璟熊小檍王鹏飞王艳春杨清武
第三军医大学新桥医院神经内科;威海市立医院神经内科
Author(s):
Chen Jing Xiong Xiaoyi Wang Pengfei Wang Yanchun Yang Qingwu

Department of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037; Department of Neurology, Weihai Municipal Hospital, Weihai, Shandong Province,264200, China

关键词:
脑出血血肿吸收炎症CD36神经功能缺损评分
Keywords:
intracerebral hemorrhage hematoma absorption inflammation CD36 neurologic deficit scores
分类号:
R341;R363.21;R743.34
文献标志码:
A
摘要:

目的      探讨CD36对脑出血患者血肿吸收及神经功能缺损的影响。      方法      选择2012年7月至2014年6月在第三军医大学新桥医院神经内科住院治疗的349例脑出血患者为研究对象,获得患者静脉全血后进行CD36突变筛查,在突变的35例患者中挑选出24例为基底节区出血的患者分入CD36缺陷组,同时在CD36正常的患者中挑选出24例基线水平一致的基底节区出血患者(CD36正常组),比较2组患者的血肿吸收、炎症变化及神经功能缺损评分。      结果      349例脑出血患者中筛选出35例CD36缺陷患者(10.03%)。2组患者的年龄、性别、入院时血肿体积、危险因素等基线水平差异无显著性(P>0.05)。发病7 d后CD36缺陷患者血肿吸收速率低于CD36正常患者[(22.4±2.4)% vs (44.8±5.1)% ,P<0.05],并且CD36缺陷患者炎症因子下降较CD36正常患者慢(P<0.05)。神经功能缺损评分显示CD36缺陷患者在第14、30、90天时显著高于CD36正常患者(P<0.05)。      结论      CD36可能在促进血肿吸收中具有重要作用进而影响患者的神经功能恢复。

Abstract:

Objective      To investigate the influence of CD36 in hematoma absorption and neurologic deficit scores (NDS) in the patients with intracerebral hemorrhage (ICH).        Methods      A total of 349 ICH patients treated in our department from July 2012 to June 2014 were selected as the research objects. Among them, 24 ICH patients with cerebral basilar hemorrhage were selected from 35 patients with CD36 mutation, and divided into CD36-deficiency group. Meanwhile, 24 CD36-normal ICH patients who had similar features with the CD36-deficency group were selected as the CD36-normal group. The hematoma absorption, inflammatory responses and NDS of the 2 groups were compared.       Results      Thirty-five patients (10.03%) with CD36 deficiency were screened from the 349 ICH patients. There were no significant differences in the age, gender, hematoma volume on admission, risk factors, and other baseline data between the 2 groups (P>0.05). On day 7 after ICH, the hematoma absorption of CD36-deficiency patients was significantly lower than that of CD36-normal patients (22.4%±2.4% vs 44.8%±5.1%, P<0.05), as well as the reduction rate of pro-inflammatory factors on day 14 after ICH (P<0.05). Moreover, on the days 14, 30 and 90 after ICH, the NDS of CD36-deficiency patients were higher than those of CD36-normal patients (P<0.05).       Conclusion      CD36 may play an important role in promoting the hematoma absorption and improving the NDS after ICH.

参考文献/References:

[1]Keep R F, Hua Y, Xi G. Intracerebral haemorrhage: mechanisms of injury and therapeutic targets[J]. Lancet Neurol, 2012, 11(8): 720-731.
[2]罗丹, 李芳芳, 王啸, 等. 自发性脑出血患者并发症的相关危险因素分析[J]. 第三军医大学学报, 2012, 34(14): 1438-1441.
[3]朱孔江, 徐广振, 杨辉. 小鼠脑出血模型血肿周围雌激素受体的表达[J]. 第三军医大学学报, 2013, 35(17): 1877-1879.
[4]Zhou Y, Wang Y, Wang J, et al. Inflammation in intracerebral hemorrhage: from mechanisms to clinical translation[J]. Prog Neurobiol, 2014, 115: 25-44.
[5]Mendelow A D, Gregson B A, Rowan E N, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial lobar intracerebral haematomas (STICH Ⅱ): a randomised trial[J]. Lancet, 2013, 382(9890): 397-408.
[6]Silverstein R L, Febbraio M. CD36, a scavenger receptor involved in immunity, metabolism, angiogenesis, and behavior[J]. Sci Signal, 2009, 2(72): re3.
[7]Silverstein R L. Inflammation, atherosclerosis, and arterial thrombosis: role of the scavenger receptor CD36[J]. Cleve Clin J Med, 2009, 76 Suppl 2: S27-S30.
[8]Zhao X, Sun G, Zhang J, et al. Hematoma resolution as a target for intracerebral hemorrhage treatment: role for peroxisome proliferator-activated receptor gamma in microglia/macrophages[J]. Ann Neurol, 2007, 61(4): 352-362.
[9]Sansing L H, Harris T H, Welsh F A, et al. Toll-like receptor 4 contributes to poor outcome after intracerebral hemorrhage[J]. Ann Neurol, 2011, 70(4): 646-656.
[10]Fang H, Chen J, Lin S, et al. CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling[J]. J Immunol, 2014, 192(12): 5984-5992.
[11]Steiner T, Kaste M, Forsting M, et al. Recommendations for the management of intracranial haemorrhage—part I: spontaneous intracerebral haemorrhage. The European Stroke Initiative Writing Committee and the Writing Committee for the EUSI Executive Committee[J]. Cerebrovasc Dis, 2006, 22(4): 294-316.
[12]Gao L, Zhao H, Liu Q, et al. Improvement of hematoma absorption and neurological function in patients with acute intracerebral hemorrhage treated with Xueshuantong[J]. J Neurol Sci, 2012, 323(1/2): 236-240.
[13]Aitman T J. CD36, insulin resistance, and coronary heart disease[J]. Lancet, 2001, 357(9257): 651-652.
[14]李大成, 蓝欲晓, 鲍自谦, 等. 深圳地区无偿献血者群体CD36抗原缺失型的表型分析[J]. 中国输血杂志, 2012, 25(4): 304-307.
[15]刘凌, 叶刚强, 李流娇, 等. 肇庆地区普通人群血小板基因HPA1-6和15基因多态性及CD36抗原缺失分析[J]. 广东医学,  2013, 34(13): 2054-2056.
[16]Li R, Qiao Z, Ling B, et al. Incidence and molecular basis of CD36 deficiency in Shanghai population[J]. Transfusion, 2015, 55(3): 666-673.
[17]Xu X, Ye X, Xia W, et al. Studies on CD36 deficiency in South China: two cases demonstrating the clinical impact of anti-CD36 antibodies[J]. Thromb Haemost, 2013, 110(6): 1199-1206.

更新日期/Last Update: 2015-04-20