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目的:探索血清CXCL16和Lp-PLA2水平与缺血性脑卒中颈动脉易损斑块的关系。方法:选取2013-08-2014-08月住院的128例缺血性脑卒中患者作为病例组,其中大动脉粥样硬化型(LAA)84例,小动脉闭塞型(SAA)44例;对照组为同期性别、年龄与病例组匹配的128例健康体检者。检测空腹血糖、血脂、LpPLA2、CXCL16等,并记录缺血性脑卒中类型、颈动脉斑块分型。结果:LAA组与对照组血清CXCL16和LpPLA2水平差异有统计学意义(P<0.05);SAA组与对照组血清CXCL16和Lp-PLA2水平差异无统计学意义(P>0.05);LAA组与SAA组血清CXCL16及Lp-PLA2差异有统计学意义(P<0.05)。无斑块组、稳定性斑块组、易损斑块组中,血清CXCL16水平及Lp-PLA2水平呈逐渐递升的趋势,且对照组与稳定斑块组、对照组与易损斑块组之间,CXCL16[0.82(0.58,1.19)vs 1.16(0.69,2.42)vs 1.36(0.79,2.04)]及Lp-PLA2[(7.71±2.89)vs(11.59±3.97)vs(13.13±3.38)]差异有统计学意义(P<0.05),而对照组与无斑块组差异无统计学意义(P>0.05);与无斑块组相比:稳定斑块组、易损斑块组,血清CXCL16及Lp-PLA2含量明显上调;稳定斑块组与易损斑块组相比:随着斑块易损性的增加,血清CXCL16及Lp-PLA2水平升高,2组差异有统计学意义(P<0.05)。分析颈动脉斑块直径与CXCL16及Lp-PLA2的相关性未发现明显统计学意义。使用CXCL16+Lp-PLA2联合诊断的诊断效能最高,ROC曲线下面积为0.885,95%CI为0.806~0.964。结论:血清CXCL16、Lp-PLA2水平可作为缺血性脑卒中的患病风险的评估指标,CXCL16、Lp-PLA2水平在LAA患者水平更高;CXCL16、Lp-PLA2水平升高与颈动脉斑块的易损性相关,在区分稳定斑块及易损斑块中具有一定临床意义。
Objective: To explore the relationship between serum CXCL16 and Lp-PLA2 levels and vulnerable carotid plaques in ischemic stroke. Methods: A total of 128 patients with ischemic stroke who were admitted to hospital from January 2013 to August 2014 were enrolled in the study. Among them, 84 cases were large atherosclerosis (LAA) and 44 cases were small artery occlusion (SAA). The control group was The same period of gender, age and case matched 128 cases of healthy people. Fasting blood glucose, blood lipids, LpPLA2 and CXCL16 were detected. The types of ischemic stroke and carotid plaque were recorded. Results: Serum levels of CXCL16 and LpPLA2 in LAA group and control group were significantly different (P <0.05). There was no significant difference in serum CXCL16 and Lp-PLA2 levels between SAA group and control group (P> 0.05) The serum CXCL16 and Lp-PLA2 difference was statistically significant (P <0.05). CXCL16 level and Lp-PLA2 level in the no-plaque group, the stable plaque group and the vulnerable plaque group showed a gradual increasing trend, and the control group and the stable plaque group, the control group and the vulnerable plaque group There was significant difference between CXCL16 [0.82 (0.58,1.19) vs 1.16 (0.69,2.42) vs 1.36 (0.79,2.04)] and Lp-PLA2 [(7.71 ± 2.89) vs (11.59 ± 3.97) vs (13.13 ± 3.38) (P <0.05), but there was no significant difference between control group and no plaque group (P> 0.05). Compared with no plaque group, stable plaque group, vulnerable plaque group, serum CXCL16 and Lp-PLA2 content was significantly increased; stable plaque group and vulnerable plaque group: with the increase of plaque vulnerability, serum CXCL16 and Lp-PLA2 levels increased, the difference between the two groups was statistically significant (P < 0.05). Analysis of carotid plaque diameter and CXCL16 and Lp-PLA2 no significant correlation was found. The diagnostic efficacy of the combination of CXCL16 + Lp-PLA2 was highest, with an area under the ROC curve of 0.885 and a 95% CI of 0.806 to 0.964. Conclusions: Serum levels of CXCL16 and Lp-PLA2 can be used as risk factors for ischemic stroke. The levels of CXCL16 and Lp-PLA2 are higher in patients with LAA. The levels of CXCL16 and Lp-PLA2 are significantly correlated with carotid plaques Vulnerability of the plaque in the distinction between stable and vulnerable plaques in a certain clinical significance.