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急性脑梗死后脾脏体积的变化及其与免疫炎性反应和血小板反应性的关系 被引量:10

The change of spleen volume after acute cerebral infarction and its relationship with inflammatory response and platelet reactivity
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摘要 目的观察急性脑梗死患者发病后脾脏体积的变化,探讨脾脏体积与血小板反应性、炎性因子水平和淋巴细胞亚群数量的关系。方法收集2017年1—6月于威海市立医院神经内科住院的急性脑梗死患者30例,分别于发病24 h内、48 h以及4、7 d时检测脾脏体积、阿司匹林治疗后花生四烯酸诱导的血小板最大聚集率(AA-MAR)、干扰素-γ、淋巴细胞亚群。选取基础资料匹配的非急性脑梗死患者20例作为对照组,于入院时检测上述指标作为基线数据。比较不同时间点的脾脏体积、AA-MAR、干扰素-γ、淋巴细胞亚群的变化。采用Pearson相关分析检测血小板反应性、炎性因子水平、淋巴细胞亚群与脾脏体积的关系。结果与对照组[(120.12±10.28) cm^3]相比,急性脑梗死患者发病24 h内[(117.48±7.93) cm^3]和发病48 h[(111.61±9.21) cm^3]的脾脏体积均显著缩小(t=-2.142, P〈0.05;t=-2.790,P〈0.01),发病4 d[(121.31±8.16) cm^3]和7 d[(126.11±10.31) cm^3]的脾脏体积均显著增大(t=2.242, P〈0.05;t=2.762, P〈0.01),4个时间点的脾脏体积变化整体呈先缩小再增大的双相趋势。与对照组相比,急性脑梗死患者上述4个时间点AA-MAR水平(对照组:20.97%±8.21%;24 h内:31.86%±9.54%, t=3.165, P〈0.01;48 h:41.38%±8.55%,t=3.254, P〈0.01;4 d:35.34%±8.15%, t=3.203,P〈0.01;7 d:29.38%±10.46%,t=2.494,P〈0.05)和干扰素-γ水平(pg/L,对照组:15.21±5.21;24 h内:29.75±4.57,t=3.262,P〈0.01;48 h:43.37±12.15,t=3.304,P〈0.01;4 d:40.44±9.86, t=3.291,P〈0.01;7 d:20.93±5.51, t=2.417,P〈0.05)均显著升高,AA-MAR水平以发病48 h最高,干扰素-γ水平以发病4 d最高;与对照组相比,急性脑梗死患者4个检测时间点的T4、B和自然杀伤淋巴细胞水平均显著升高,总体均呈现逐渐升高趋势,T8淋巴细胞水平在4个时间点的变化差异无统计学意义。急性脑梗死患者发病24 h内、48 h、4 d的AA-MAR(r=-0.397,P〈0.05;r=-0.515,P〈0.01;r=-0.382,P〈0.05)和干扰素-γ(r=-0.408,P〈0.05;r=-0.479,P〈0.01;r=-0.378,P〈0.05)与脾脏体积均存在负相关,急性脑梗死患者发病24 h内和发病48 h的T4、B和自然杀伤淋巴细胞与脾脏体积均存在负相关。结论急性脑梗死后患者脾脏体积呈缩小再增大趋势,血小板反应性、炎性因子水平、淋巴细胞亚群水平均与脾脏的体积具有相关性,脾脏可能通过释放血小板、炎性因子和淋巴细胞加剧了缺血性脑损伤。 ObjectiveTo observe the changes of spleen volume in patients with acute cerebral infarction, and to explore the relationship between the spleen volume and platelet reactivity, inflammatory factors' lymphocyte subsets.MethodsThis is a case control study. Thirty patients with acute cerebral infarction from January 2017 to June 2017 in Department of Neurology, Weihai Municipal Hospital were included. The spleen volume, arachidonic acid-induced maximum platelet aggregation ratio (AA-MAR), interferon gamma (IFN-γ) and lymphocyte subsets of patients were monitored in 24 hours of stroke, at 48 hours of stroke, at four days of stroke and at seven days of stroke. Twenty patients without acute cerebral infarction with the same baseline data were selected as the control group, to determine the baseline of spleen volume, AA-MAR, IFN-γ and lymphocyte subsets. A t test was used to describe the changes of spleen volume, AA-MAR, IFN-γ and lymphocyte subsets at different time points, and Pearson's correlation analysis was used to estimate the relationship between the spleen volume and these variables.ResultsCompared with the control group ((120.12±10.28) cm^3), the patients with acute cerebral infarction in 24 hours of stroke ((117.48±7.93) cm^3) and at 48 hours of stroke ((111.61±9.21) cm^3) had smaller spleen volume (t=-2.142, P〈0.05; t=-2.790, P〈0.01), whereas at four days ((121.31±8.16) cm3) and seven days of stroke ((126.11±10.31) cm^3) had bigger spleen volume (t=2.242, P〈0.05; t=2.762, P〈0.01), with the spleen volume decreased first and increased later. Compared with the control group, the patients with acute cerebral infarction had more AA-MAR (control group: 20.97%±8.21%; 24 h: 31.86%±9.54%, t=3.165, P〈0.01; 48 h: 41.38%±8.55%, t=3.254, P〈0.01; 4 d: 35.34%±8.15%, t=3.203, P〈0.01; 7 d: 29.38%±10.46%, t=2.494, P〈0.05) and IFN-γ(pg/L, control group: 15.21±5.21; 24 h: 29.75±4.57, t=3.262, P〈0.01; 48 h: 43.37±12.15, t=3.304, P〈0.01; 4 d: 40.44±9.86, t=3.291, P〈0.01; 7 d: 20.93±5.51, t=2.417, P〈0.05) at different time points, with the most AA-MAR at 48 hours of onset, and the most IFN-γ at four days of stroke. Compared with the control group, the patients with acute cerebral infarction had more T4, B lymphocytes and natural killer lymphocytes at the four time points, while the level of T8 lymphocytes did not show statistically significant difference even though also increased at the four time points. The correlation analysis results showed that in patients with acute cerebral infarction, the level of AA-MAR (r=-0.397, P〈0.05; r=-0.515, P〈0.01; r=-0.382, P〈0.05) and IFN-γ (r=-0.408, P〈0.05; r=-0.479, P〈0.01; r=-0.378, P〈0.05) was negatively corelated with the spleen volume in 24 hours of onset, at 48 hours of stroke and at four days of stroke; the level of T4, B and natural killer lymphocytes were negatively corelated with the spleen volume in 24 hours of stroke and at 48 hours of stroke.ConclusionAfter the acute cerebral infarction onset, the spleen volume tends to reduce and then increases, the levels of platelet reactivity, inflammatory factors and lymphocyte subsets are correlated with the spleen volume, and the spleen may aggravate the brain injury by releasing platelets inflammatory factors and lymphocyte subsets.
作者 崔兴华 王晶 孙超 王彤 沈腾群 徐新美 李振光 张金彪 Cui Xinghua;Wang Jing;Sun Chao;Wang Tong;Shen Tengqun;Xu Xinmei;Li Zhenguang;Zhang Jinbiao(Department of Neurology,Weihai Municipal Hospital,Weihai,Shandong 264200,Chin)
出处 《中华神经科杂志》 CAS CSCD 北大核心 2018年第7期526-532,共7页 Chinese Journal of Neurology
关键词 卒中 血小板聚集 干扰素Γ 淋巴细胞 Stroke Spleen Platelet aggregation Interferon-gamma Lymphocytes
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