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脑血管疾病为致人死亡的重要原因,发病风险及病死风险均较高,其中有很多属于缺血性脑血管疾病。急性缺血性脑卒中即急性脑梗死,是由于颅内的血管内出现血液供应障碍、血管闭塞(不同因素导致),导致局部的脑组织出现缺血性病变,其严重程度与脑梗死发病部位、血管狭窄部位、不良生活习惯等有关,且对预后亦有一定影响[1-2]。血常规在临床上应用比较广泛,其检验结果能够反映体内的病理变化,亦可用于评价治疗效果、康复状况。脑梗死的演变过程中均可能有炎性反应的参与,如动脉粥样硬化斑块形成以及治疗后脑组织恢复及预后等。检验指标水平及炎性因子的检测与颈动脉粥样硬化斑块的稳定性等有关,对脑梗死病情发展能够产生一定的影响[3-4]。血常规检验中平均血小板体积(mean platelet volume,MPV)、平均血小板体积与淋巴细胞比值(mean platelet volume to lymphocyte ratio,MPVLR)等检测对于诊断、评估治疗效果等能够发挥积极作用。MPV升高已被确认为急性脑梗死的独立危险因素,并且MPV水平被认为是急性脑梗死病人预后的影响因子[5-6]。既往研究表明,脑梗死后淋巴细胞数量会立即下降,然而其在接下来的14 d内会逐步升高[7]。脑梗死病灶面积的增加及神经功能的恶化与淋巴细胞计数的降低有关[8-9]。此外,MPVLR作为一种新型炎症指标,与急性冠状动脉综合征病人冠状动脉病变的严重程度和长远的生存率密切相关[10]。由于心脑血管发病机制上有相似性,本研究旨在探讨入院时MPVLR检测对预测急性脑梗死严重程度的价值,现作报道。
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2组病人在年龄、性别等方面差异均无统计学意义(P>0.05)(见表 1)。
指标 轻度组
(n=64)中重度组
(n=45)χ2 P 年龄[P50(P25, P75)]/岁 66.00(56.00, 75.00) 66.00(51.00, 76.00) 0.46* >0.05 男/女 42/22 23/22 2.31 >0.05 吸烟 32(50.00) 23(51.11) 0.01 >0.05 饮酒 29(45.31) 27(60.00) 2.28 >0.05 高血压 44(68.75) 36(80) 1.71 >0.05 糖尿病 22(34.38) 17(37.78) 0.13 >0.05 高脂血症 23(35.93) 19(42.22) 0.44 >0.05 冠心病 9(14.06) 13(28.88) 3.61 >0.05 心房颤动 5(7.81) 5(11.11) 0.35 >0.05 *示uc值 表 1 一般临床资料的比较[n;百分率(%)]
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中重度组病人MPVLR及单核细胞计数均高于轻度组,差异有统计学意义(P < 0.05),其他实验室指标2组差异均无统计学意义(P>0.05)(见表 2)。
指标 轻度组(n=64) 中重度组(n=45) uc P MPVLR 4.90(3.96, 6.70) 7.25(5.44, 9.26) 4.35 < 0.05 单核细胞计数/(×109/L) 0.33(0.21, 0.54) 0.43(0.34, 0.49) 2.41 ﹤0.05 中性粒细胞计数/(×109/L) 4.28(3.05, 5.61) 4.73(3.40, 6.51) 0.85 >0.05 白细胞计数/(×109/L) 7.28±2.54 7.14±3.15 0.27* >0.05 低密度脂蛋白/(mmol/L) 2.33±7.09 2.21±0.71 0.85* >0.05 总胆固醇/(mmol/L) 3.83±1.03 3.75±1.09 0.37* >0.05 尿酸/(μmol/L) 289.25±102.36 310.42±95.24 1.09* >0.05 血小板计数/(×109/L) 205.00(157.50, 253.75) 185.00(153.00, 240.50) 1.16 >0.05 D-二聚体/(mg/L) 0.46(0.22, 0.76) 0.47(0.31, 1.41) 1.42 >0.05 高密度脂蛋白/(mmol/L) 0.94(0.76, 1.21) 1.06(0.84, 1.26) 1.60 >0.05 三酰甘油/(mmol/L) 1.39(1.03, 1.82) 1.41(1.01, 1.87) 0.19 >0.05 空腹血糖/(mmol/L) 5.55(4.60, 7.35) 5.83(4.93, 7.43) 0.90 >0.05 胱抑素C/(mg/L) 0.90(0.78, 1.02) 0.99(0.84, 1.10) 1.59 >0.05 *示t值 表 2 实验室指标比较[P50(P25, P75)]
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将MPVLR及单核细胞计数纳入logistic回归分析,结果显示MPVLR升高是急性脑梗死严重程度的独立危险因素(P < 0.01)(见表 3)。
变量 B SE Waldχ2 P OR(95%CI) MPVLR 0.244 0.076 10.40 < 0.01 1.277(1.101~1.481) 单核细胞 1.862 1.084 2.95 >0.05 6.438(0.769~53.895) 表 3 二分类logistic回归分析
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ROC曲线分析显示,MPVLR预测急性脑梗死严重程度的曲线下面积为0.745(95%CI: 0.653~0.824),最佳截断值为5.36,敏感度与特异度分别为80.0%和62.5% (见图 1)。
平均血小板体积/淋巴细胞比值对急性脑梗死严重程度的预测价值
The predictive value of mean platelet volume-to-lymphocyte ratio in the severity of acute cerebral infarction
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摘要:
目的探讨平均血小板体积/淋巴细胞比值(mean platelet volume-to-lymphocyte ratio,MPVLR)对急性脑梗死严重程度的预测价值。 方法回顾性分析109例急性脑梗死病人的临床资料,根据NIHSS评分将其分为轻度组(n=64)和中重度组(n=45)。根据2组血常规相关指标,计算MPVLR。采用二分类logistic回归分析急性脑梗死病情的影响因素,利用ROC曲线评价入院时MPVLR水平对急性脑梗死病变严重程度的预测价值。 结果轻度组MPVLR、单核细胞计数均低于中重度组,差异均有统计学意义(P < 0.05)。二元logistic回归分析显示,入院时MPVLR水平的增加,为急性脑梗死病情严重程度的独立危险因素。ROC曲线显示,MPVLR预测急性脑梗死严重程度的ROC曲线下面积为0.745(95%CI:0.653~0.824),最佳截断值为5.36,敏感度为80.0%,特异度为62.5%。 结论MPVLR对急性脑梗死严重程度具有一定预测价值。 -
关键词:
- 急性脑梗死 /
- 平均血小板体积/淋巴细胞比值
Abstract:ObjectiveTo explore the predictive value of the mean platelet volume-to-lymphocyte ratio(MPVLR) in the severity of acute cerebral infarction. MethodsA total of 109 patients with acute cerebral infarction were retrospectively analyzed, and divided into the mild group(n=64) and moderate-severe group(n=45) according to the NIHSS score.The MPVLR was calculated according to the blood routine indexes of two groups.The influencing factors of acute cerebral infarction were analyzed using dichotomous logistic regression, and the predictive value of MPVLR level on admission in the severity of acute cerebral infarction was evaluated using ROC curve. ResultsThe MPVLR and monocyte counts in mild group were lower than those in moderate group(P < 0.05).The results of binary logistic regression analysis showed that the increasing of MPVLR level on admission was an independent predictor of acute cerebral infarction.The results of ROC curve showed that the area under the curve of MPVLR predicting the severity of acute cerebral infarction was 0.745(95%CI: 0.653~0.824), and the best cutoff value, sensitivity and specificity were 5.36, 80.0% and 62.5%, respectively. ConclusionsThe MPVLR has certain predictive value in judging the severity of acute cerebral infarction. -
表 1 一般临床资料的比较[n;百分率(%)]
指标 轻度组
(n=64)中重度组
(n=45)χ2 P 年龄[P50(P25, P75)]/岁 66.00(56.00, 75.00) 66.00(51.00, 76.00) 0.46* >0.05 男/女 42/22 23/22 2.31 >0.05 吸烟 32(50.00) 23(51.11) 0.01 >0.05 饮酒 29(45.31) 27(60.00) 2.28 >0.05 高血压 44(68.75) 36(80) 1.71 >0.05 糖尿病 22(34.38) 17(37.78) 0.13 >0.05 高脂血症 23(35.93) 19(42.22) 0.44 >0.05 冠心病 9(14.06) 13(28.88) 3.61 >0.05 心房颤动 5(7.81) 5(11.11) 0.35 >0.05 *示uc值 表 2 实验室指标比较[P50(P25, P75)]
指标 轻度组(n=64) 中重度组(n=45) uc P MPVLR 4.90(3.96, 6.70) 7.25(5.44, 9.26) 4.35 < 0.05 单核细胞计数/(×109/L) 0.33(0.21, 0.54) 0.43(0.34, 0.49) 2.41 ﹤0.05 中性粒细胞计数/(×109/L) 4.28(3.05, 5.61) 4.73(3.40, 6.51) 0.85 >0.05 白细胞计数/(×109/L) 7.28±2.54 7.14±3.15 0.27* >0.05 低密度脂蛋白/(mmol/L) 2.33±7.09 2.21±0.71 0.85* >0.05 总胆固醇/(mmol/L) 3.83±1.03 3.75±1.09 0.37* >0.05 尿酸/(μmol/L) 289.25±102.36 310.42±95.24 1.09* >0.05 血小板计数/(×109/L) 205.00(157.50, 253.75) 185.00(153.00, 240.50) 1.16 >0.05 D-二聚体/(mg/L) 0.46(0.22, 0.76) 0.47(0.31, 1.41) 1.42 >0.05 高密度脂蛋白/(mmol/L) 0.94(0.76, 1.21) 1.06(0.84, 1.26) 1.60 >0.05 三酰甘油/(mmol/L) 1.39(1.03, 1.82) 1.41(1.01, 1.87) 0.19 >0.05 空腹血糖/(mmol/L) 5.55(4.60, 7.35) 5.83(4.93, 7.43) 0.90 >0.05 胱抑素C/(mg/L) 0.90(0.78, 1.02) 0.99(0.84, 1.10) 1.59 >0.05 *示t值 表 3 二分类logistic回归分析
变量 B SE Waldχ2 P OR(95%CI) MPVLR 0.244 0.076 10.40 < 0.01 1.277(1.101~1.481) 单核细胞 1.862 1.084 2.95 >0.05 6.438(0.769~53.895) -
[1] CHEN Y, LIU Y, LUO C, et al. Analysis of multiple factors involved in acute progressive cerebral infarction and extra- and intracranial arterial lesions[J]. Exp Ther Med, 2014, 7(6): 1495. doi: 10.3892/etm.2014.1624 [2] MILLÁN M, REMOLLO S, QUESADA H, et al. Vessel patency at 24 hours and its relationship with clinical outcomes and infarct volume in REVASCAT trial(randomized trial of revascularization with solitaire FR device versus best medical therapy in the treatment of acute stroke due to anterior circulation large vessel occlusion presenting within eight hours of symptom onset)[J]. Stroke, 2017, 48(4): 983. doi: 10.1161/STROKEAHA.116.015455 [3] YANG Y, XUE T, ZHU J, et al. Serum lipoprotein-associated phospholipase A2 predicts the formation of carotid artery plaque and its vulnerability in anterior circulation cerebral infarction[J]. Clin Neurol Neurosurg, 2017, 160: 40. doi: 10.1016/j.clineuro.2017.06.007 [4] XUE QZ, MENG AG, WANG T, et al. Correlation between of small dense low-density lipoprotein cholesterol with acute cerebral infarction and carotid atherosclerotic plaque stability[J]. J Clin Lab Anal, 2019, 33(6): e22891. [5] GREISENEGGER S, ENDLER G, HSIEH K, et al. Is elevated mean platelet volume associated with a worse outcome in patients with acute ischemic cerebrovascular events[J]. Stroke, 2004, 35(7): 1688. doi: 10.1161/01.STR.0000130512.81212.a2 [6] LIN CY, CHANG CY, SUN CH, et al. Platelet count and early outcome in patients with spontaneous cerebellar hemorrhage: a retrospective study[J]. PLoS One, 2015, 10(3): e0119109. doi: 10.1371/journal.pone.0119109 [7] PARK MG, KIM MK, CHAE SH, et al. Lymphocyte-to-monocyte ratio on day 7 is associated with outcomes in acute ischemic stroke[J]. Neurol Sci, 2018, 39(2): 243. doi: 10.1007/s10072-017-3163-7 [8] REN X, AKIYOSHI K, DZIENNIS S, et al. Regulatory B cells limit CNS inflammation and neurologic deficits in murine experimental stroke[J]. J Neurosci, 2011, 31(23): 8556. doi: 10.1523/JNEUROSCI.1623-11.2011 [9] LIESZ A, SURI-PAYER E, VELTKAMP C, et al. Regulatory T cells are key cerebroprotective immunomodulators in acute experimental stroke[J]. Nat Med, 2009, 15(2): 192. doi: 10.1038/nm.1927 [10] KILIC A, KURTUL A. RETRACTED: Mean platelet volume-to-lymphocyte ratio as a novel marker for severity and complexity of coronary atherosclerosis in patients with acute coronary syndrome[J]. Angiology, 2017: 3319717724274. [11] 中华医学会神经病学分会, 中华医学会神经病学分会脑血管病学组. 中国急性缺血性脑卒中诊治指南2018[J]. 中华神经科杂志, 2018, 51(9): 666. doi: 10.3760/cma.j.issn.1006-7876.2018.09.004 [12] 王伊龙, 赵性泉, 刘新峰, 等. 高危非致残性缺血性脑血管事件诊疗指南[J]. 中国卒中杂志, 2016, 11(6): 481. doi: 10.3969/j.issn.1673-5765.2016.06.011 [13] BARON T, BESKOW A, JAMES S, et al. Biobank linked to SWEDEHEART quality registry-routine blood sample collection opens new opportunities for cardiovascular research[J]. Ups J Med Sci, 2019, 124(1): 12. doi: 10.1080/03009734.2018.1498957 [14] MO L, CHEN Y, LI Z, et al. Red blood cell distribution width as a marker of cerebral infarction in hemodialysis patients[J]. Ren Fail, 2017, 39(1): 712. doi: 10.1080/0886022X.2017.1398664 [15] LIEN LM, LIN KH, HUANG LT, et al. Licochalcone a prevents platelet activation and thrombus formation through the inhibition of PLCγ2-PKC, Akt, and MAPK pathways[J]. Int J Mol Sci, 2017, 18(7): 1500. doi: 10.3390/ijms18071500 [16] KURTUL A, ACIKGOZ SK. Usefulness of mean platelet volume-to-lymphocyte ratio for predicting angiographic no-reflow and short-term prognosis after primary percutaneous coronary intervention in patients with st-segment elevation myocardial infarction[J]. Am J Cardiol, 2017, 120(4): 534. doi: 10.1016/j.amjcard.2017.05.020 [17] HUDZIK B, SZKODZIŃSKI J, LEKSTON A, et al. Mean platelet volume-to-lymphocyte ratio: a novel marker of poor short- and long-term prognosis in patients with diabetes mellitus and acute myocardial infarction[J]. J Diabetes Complications, 2016, 30(6): 1097. doi: 10.1016/j.jdiacomp.2016.04.010 [18] STEGNER D, KLAUS V, NIESWANDT B. Platelets as modulators of cerebral ischemia/reperfusion injury[J]. Front Immunol, 2019, 10: 2505. doi: 10.3389/fimmu.2019.02505 [19] JENNINGS LK. Mechanisms of platelet activation: need for new strategies to protect against platelet-mediated atherothrombosis[J]. Thromb Haemost, 2009, 102(2): 248. [20] CHEN SY, LIN YS, CHENG YF, et al. Mean platelet volume-to-lymphocyte ratio predicts poor functional outcomes among ischemic stroke patients treated with intravenous thrombolysis[J]. Front Neurol, 2019, 10: 1274. doi: 10.3389/fneur.2019.01274 [21] 李玲玲, 李永娟, 陈志斌. 急性脑梗死严重程度的影响因素及与淋巴细胞/单核细胞比值的关系[J]. 中国医学导报, 2018, 15(26): 62. [22] CHAUHAN A, HUDOBENKO J, Al MAMUN A, et al. Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke[J]. J Neuroinflammation, 2018, 15(1): 148. doi: 10.1186/s12974-018-1188-3