无症状性脑梗死患者血清炎性因子和纤溶及抗纤溶活性的变化

目的观察无症状性脑梗死(silent cerebral infarction,SCI)患者血清炎性因子和纤溶及抗纤溶活性的变化。方法选择SCI患者53例(SCI组)和健康体检者55例(对照组),分别检测血清高敏C反应蛋白(hs-CRP)、血浆纤溶酶原活性(PLG:A)、纤溶酶活性(PLM:A)、组织型纤溶酶原激活物(t-PA)活性、D-二聚体(D-D)含量、_2α-纤溶酶抑制剂(α_2-PI)和纤溶酶原激活物抑制剂(PAI)活性。结果 SCI组hs-CRP水平明显高于对照组(15.36±4.30)mg/L vs (10.26±2.61)mg/L,P<0.01],SCI组PLM:A、t-PA和D-D含量均明显低于对照组(35.84±10.23)% vs (68.74±18.41)%,(0.11±0.01)U/ml vs (0.49±0.12)U/mL(0.36±0.14)mg/L vs (0.68±0.16)mg/L,P<0.01)],SCI组PLG:A与对照组比较差异无统计学意义(P>0.05),SCI组α_2-PI活性和PAI活性明显高于对照组(128.46±23.75)% vs (96.36±19.34)%,(0.86±0.22)AU/ml vs (0.48±0.10)AU/ml.P<0.01]。结论炎症过程和纤溶及抗纤溶系统的功能失调与SCl的形成有关。

Changes of serum inflammatory cytokine, fibrinolytic and antifibrinolytic activities in patients with SCI

Objective To observe the changes of serum inflammatory cytokine,fibrinolytic and antifibrinolytic activities in patients with silent cerebral infarction(SCI). Methods The serum level of high-sensitivity C-reactive protein(hs-CRP) was measured by immunodiffusion turbidimetry in 53 patients with SCI and 55 cases of control group. The plasminogen activity(PLG : A),plasmin activity(PLM : A), tissue-type plasminogen activator (t-PA) activity, D-dimer (D-D), α_2-plasmin inhibitor(α_2-PI) activity and plasminogen activator inhibitor(PAI) activity were also measured in both groups. Results The level of hs-CRP was significantly higher in patients with SCI than in the control group(15.36±4.30) mg/L vs (10.26±2.61) mg/L, P<0.01]. The levels of PLM : A,t-PA and D-D were markedly lower in SCI group than in the control group (35.84± 10.23)% vs (68.74±18.41)%,(0.11±0.01) U/ml vs (0.49±0.12) U/ml, and(0.36±0.14) mg/L vs (0.68±0.16) mg/L, P<0.01, respectively],but PLG : A was not significantly different between the two groups (P>0.05). The α_2-PI activity and PAI activity were significantly higher in SCI group than in the control group(128.46±23.75)% vs (96.36±19.34)%,(0.86± 0.22) AU/ml vs (0.48±0.10) AU/ml, P<0.01, respectively]. Conclusion Inflammatory processes and dysfunction of fibrinolytic and antifibrinolytic systems are involved in the pathogenesis of SCI.