急性冠脉综合征患者血清巨噬细胞集落刺激因子和白介素-10水平变化的临床意义

目的观察血清巨噬细胞集落刺激因子 (M-CSF)、白介素-10 (IL-10) 水平在急性冠脉综合征(ACS)患者中的变化,探讨其与斑块稳定性的关系.方法 ACS患者38 例(ACS组):急性心肌梗死(AMI)组20例,不稳定型心绞痛(UAP) 组18 例;稳定型心绞痛(SAP) 组17 例;对照组17 例.用ELISA法测定血清巨噬细胞集落刺激因子及白介素-10水平.结果血清M-CSF水平AMI组高于SAP组和对照组(P均<0.05),UAP组高与SAP组和对照组(P均<0.05),AMI组与UAP 组比较差异无显著性(P>0.05);血清IL-10水平AMI组高于UAP组、SAP组和对照组(P均<0.05), UA组高于SAP组和对照组(P均<0.05);ACS病人血清IL-10和M-CSF水平呈正相关关系(r=0.352,P<0.05).结论 (1)ACS患者血清M-CSF升高反映斑块的不稳定性.(2)急性冠脉综合征患者血清IL-10升高,并且与血清M-CSF水平呈正相关关系反映了在动脉粥样硬化斑块中作为抗炎因子的IL-10与其他炎症因子相互作用的复杂性.

Clinical Significance of the Serum Level of Macrophage Colony-Stimulating Factor and Interleukin-10 in Patients With Acute Coronary Syndromes

Objective To observe the serum levels of macrophages colony-stimulating factor (M-CSF) and interluekin-10 (IL-10) in patients with acute coronary syndromes (ACS) and to investigate their relationship with stability of plaques.Methods 38 patients with ACS, including 20 patients with acute myocardial infarction (AMI),18 patients with unstable angina (UA).The study also included 17 patients with stable angina (SA) and 17 age-matched control subjects.The serum M-CSF and IL-10 concentrations were measured by ELISA.Results ACS patients exhibited significantly higher serum levels of M-CSF as compared with those of SA patients and controls (P<0.05).There was no significant difference in M-CSF levels between AMI patients and UA patients (P>0.05).The serum IL-10 levels in patients with AMI was significantly higher than that in patients with UA,SA and in controls (P<0.05).The serum levels of IL-10 in patients with UA was higher than that in patients with SA and controls (P<0.05).In ACS patients there was a statistically significant positive correlation of serum IL-10 with the levels of M-CSF(r=0.352,P<0.05).Conclusions (1) An increased circulating M-CSF is associated with the unstability of plaque.(2) The increased serum level of IL-10 and the positive correlation with M-CSF levels reflects the interactional complexity between Il-10 and others inflammatory factor in atherogenesis plaques.