论文部分内容阅读
目的对β-珠蛋白生成障碍性贫血患者的血清内皮粘附分子进行分析,探讨β-珠蛋白生成障碍性贫血的血管内皮损伤程度。方法通过酶联免疫吸附法分析130例β-珠蛋白生成障碍性贫血患者的血清血管细胞粘附分子1、细胞间粘附分子1、P-选择素及E-选择素浓度,并与健康对照组进行比较。结果β-珠蛋白生成障碍性贫血患者的血清血管细胞粘附分子1、细胞间粘附分子1、P-选择素及E-选择素浓度分别为(1009.1±409.3)μg/L、(566.4±240.8)μg/L、(93.1±30.6)μg/L、(63.7±28.5)μg/L,显著高于健康对照组的(508.2±239.5)μg/L、(235.5±73.6)μg/L、(57.9±10.1)μg/L、(42.5±10.7)μg/L(P<0.01)。结论β-珠蛋白生成障碍性贫血患者的血管内皮细胞在一定程度被活化,进而导致患者血管内皮损伤。
Objective To analyze the serum endothelium adhesion molecules in patients with β-globin aplastic anemia and to explore the extent of vascular endothelial damage of β-globinogenic anemia. Methods The levels of serum vascular cell adhesion molecule-1, intercellular adhesion molecule-1, P-selectin and E-selectin in 130 patients with β-globinbacillary dysplasia were analyzed by enzyme-linked immunosorbent assay and compared with healthy controls Group to compare. Results Serum levels of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, P-selectin and E-selectin were (1009.1 ± 409.3) μg / L in patients with β-globinbacillary dysplasia, 240.8 μg / L, 93.1 ± 30.6 μg / L and 63.7 ± 28.5 μg / L, respectively, which were significantly higher than those in healthy controls (508.2 ± 239.5 μg / L, 235.5 ± 73.6 μg / L, 57.9 ± 10.1) μg / L and (42.5 ± 10.7) μg / L, respectively (P <0.01). Conclusion Vascular endothelial cells in patients with β-globin aplasia are activated to a certain extent, leading to vascular endothelial injury in patients.