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目的研究再生障碍性贫血(AA)患者骨髓微血管密度(MVD)及血管内皮生长因子(VEGF)的表达,探讨作为骨髓造血微环境重要组成成分的微血管以及调节因子 VEGF 在 AA 是否存在异常及其临床意义。方法应用免疫组化方法,以抗Ⅷ因子相关抗原及 VEGF 单克隆抗体标记骨髓活检组织切片,检测51例初诊 AA 患者及10例对照者骨髓 MVD 及 VEGF 表达,比较 AA 患者与对照者以及 AA 患者免疫抑制治疗后 MVD 及 VEGF 表达变化。结果 AA 患者骨髓 MVD 为5.5±3.5,明显低于对照组(8.7±3.4,P<0.05)。非重型 AA(NSAA)与重型 AA(SAA)患者的 MVD 分别为7.4±2.9和4.3±3.4,差异有统计学意义(P<0.01)。AA 患者骨髓 VEGF 阳性细胞百分率明显低于对照组[分别为(6.7±8.4)%和(14.7±6.1)%,P<0.01],但 NSAA 与 SAA 患者的骨髓 VEGF 阳性细胞百分率差异无统计学意义(P>0.05)。22例经免疫抑制治疗后获得治疗反应的患者骨髓 MVD 及VEGF 阳性细胞百分率均较治疗前明显增加。结论 AA 患者骨髓 MVD 减少及 VEGF 表达减低,可能是 AA 骨髓造血衰竭的病理生理机制之一。促进血管生成以及改善骨髓血液循环的药物在免疫抑制治疗的基础上或可加快造血恢复。
Objective To investigate the expression of bone marrow microvessel density (MVD) and vascular endothelial growth factor (VEGF) in patients with aplastic anemia (AA) and to investigate whether there is an abnormality of microvessel and VEGF, an important component of hematopoietic microenvironment in bone marrow, significance. Methods Immunohistochemistry was used to detect the bone marrow biopsy tissue sections by anti-factor Ⅷ-related antigen and VEGF monoclonal antibody. MVD and VEGF expression were detected in 51 cases of newly diagnosed AA patients and 10 cases of control. Compared with AA patients and controls and AA patients Changes of MVD and VEGF expression after immunosuppressive therapy. Results The bone marrow MVD in patients with AA was 5.5 ± 3.5, significantly lower than that in the control group (8.7 ± 3.4, P <0.05). The MVD in patients with non-heavy AA (AAAA) and severe AA (SAA) were 7.4 ± 2.9 and 4.3 ± 3.4, respectively, with significant difference (P <0.01). The percentage of VEGF-positive cells in bone marrow of AA patients was significantly lower than that of controls [(6.7 ± 8.4)% vs (14.7 ± 6.1)%, P <0.01], but there was no significant difference in the percentage of VEGF-positive cells (P> 0.05). The percentage of MVD and VEGF positive cells in bone marrow of 22 patients treated with immunosuppressive therapy was significantly higher than that before treatment. Conclusion The decrease of MVD and VEGF expression in AA patients may be one of the pathophysiological mechanisms of AA bone marrow failure. Drugs that promote angiogenesis and improve blood circulation to the bone marrow can speed up hematopoietic recovery on the basis of immunosuppressive therapy.