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再生障碍性贫血患者骨髓微血管密度及血管内皮生长因子表达的意义

Bone marrow microvessel density and vascular endothelial growth factor expression in patients with aplastic anemia

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【作者】 张莉王慧君李洪强杨栋林阎嶂松吴玉红周康储榆林陈辉树张凤奎

【Author】 ZHANG Li WANG Hui-jun LI Hong-qiang YANG Dong-lin YAN Zhang-song WU Yu-hong ZHOU Kang CHU Yu-lin CHEN Hui-shu ZHANG Feng-kui Institute of Hematology and Blood Diseases Hospital,CAMS & PUMC,Tianjin 300020,China

【机构】 中国医学科学院、中国协和医科大学血液学研究所、血液病医院

【摘要】 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。

【Abstract】 Objective To study the bone marrow microvessel density(MVD)and vascular endotheli- al growth factor(VEGF)expression and their clinical significance in patients with aplastic anemia(AA). Methods Bone marrow biopsies in 51 newly diagnosed patients with AA were evaluated the MVD and VEGF expression by immunostainiug with anti-factor Ⅷ related antigen and VEGF monoclonal antibodies at regular time points after immunosuppressive therapy(IT).Results The mean bone marrow MVD in AA group was 5.5±3.5,being significantly lower than that in normal control group(8.7±3.4,P<0.05).MVDs of SAA and NSAA patients were 7.4±2.9 and 4.3±3.4,respectively,being significantly different(P<0.01). The VEGF expression in AA group was significantly lower than that in control group[(6.7±8.4)% vs (14.7±6.1)%,P<0.01],but there was no difference between SAA and NSAA.Bone marrow MVD and VEGF were significantly increased after IT in 22 responded AA patients.Conclusion Bone marrow MVD and VEGF expression are low in AA patients which may be one of pathophysiologic mechanisms of bone mar- row failure in AA.Proangiogenie and ameliorating microcirculation agents together with IT might accelerate the recovery of hematopoisis in AA patients.

  • 【文献出处】 中华血液学杂志 ,Chinese Journal of Hematology , 编辑部邮箱 ,2007年08期
  • 【分类号】R556
  • 【被引频次】15
  • 【下载频次】34
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