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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
引用本文: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.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[J].中华血液学杂志,2007,28(8):528-531.
作者姓名: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
作者单位:300020,天津,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。

关 键 词:微血管密度  贫血  再生障碍性  血管内皮生长因子  骨髓
修稿时间:2006-11-07

Bone marrow microvessel density and vascular endothelial growth factor expression in patients with aplastic anemia
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.Bone marrow microvessel density and vascular endothelial growth factor expression in patients with aplastic anemia[J].Chinese Journal of Hematology,2007,28(8):528-531.
Authors: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
Institution:Institute of Hematology and Blood Diseases Hospital, CAMS & PUMC, Tianjin, China.
Abstract:OBJECTIVE: To study the bone marrow microvessel density (MVD) and vascular endothelial 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 immunostaining 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 marrow failure in AA. Proangiogenic and ameliorating microcirculation agents together with IT might accelerate the recovery of hematopoisis in AA patients.
Keywords:Microvessel density  Anemia  aplastic  Vascular endothelial growth factor  Bone marrow
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