中国实验血液学杂志
中國實驗血液學雜誌
중국실험혈액학잡지
JOURNAL OF EXPERIMENTAL HEMATOLOGY
2006年
1期
79-82
,共4页
季健玲%徐美玉%黄锋%刘红
季健玲%徐美玉%黃鋒%劉紅
계건령%서미옥%황봉%류홍
再生障碍性贫血%血管生成%CD34细胞%骨髓
再生障礙性貧血%血管生成%CD34細胞%骨髓
재생장애성빈혈%혈관생성%CD34세포%골수
aplastic anemia%angiogenesis%CD34%bone marrow
本研究目的为探讨再生障碍性贫血骨髓血管生成的状况.采用免疫组织化学SP法检测32例再生障碍性贫血患者和16例正常人骨髓活检组织中血管内皮细胞标记CD34的表达,用盲法计数骨髓微血管密度(MVD)并对骨髓血管生成进行简单分级.结果表明,再生障碍性贫血患者骨髓MVD显著低于正常人(P<0.01),其中重型再生障碍性贫血和非重型再生障碍性贫血的MVD都显著低于正常人(P<0.01),而重型再生障碍性贫血MVD值低于非重型再生障碍性贫血(P<0.05).再生障碍性贫血患者MVD与血管简单分级之间存在正相关性(r=0.64,P<0.01).结论:再生障碍性贫血患者骨髓血管生成缺陷可能导致或加重骨髓造血障碍.
本研究目的為探討再生障礙性貧血骨髓血管生成的狀況.採用免疫組織化學SP法檢測32例再生障礙性貧血患者和16例正常人骨髓活檢組織中血管內皮細胞標記CD34的錶達,用盲法計數骨髓微血管密度(MVD)併對骨髓血管生成進行簡單分級.結果錶明,再生障礙性貧血患者骨髓MVD顯著低于正常人(P<0.01),其中重型再生障礙性貧血和非重型再生障礙性貧血的MVD都顯著低于正常人(P<0.01),而重型再生障礙性貧血MVD值低于非重型再生障礙性貧血(P<0.05).再生障礙性貧血患者MVD與血管簡單分級之間存在正相關性(r=0.64,P<0.01).結論:再生障礙性貧血患者骨髓血管生成缺陷可能導緻或加重骨髓造血障礙.
본연구목적위탐토재생장애성빈혈골수혈관생성적상황.채용면역조직화학SP법검측32례재생장애성빈혈환자화16례정상인골수활검조직중혈관내피세포표기CD34적표체,용맹법계수골수미혈관밀도(MVD)병대골수혈관생성진행간단분급.결과표명,재생장애성빈혈환자골수MVD현저저우정상인(P<0.01),기중중형재생장애성빈혈화비중형재생장애성빈혈적MVD도현저저우정상인(P<0.01),이중형재생장애성빈혈MVD치저우비중형재생장애성빈혈(P<0.05).재생장애성빈혈환자MVD여혈관간단분급지간존재정상관성(r=0.64,P<0.01).결론:재생장애성빈혈환자골수혈관생성결함가능도치혹가중골수조혈장애.
The objective of this study was to investigate the status of bone marrow angiogenesis in aplastic anemia (AA). Bone marrow specimens from 32 patients with AA and 16 normal controls were studied. The number of bone marrow microvessels was examined by means of immunohistochemical staining for CD34. Determination of microvessel density (MVD) and angiogenesis grading were done in a blinded manner. The results showed that the bone marrow MVD in patients with AA was significantly lower than that in healthy subjects (P<0.01 ). MVD in patients with severe and moderate AA was lower than that in control group, respectively (P<0.01). There is significant MVD difference between severe AA and moderate AA (P<0.05). Angiogenesis grade and MVD in AA were positively correlated(r=0.64, P<0.01).It is concluded that bone marrow angiogenesis in AA patients is lower than that in normal controls. Defect of angiogenesis in bone marrow may play a role resulting in or aggravating hematopoietic aplasia in patients with AA.