中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2012年
8期
799-803
,共5页
海绵状血管畸形%免疫组织化学染色%中枢神经系统
海綿狀血管畸形%免疫組織化學染色%中樞神經繫統
해면상혈관기형%면역조직화학염색%중추신경계통
Cavernous malformation%Immunohistochemistry%Central nervous system
目的 应用免疫组化染色观察不同类型中枢神经系统海绵状血管畸形的内皮细胞标记物、血管生成和增殖活性,探讨病变出血的分子基础. 方法 以自2004年4月至2008年8月南方医院神经外科经显微手术切除的97例中枢神经系统轴内海绵状血管畸形的病理标本为观察对象,根据患者MRI表现分类及其与术中病理形态的比较将所有患者分为出血组(47例)和非出血组50例；另设正常对照组20例,标本来自颅脑外伤患者切除的脑组织.将3组病理标本进行CD34、α-平滑肌肌动蛋白(α-SMA)及血管内皮生长因子(VEGF)免疫组化染色并比较. 结果 海绵状血管畸形内皮层中,CD34呈不同程度的表达,有明显的不连续性；管腔小的病变血管中.CD34染色层较厚；而在管腔大的病变血管中,CD34染色层却较薄,且常不连续.α-SMA表现为阴性或弱阳性(-)～(++).弥散地分布于内皮下层.VEGF有较明显的表达(-)～(++),主要弥散地位于内皮层、内皮下层以及病变血管之间的纤维结缔组织中.正常对照组、出血组与非出血组之间CD34、α-SMA及VEGF免疫组化染色经Kruskal-Wallis H检验示差异均有统计学意义(P＜0.05).所有标本Ki-67染色均呈阴性. 结论 血管结构上缺乏平滑肌可能是部分海绵状血管畸形容易出血的原因之一；VEGF弥散性的表达增多,可能与出血诱导的非特异上调有关；Ki-67染色呈阴性表明至少在标本取得时不存在增殖状态.
目的 應用免疫組化染色觀察不同類型中樞神經繫統海綿狀血管畸形的內皮細胞標記物、血管生成和增殖活性,探討病變齣血的分子基礎. 方法 以自2004年4月至2008年8月南方醫院神經外科經顯微手術切除的97例中樞神經繫統軸內海綿狀血管畸形的病理標本為觀察對象,根據患者MRI錶現分類及其與術中病理形態的比較將所有患者分為齣血組(47例)和非齣血組50例；另設正常對照組20例,標本來自顱腦外傷患者切除的腦組織.將3組病理標本進行CD34、α-平滑肌肌動蛋白(α-SMA)及血管內皮生長因子(VEGF)免疫組化染色併比較. 結果 海綿狀血管畸形內皮層中,CD34呈不同程度的錶達,有明顯的不連續性；管腔小的病變血管中.CD34染色層較厚；而在管腔大的病變血管中,CD34染色層卻較薄,且常不連續.α-SMA錶現為陰性或弱暘性(-)～(++).瀰散地分佈于內皮下層.VEGF有較明顯的錶達(-)～(++),主要瀰散地位于內皮層、內皮下層以及病變血管之間的纖維結締組織中.正常對照組、齣血組與非齣血組之間CD34、α-SMA及VEGF免疫組化染色經Kruskal-Wallis H檢驗示差異均有統計學意義(P＜0.05).所有標本Ki-67染色均呈陰性. 結論 血管結構上缺乏平滑肌可能是部分海綿狀血管畸形容易齣血的原因之一；VEGF瀰散性的錶達增多,可能與齣血誘導的非特異上調有關；Ki-67染色呈陰性錶明至少在標本取得時不存在增殖狀態.
목적 응용면역조화염색관찰불동류형중추신경계통해면상혈관기형적내피세포표기물、혈관생성화증식활성,탐토병변출혈적분자기출. 방법 이자2004년4월지2008년8월남방의원신경외과경현미수술절제적97례중추신경계통축내해면상혈관기형적병리표본위관찰대상,근거환자MRI표현분류급기여술중병리형태적비교장소유환자분위출혈조(47례)화비출혈조50례；령설정상대조조20례,표본래자로뇌외상환자절제적뇌조직.장3조병리표본진행CD34、α-평활기기동단백(α-SMA)급혈관내피생장인자(VEGF)면역조화염색병비교. 결과 해면상혈관기형내피층중,CD34정불동정도적표체,유명현적불련속성；관강소적병변혈관중.CD34염색층교후；이재관강대적병변혈관중,CD34염색층각교박,차상불련속.α-SMA표현위음성혹약양성(-)～(++).미산지분포우내피하층.VEGF유교명현적표체(-)～(++),주요미산지위우내피층、내피하층이급병변혈관지간적섬유결체조직중.정상대조조、출혈조여비출혈조지간CD34、α-SMA급VEGF면역조화염색경Kruskal-Wallis H검험시차이균유통계학의의(P＜0.05).소유표본Ki-67염색균정음성. 결론 혈관결구상결핍평활기가능시부분해면상혈관기형용역출혈적원인지일；VEGF미산성적표체증다,가능여출혈유도적비특이상조유관；Ki-67염색정음성표명지소재표본취득시불존재증식상태.
Objective To explore the endothelial cell markers,angiogenesis and proliferative activity ofcavemous malformation (CM) ofthe central nervous system by immunohistochemical study.Methods Ninety-seven patients with CM performed excision and confirmed by pathologic examination from April 2004 to August 2008 were chosen in our study.According to the MRI manifestations and their pathological features,they were divided into bleeding group (n=47) and non-bleeding group (n=50); and 20 normal brain samples from patients of open cranial-cerebral trauma were chosen as controls. All samples were stained by immunohistochemistry with CD34, α-smooth muscle actin (α-SMA), and vascular endothelial growth factor (VEGF),respectively. Results CD34 expressed in the endothelium of CM discontinuously; in CM with small lumen,thick layer of immunohistochemistry with CD34 was noted,while in CM with large lumen,thin layer of that was observed discontinuously; and the α-SMA expressed in the sub endothelium of CM with diffuse distribution. VEGF expressed obviously in endothelium,sub endothelium and intervascular spaces with diffuse distribution; significant differences of them were noted between each 2 groups (control group,bleeding group and non-bleeding group,P＜0.05).Ki-67 was negative in all samples. Conclusion Lack of vessel smooth muscle may relevant to bleeding tendency of CM; the up-regulation of VEGF may be the result of bleeding stimulation and absence of Ki67 indicates no proliferation in CM.
