Pistolesi S, Fontanini G, Camacci T, De Ieso K, Boldrini L, Lupi G, Padolecchia R, Pingitore R, Parenti G
Department of Surgery, Pisa University, Pisa, Italy.
J Neurooncol. 2002 Nov;60(2):159-64. doi: 10.1023/a:1020624119944.
Approximately 60% of meningiomas are associated with perilesional brain oedema. Several aspects have been evaluated in order to understand the pathophysiological mechanisms of oedema (age, sex of the patient, size and location of the tumour, histotype, grading), although at present they have yet to be completely clarified. We focused on pial blood supply, microvascular density (MVD) and angiogenic growth factors (i.e. vascular endothelial growth factor--VEGF) in order to evaluate their putative role in the development of brain oedema.
We retrospectively studied 55 patients with intracranial meningiomas. Computerized tomography (CT) and angiographic studies were obtained in all cases. The angiograms provided an accurate differentiation between pial and dural blood supply, concomitantly with its semi-quantitative evaluation. The location and the volume of oedema, in relation to the meningioma surface, was evaluated using CT scans, as an oedema index (E/I). We also determined the expression of VEGF and MVD using standard immunohistochemical methods.
Thirty-two out of 55 meningiomas presented peritumoural oedema, with an angiographic blush ranging from 2 to 4; VEGF protein was expressed in 27 out of 32 cases, independent of grade or histotype of tumours. In all patients, MVD ranged from 4 to 33.3 vessels (median value: 10.6). A significant relationship was found between the expression of VEGF and MVD (p = 0.0003) and between VEGF and E/I (p = 0.0023). Moreover, the E/I ratio was related to the blush (p = 0.0005). A significant association was also present between VEGF expression and pial blush (p = 0.0001).
Our data confirm the central role of VEGF and pial blood supply in the pathogenesis of peritumoural oedema and support the hypothesis that the development of oedema in meningioma is vasogenic in type.
约60%的脑膜瘤伴有瘤周脑水肿。为了解脑水肿的病理生理机制,已对多个方面进行了评估(患者的年龄、性别、肿瘤大小和位置、组织学类型、分级),尽管目前这些机制尚未完全阐明。我们聚焦于软脑膜血供、微血管密度(MVD)和血管生成生长因子(即血管内皮生长因子-VEGF),以评估它们在脑水肿发生发展中可能的作用。
我们回顾性研究了55例颅内脑膜瘤患者。所有病例均进行了计算机断层扫描(CT)和血管造影检查。血管造影可准确区分软脑膜和硬脑膜血供,并同时进行半定量评估。使用CT扫描评估与脑膜瘤表面相关的水肿位置和体积,作为水肿指数(E/I)。我们还使用标准免疫组织化学方法测定VEGF的表达和MVD。
55例脑膜瘤中有32例出现瘤周水肿,血管造影造影剂外溢范围为2至4级;32例中有27例表达VEGF蛋白,与肿瘤的分级或组织学类型无关。所有患者的MVD范围为4至33.3个血管(中位数:10.6)。发现VEGF表达与MVD之间存在显著相关性(p = 0.0003),VEGF与E/I之间也存在显著相关性(p = 0.0023)。此外,E/I比值与造影剂外溢相关(p = 0.0005)。VEGF表达与软脑膜造影剂外溢之间也存在显著相关性(p = 0.0001)。
我们的数据证实了VEGF和软脑膜血供在瘤周脑水肿发病机制中的核心作用,并支持脑膜瘤中水肿的发生是血管源性的这一假说。