Hefti Martin, von Campe G, Schneider C, Roelcke U, Landolt H
UKSH, Neurosurgery, Kiel, Germany.
Cent Eur Neurosurg. 2010 Feb;71(1):20-5. doi: 10.1055/s-0029-1241190. Epub 2010 Feb 19.
Improvements in microneurosurgical techniques, radiotherapy and chemotherapy for the treatment of high grade gliomas resulted in better local tumor control and longer progression-free survival. Multicentric (MC) lesions located distant from the initial resection area contribute to treatment failure in a growing number of patients. These MC lesions may develop within the course of the disease (metachronous) or may already be present at the time of first tumor manifestation (synchronous). To look for mechanisms and regular patterns behind MC glioma manifestations and to investigate whether they are "a second primary tumor" or the result of continuous diffuse glioblastoma cell invasion, we retrospectively analyzed the initial and all follow-up MR studies of our high grade glioma (HGG) patients.
MR studies of 247 consecutive patients treated for HGG at a single institution were analyzed. MC tumor manifestation was defined as more than one gadolinium enhancing lesion within the brain on MRI without a connecting signal alteration in T2 sequences and/or without a connecting hypointense mass in T1 sequences. The minimal distance to define two solitary lesions was set at >10 mm. According to these specifications 40 patients showed MC tumor manifestations in their MR studies on admission or during treatment of their disease. The MR studies of these cases were retrospectively analyzed for patterns in MC tumor manifestation and progression. Topographical specifications and delay in manifestation were used to explain possible pathways of development. Kaplan Meyer survival graphs for metachronous and synchronous MC disease were calculated.
24 patients showed MC tumor manifestation at the time of admission. 16 cases developed MC manifestation within a follow-up period of 3-57 months. The location of all lesions could be categorized into one of three distinct patterns (white matter, subependymal, intraventricular). The patterns showed individual and location-specific time gaps to metachronous manifestation. Calculated from the time of first tumor diagnosis, the median survival was longer for patients with metachronous MC lesions (353 days, p<0.05) compared to patients with synchronous MC lesions (110 days) or patients without multicentricity (234 days). Patients with metachronous lesions showed a similar survival (72 days) as patients with synchronous MC lesions (110 days) once they developed MC disease.
The topographical patterns and temporal characteristics of MC disease suggest that all manifestations share common mechanisms such as an active migratory process. Our data therefore do not support the concept of an independent MC development of multiple gliomas.
显微神经外科技术、放疗和化疗在高级别胶质瘤治疗方面的改进，使得局部肿瘤控制更好，无进展生存期更长。越来越多患者的治疗失败是由远离初始切除区域的多中心（MC）病变导致的。这些MC病变可能在疾病过程中出现（异时性），也可能在首次肿瘤表现时就已存在（同时性）。为了探寻MC胶质瘤表现背后的机制和规律模式，并研究它们是“第二原发性肿瘤”还是持续性弥漫性胶质母细胞瘤细胞侵袭的结果，我们回顾性分析了我们的高级别胶质瘤（HGG）患者的初始及所有随访磁共振成像（MR）研究。
对在单一机构接受HGG治疗的247例连续患者的MR研究进行分析。MC肿瘤表现定义为MRI上脑内有一个以上钆增强病变，T2序列无连接信号改变和/或T1序列无连接低信号肿块。定义两个孤立病变的最小距离设定为>10毫米。根据这些标准，40例患者在入院时或疾病治疗期间的MR研究中显示有MC肿瘤表现。对这些病例的MR研究进行回顾性分析，以探寻MC肿瘤表现和进展的模式。利用地形学特征和表现延迟来解释可能的发展途径。计算异时性和同时性MC疾病的Kaplan - Meyer生存曲线。
24例患者入院时显示有MC肿瘤表现。16例在3 - 57个月的随访期内出现MC表现。所有病变的位置可分为三种不同模式之一（白质、室管膜下、脑室内）。这些模式显示出异时性表现的个体和位置特异性时间间隔。从首次肿瘤诊断时间算起，异时性MC病变患者的中位生存期（353天，p<0.05）比同时性MC病变患者（110天）或无多中心性的患者（234天）更长。一旦出现MC疾病，异时性病变患者的生存期（72天）与同时性MC病变患者（110天）相似。
MC疾病的地形学模式和时间特征表明，所有表现都有共同机制，如活跃的迁移过程。因此，我们的数据不支持多个胶质瘤独立发生MC的概念。
