Department of Pathology, Immunology, and Laboratory Medicine, University of Florida College of Medicine, Gainesville, USA.
Adv Anat Pathol. 2012 Jul;19(4):239-49. doi: 10.1097/PAP.0b013e31825c6a04.
A major challenge in the routine practice of surgical neuropathology is the distinction between reactive astrocytosis, which may be because of non-neoplastic and neoplastic conditions, and a low-grade infiltrating diffuse astrocytoma [World Health Organization (WHO) grade II]. This can be particularly challenging with small biopsies that often yield limited amounts of tissue for pathologic study, especially considering the marked differences in prognosis and therapy after a pathologic diagnosis. This paper will review some basic principles of gliosis as an astrocytic reaction to a wide range of central nervous system insults and focus on some common diagnostic pitfalls such as (1) gliosis associated with brain tumor mimics, including demyelinating disease and infections, (2) gliosis associated with nonglial tumors such as craniopharyngioma, hemangioblastoma, metastases, and central nervous system lymphoma. New diagnostic methods have facilitated the differentiation between reactive astrocytosis and the diffuse gliomas. Of these, the use of mutated isocitrate dehydrogenase-1 (IDH-1) as a marker of diffuse infiltrating astroctomas, oligodendrogliomas, and a subset of glioblastomas (secondary glioblastomas) is particularly exciting for tissue diagnosis and patient prognosis. In addition IDH-1 may be useful to distinguish a diffuse infiltrating glioma from low-grade "focal" neoplasms such as the pilocytic astocytoma in histologically ambiguous cases. The discovery of BRAF mutations as molecular signatures of some pilocytic astrocytomas, gangliogliomas, and pleomorphic xanthoastrocytomas has provided another diagnostic tool for the pathologist. Only after a definitive diagnosis of a diffuse infiltrating glioma or a focal glioma is made should a tumor grade be applied and some practical issues in current glioma grading are provided.
在外科神经病理学的常规实践中，一个主要挑战是区分反应性星形胶质增生，其可能是由于非肿瘤性和肿瘤性病变引起的，与低级浸润性弥漫性星形细胞瘤[世界卫生组织（WHO）分级 II]。对于经常获得用于病理研究的有限量组织的小活检，这可能特别具有挑战性，尤其是考虑到病理诊断后预后和治疗的显著差异。本文将回顾神经胶质增生作为星形细胞对广泛的中枢神经系统损伤的反应的一些基本原则，并重点介绍一些常见的诊断陷阱，例如：（1）与脑瘤相关的神经胶质增生模仿物，包括脱髓鞘疾病和感染；（2）与非神经胶质肿瘤相关的神经胶质增生，如颅咽管瘤、血管母细胞瘤、转移瘤和中枢神经系统淋巴瘤。新的诊断方法促进了反应性星形胶质增生与弥漫性神经胶质瘤之间的区分。其中，使用突变型异柠檬酸脱氢酶-1（IDH-1）作为弥漫浸润性星形细胞瘤、少突胶质细胞瘤和一部分胶质母细胞瘤（继发性胶质母细胞瘤）的标志物，对于组织诊断和患者预后特别令人兴奋。此外，IDH-1 可能有助于在组织学上不明确的病例中，从低级别“局灶性”肿瘤（如毛细胞星形细胞瘤）中区分弥漫浸润性胶质瘤。BRAF 突变作为一些毛细胞星形细胞瘤、神经节胶质瘤和多形性黄色星形细胞瘤的分子特征的发现，为病理学家提供了另一种诊断工具。只有在明确诊断为弥漫浸润性胶质瘤或局灶性胶质瘤后，才能应用肿瘤分级，并且提供了当前胶质瘤分级中的一些实际问题。
