Meningothelial hyperplasia: a detailed clinicopathologic, immunohistochemical and genetic study of 11 cases.
Meningothelial hyperplasia: a detailed clinicopathologic, immunohistochemical and genetic study of 11 cases.
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脑膜上皮增生：11 例详细的临床病理学、免疫组织化学和遗传学研究。
DOI：
10.1111/j.1750-3639.2005.tb00505.x
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Gutmann,DavidH
中科院分区：
文献类型：
--
作者：
Perry,Arie;Lusis,EriksA;Gutmann,DavidH
脑膜上皮增生是一种特征不明的实体，通常与高龄、慢性肾衰竭、创伤、出血和肿瘤有关。为了阐明这种病变的性质，将 11 例定义为存在 10 层或以上细胞层厚的巢的病例与正常蛛网膜帽细胞和脑膜瘤进行了比较。进行免疫组织化学和 FISH 以确定 NF2(merlin)、蛋白 4.1 B、EMA、孕激素受体 (PR)、EGFR、生存素、VEGF、PDGF-BB、PDGFRβ、E-钙粘蛋白和组织蛋白酶 D 状态。所有病例均具有至少一种假定的诱发因素，包括出血（7）、慢性肾病（5）、年老（5）、创伤（1）和邻近视神经毛细胞星形细胞瘤（1）。通常存在不连续的生长模式，没有侵入周围的正常组织。 2例中可见散在的多倍体细胞，但未发现基因缺失。免疫特征与正常帽细胞相似，但有一个例外：正常细胞的 PR 均呈阴性，而 64% 的增生细胞呈核阳性，这一频率与良性脑膜瘤相似。我们的数据表明，脑膜上皮增生是一种反应过程，通常可根据临床病理学和遗传特征与脑膜瘤区分开来。在某些情况下，它可能是肿瘤前的，但需要进一步的研究来检验这一假设。摘要根据我们和其他人的数据，我们得出结论，脑膜上皮增生是一种反应性过程，其特征是蛛网膜帽细胞的增殖，通常是非侵入性的、多中心的，并且至少局部达到 10 层或更多细胞层的厚度。华丽的例子通常很难与脑膜瘤区分开来。然而，它们通常与诱发因素有关，例如慢性肾病、出血、创伤、颅内低血压和肿瘤，特别是视神经胶质瘤。尽管脑膜上皮增生与正常帽细胞具有许多相同的免疫组织化学和遗传特征，但其不同之处在于其频繁的 PR 免疫反应性和偶尔的多倍体细胞。与经典脑膜瘤相反，FISH 或 merlin 没有证据表明 NF2 或 4.1 B 基因缺失，免疫组织化学没有证据表明 4.1 B 蛋白表达缺失。数据表明，在某些情况下，脑膜上皮增生可能代表肿瘤前病变，尽管需要更多的研究来严格检验这一假设。
Meningothelial hyperplasia is a poorly characterized entity, often associated with advanced age, chronic renal failure, trauma, hemorrhage, and neoplasia. In order to elucidate the nature of this lesion, 11 cases defined by the presence of nests of 10 or more cell layers thick, were compared with normal arachnoidal cap cells and meningiomas. Immunohistochemistry and FISH were performed to determineNF2(merlin), protein 4.1 B, EMA, progesterone receptor (PR), EGFR, survivin, VEGF, PDGF‐BB, PDGFRβ, E‐cadherin, and cathepsin D status. All cases had at least one putative predisposing factor, including hemorrhage (7), chronic renal disease (5), old age (5), trauma (1), and an adjacent optic nerve pilocytic astrocytoma (1). There was typically a discontinuous growth pattern, with no invasion of surrounding normal tissue. No gene deletions were found, though scattered polyploid cells were seen in 2 cases. The immunoprofile was similar to normal cap cells with one exception; whereas normal cells were uniformly negative for PR, nuclear positivity was seen in 64% of hyperplasias, a frequency similar to that of benign meningiomas. Our data suggest that meningothelial hyperplasia is a reactive process that is usually distinguishable from meningioma based on clinicopathologic and genetic features. It may be preneoplastic in some, though further studies are needed to test this hypothesis.SUMMARYBased on our data and that of others, we conclude that meningothelial hyperplasia is a reactive process characterized by a proliferation of arachnoidal cap cells that is often non‐invasive, multicentric, and at least focally reaches a thickness of 10 or more cell layers. Florid examples are often difficult to distinguish from meningioma. However, they are commonly associated with inciting factors, such as chronic renal disease, hemorrhage, trauma, intracranial hypotension, and neoplasia, particularly optic pathway gliomas. Although meningothelial hyperplasia shares many immunohistochemical and genetic features with normal cap cells, it differs in terms of its frequent PR immunoreactivity and occasional polyploid cells. In contrast to classic meningiomas, there is no evidence for eitherNF2or4.1 Bgene deletions by FISH or merlin or protein 4.1 B losses of expression by immunohistochemistry. The data suggest that meningothelial hyperplasia may represent a preneoplastic lesion in some cases, although additional studies are needed to rigorously test this hypothesis.