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. 2006 Apr 5;15(2):109–115. doi: 10.1111/j.1750-3639.2005.tb00505.x

Meningothelial Hyperplasia: A Detailed Clinicopathologic, Immunohistochemical and Genetic Study of 11 Cases

Arie Perry 1,✉, Eriks A Lusis 1, David H Gutmann 2
PMCID: PMC8095984  PMID: 15912882

Abstract

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 determine NF2 (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.

SUMMARY

Based 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 either NF2 or 4.1 B gene 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.

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