Massive gliosis of the retina: report of a case investigated by immunohistochemistry and clonality assays

Inayama, Yoshiaki; Hanashi, Miho; Yazawa, Takuya; Mitsui, Hideaki; Kimura, Ayako; Ito, Daizo

doi:10.1016/j.humpath.2005.04.013

Cited by 11 publications

(8 citation statements)

References 5 publications

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“…25 One lesion manifested a focus of bland infarctive necrosis at its apex with obliterative hyalinization of the vessels in the subjacent viable tissue; intratumoral hemorrhage was not found. Massive retinal gliosis that fills the vitreous cavity is probably an advanced example of the entity we are describing here, 27,28 but there has never been a case of a small tumor like ours that has been directly observed and documented over time to progress to the stage of filling the entire vitreous cavity.…”

Section: Discussionmentioning

confidence: 69%

“…Massive gliosis of the retina and vitreous has been reported bilaterally in an infant with retinopathy of prematurity 60 and an investigation of a case of massive retinal gliosis in a female patient with a microphthalmic eye revealed that the gliotic mass contained multiple clones determined by the HUMARA methodology (human androgen receptor gene assay for clonality utilizing X chromosome inactivation in female subjects), findings in both cases that are consistent with a reactive proliferation. 28 The association of many “vasoproliferative tumors” of the retina with other ocular diseases such as uveitis (as in our index case), retinal detachment, retinopathy of prematurity, Coats disease, and trauma has led other investigators to suggest that these tumors may form as a reactive process to an antecedent insult. 22 The idiopathic lesions described by Shields and associates, 2 as well as by others, may actually have formed in the wake of a subclinical or cryptic event that was never reported or was forgotten by the patient, or a prior episode of mild inflammation that went untreated.…”

Section: Discussionmentioning

confidence: 80%

“…In 2 cases of massive gliosis of the retina and vitreous body, isoenzyme C of carbonic anhydrase has been detected histochemically and is regarded as a reliable marker for Müller cells. 27,28 …”

Section: Discussionmentioning

confidence: 99%

“…The modifier “astrocytic” is preferable to “glial” because the latter term is more generic and subsumes oligodendroglia and microglia (macrophages) as well as astroglia. Further studies to better define the cell types involved (fibrous astrocytes vs Müller cells that acquire glial filaments), and to more completely characterize these proliferations as reactive and polyclonal, 27,28 would be essential for advancing our understanding of this disease spectrum.…”

Section: Discussionmentioning

confidence: 99%

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Reactive Retinal Astrocytic Tumors (So-called Vasoproliferative Tumors): Histopathologic, Immunohistochemical, and Genetic Studies of Four Cases

Perry

Jakobiec

Zakka

et al. 2013

American Journal of Ophthalmology

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Purpose To evaluate the cellular nature of and diagnostic terminology used in connection with acquired retinal “vasoproliferative tumors.” Design Retrospective clinicopathologic study. Methods Clinical records and microscopic slides of 4 enucleated globes were reviewed. Special stains and immunohistochemical probes for CD31, CD34, p53, glial fibrillary acidic protein (GFAP), CD163, and Ki67 (cell replication) were employed; ultrastructural and fluorescence in situ hybridization (FISH) analyses were performed. Results Tumors were located inferotemporally in middle-aged patients. They were uniformly composed of compacted elongated, GFAP-positive spindle cells (due to intermediate filaments identified ultrastructurally) with a Ki67 index of less than 1%. Rosenthal fibers and eosinophilic granular bodies were observed. Hyalinized periodic acid–Schiff-positive vessels were widely separated. CD31 and CD34 revealed a sparse microvasculature. Tumor-associated exudate spread predominantly subretinally. The retinal pigment epithelium had undergone extensive placoid fibrous metaplasia with focal ossification. P53 upregulation, BRAF-KIAA gene rearrangement, and IDH1 R132H mutation typically associated with low-grade astrocytic neoplasms were absent. Conclusions Retinal “vasoproliferative” tumors have been mischaracterized, because they actually display a paucity of microvessels. Proliferating fibrous astrocytes with a very low proliferation index predominate, without immunohistochemical or genetic evidence favoring a neoplasm. Subretinal exudate appeared capable of provoking widespread fibrous metaplasia of the pigment epithelium that was mainly responsible for secondary retinal damage. The term “reactive retinal astrocytic tumor” is proposed as more appropriate for this entity. In carefully selected progressive lesions, consideration should be given to earlier surgical intervention before extensive subretinal exudate accumulates and pigment epithelial proliferation with fibrous metaplasia ensues.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Reactive Retinal Astrocytic Tumors (So-called Vasoproliferative Tumors): Histopathologic, Immunohistochemical, and Genetic Studies of Four Cases

Perry

Jakobiec

Zakka

et al. 2013

American Journal of Ophthalmology

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“…These elongated oval or spindle-shaped cells contain varying amounts of fibrillated eosinophilic cytoplasm and show diffuse immunopositivity for GFAP [1,5,20,21,22,23]. Previous electron microscopy studies demonstrated features consistent with astrocytes, with absence of the abundant smooth and rough endoplasmic reticulum and interdigitating villous processes characteristic of Müller cells [4,24].…”

Section: Discussionmentioning

confidence: 99%

Reactive Retinal Astrocytic Tumor (Focal Nodular Gliosis): A Case Report

Hudson¹,

Mendoza

Yan³

et al. 2016

Ocul Oncol Pathol

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Purpose: To report the clinical and histopathological findings of a reactive retinal astrocytic tumor (RRAT) that progressed to massive retinal gliosis. Observations: The patient presented with an elevated, white-yellow retinal mass and extensive retinal exudation in the left eye. Progressive enlargement of the mass and proliferative vitreoretinopathy eventually led to phthisis bulbi and enucleation. Histologically, the mass showed a predominant astrocytic component with intense glial fibrillary acidic protein staining, hyperplasia, fibrous metaplasia, and osseous metaplasia of the retinal pigment epithelium. The Ki-67 proliferative index was <5%, and few scattered vascular channels were observed. Conclusions and Importance: These findings show that this tumor is the result of a reactive glial process rather than of neoplastic vascular proliferation. Massive retinal gliosis probably represents the advanced stage of RRAT.

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