Lamellar Hole–associated Epiretinal Proliferation

In Brief Purpose: To correlate clinical and optical coherence tomographic features with histopathological and immunohistochemical findings in an eye undergoing surgical excision of lamellar hole–associated epiretinal proliferation (LHEP). Methods: An eye with a lamellar macular hole and LHEP without a tractional epiretinal membrane component was identified with spectral-domain optical coherence tomographic imaging and underwent pars plana vitrectomy with LHEP and internal limiting membrane peeling and gas tamponade. The surgically excised LHEP specimen was analyzed with histopathological and immunohistochemical staining using flat-mount preparation techniques. Postsurgical outcomes including visual acuity and optical coherence tomographic imaging were reviewed. Results: With spectral-domain optical coherence tomography, the lamellar macular hole was found to be closed with no residual LHEP after the surgery. Visual acuity improved from 20/200 preoperatively to 20/40 at 6 months after the surgery. Histopathological and immunohistochemical analyses of the LHEP specimen revealed retinal glial cells that reacted positively with anti–glial fibrillary acidic protein and anti–glutamine synthetase, a Müller cell–specific antibody. Conclusion: Lamellar macular hole with LHEP may demonstrate closure after pars plana vitrectomy with LHEP and internal limiting membrane peeling and gas tamponade. There was considerable improvement in visual acuity. It is possible that LHEP originates from middle retinal layers of the lamellar hole defect because it contains retinal glial cells, specifically Müller cells. Lamellar hole–associated epiretinal proliferation was found on immunohistochemical analysis to contain retinal glial cells, which reacted positively with anti–glial fibrillary acidic protein and anti–glutamine synthetase, a Müller cell–specific antibody. Hence, it is plausible that this entity originates from middle retinal layers of the lamellar hole defect.