Surgical management and ultrastructural study of choroidal neovascularization in punctate inner choroidopathy after bevacizumab

J Ophthalmic Inflamm Infect. 2012 Mar;2(1):29-37. doi: 10.1007/s12348-011-0050-x. Epub 2011 Nov 27.

Abstract

Purpose: This study aims to describe surgical management results and the pathologic features of choroidal neovascularization (CNV) secondary to punctate inner choroidopathy (PIC) following anti-vascular endothelial growth factor treatment.

Design: This study is a case report on the surgical management and ultrastructural study of choroidal neovascularization.

Methods: Clinicopathologic and ultrastructural report of CNV membranes excised from both eyes of one patient was presented.

Results: The right eye responded to bevacizumab, and recurrence 17 months later did not; the left eye never responded. Excision of the active CNVs was performed 3 months after the last injection. In the right eye, there was no recurrence 23 months after surgery. In the left eye, CNV recurred after 6 months, with no response to bevacizumab. Electron microscopy revealed subretinal neovascular tissue and, additionally, Bruch's membrane and inner choroid in the left. In the right eye, lumens of many neovascular channels were occluded by microfibrils and pericytes were infrequent. In the left eye, patent CNV units with pericytes were present. There were scattered macrophages but no lymphocytes in either membrane. An inner focal choroidal lymphocytic infiltrate was discovered.

Conclusions: Submacular surgery did not cause complications following treatment with bevacizumab. Mostly nonfunctional capillaries in the right membrane failed to display pericytes. The left membrane, which was unresponsive to bevacizumab, displayed well-formed neovascular units consistently exhibiting pericytes. A focus of inner choroidal lymphocytic infiltration was found in the left eye despite the absence of overt clinical intraocular inflammation. This is the first pathological study employing human tissue that points to pericytes as a potential critical therapeutic target with the aggravating influence of inner choroidal chronic inflammation in PIC.