Proliferative vitreoretinopathy (PVR) is an abnormal and prolonged healing response to retinal injury (retinal detachment, post retinal detachment surgery) characterised by: pre/subretinal membrane formation; retinal gliosis and retinal shortening, retinal pigment epithelium cell proliferation; and increased glial (mainly Mu¨ller cells), fibroblast and inflammatory cell (macrophage, lymphocyte) activity, leading to tractional retinal holes/breaks and multiple costly eye operations suffered by patients. PVR can cause retinal re-detachment following primary surgical intervention for rhegmatogenous retinal detachment. Vitrectomy and scleral buckling surgery are the main approaches for treating PVR complications of retinal detachment. Patients require many operations to remove the scar tissue but vision results are suboptimal, and do not meet patient expectations. Over the past 40 years, this has been one of the greatest challenges for vitreoretinal surgeons and patients. Despite previous large clinical trials of multiple candidate drug therapeutics, no proven adjunctive treatment currently exists to either prevent, reduce, or treat PVR formation in retinal detachment. Both cellular proliferation and the intraocular inflammatory response are realistic targets for adjunctive treatments in PVR. The cellular components of PVR periretinal membranes (retinal pigment epithelial, glial, inflammatory and fibroblastic cells) proliferate and are thus targets for antiproliferative agents. In recent years, several new therapeutics have been tested, and we present an updated review of the clinical therapeutics for PVR in retinal detachment.
Keywords: 5-fluorouracil and low molecular weight heparin; Intravitreal methotrexate; Mitomycin-C; Pars plana vitrectomy; Proliferative vitreoretinopathy (PVR); Retinoic acid.
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