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Andrius Kazlauskas - One of the best experts on this subject based on the ideXlab platform.
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su9518 inhibits Proliferative Vitreoretinopathy in fibroblast and genetically modified muller cell induced rabbit models
Investigative Ophthalmology & Visual Science, 2013Co-Authors: Gisela Velez, Andrius Kazlauskas, Alexa R Weingarden, Hetian Lei, Guangping GaoAbstract:Purpose. Proliferative Vitreoretinopathy (PVR) is a complication of retinal detachment that can lead to surgical failure and vision loss. Previous studies suggest that a variety of retinal cells, including RPE and Muller glia, may be responsible. Platelet-derived growth factor receptor alpha (PDGFRα) has been strongly implicated in the pathogenesis, and found to be intrinsic to the development of PVR in rabbit models. We examine whether SU9518, a tyrosine kinase inhibitor with PDGFRα specificity, can inhibit the development of PVR in fibroblast and Muller cell rabbit models of PVR.
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a novel strategy to develop therapeutic approaches to prevent Proliferative Vitreoretinopathy
American Journal of Pathology, 2011Co-Authors: Marcandre Rheaume, Steven Pennock, Shizuo Mukai, Andrius KazlauskasAbstract:Proliferative Vitreoretinopathy (PVR) thwarts the repair of rhegmatogenous retinal detachments. Currently, there is no effective prevention for PVR. Platelet-derived growth factor receptor α (PDGFRα) is associated with PVR in humans and strongly promotes experimental PVR driven by multiple vitreal growth factors outside the PDGF family. We sought to identify vitreal factors required for experimental PVR and to establish a potential approach to prevent PVR. Vitreous was obtained from normal rabbits or those in which PVR was either developing or stabilized. Normal vitreous contained substantial levels of growth factors and cytokines, which changed quantitatively and/or qualitatively as PVR progressed and stabilized. Neutralizing a subset of these agents in rabbit vitreous eliminated their ability to induce PVR-relevant signaling and cellular responses. A single intravitreal injection of neutralizing reagents for this subset prevented experimental PVR. To identify growth factors and cytokines likely driving PVR in humans, we subjected vitreous from patients with or without PVR to a similar series of analyses. This analysis accurately identified those agents required for vitreous-induced contraction of cells from a patient PVR membrane. We conclude that combination therapy encompassing a subset of vitreal growth factors and cytokines is a potential approach to prevent PVR.
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n acetylcysteine suppresses retinal detachment in an experimental model of Proliferative Vitreoretinopathy
American Journal of Pathology, 2010Co-Authors: Hetian Lei, David Maberley, Arif Samad, Joanne A Matsubara, Gisela Velez, Jing Cui, Andrius KazlauskasAbstract:Proliferative Vitreoretinopathy (PVR) is a complication that develops in 5% to 10% of patients who undergo surgery to correct a detached retina. The only treatment option for PVR is surgical intervention, which has a limited success rate that diminishes in patients with recurring PVR. Our recent studies revealed that antioxidants prevented intracellular signaling events that were essential for experimental PVR. The purpose of this study was to test whether N-acetyl-cysteine (NAC), an antioxidant used in a variety of clinical settings, was capable of protecting rabbits from PVR. Vitreous-driven activation of PDGFRα and cellular responses intrinsic to PVR (contraction of collagen gels and cell proliferation) were blocked by concentrations of NAC that were well below the maximum tolerated dose. Furthermore, intravitreal injection of NAC effectively protected rabbits from developing retinal detachment, which is the sight-robbing phase of PVR. Finally, these observations with an animal model appear relevant to clinical PVR because NAC prevented human PVR vitreous-induced contraction of primary RPE cells derived from a human PVR membrane. Our observations demonstrate that antioxidants significantly inhibited experimental PVR, and suggest that antioxidants have the potential to function as a PVR prophylactic in patients undergoing retinal surgery to repair a detached retina.
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platelet derived growth factor plays a key role in Proliferative Vitreoretinopathy
Investigative Ophthalmology & Visual Science, 1999Co-Authors: Anthony Andrews, Michelle D Tallquist, Philippe Soriano, Egle Balciunaite, Fee Lai Leong, Miguel F Refojo, Andrius KazlauskasAbstract:PURPOSE The action of growth factors is thought to make a substantial contribution to the events leading to Proliferative Vitreoretinopathy (PVR). In this study, the importance of platelet-derived growth factor (PDGF) was tested in a rabbit model of PVR. METHODS The approach was to compare the extent of PVR induced by cells that do or do not express the receptors for PDGF and therefore differ in their ability to respond to PDGF. RESULTS Mouse embryo fibroblasts derived from PDGF receptor knock-out embryos that do not express either of the two PDGF receptors induced PVR poorly when injected into the eyes of rabbits that had previously undergone gas vitrectomy. Re-expression of the PDGF beta receptor in these cells did not improve the ability of the cells to cause PVR. In contrast, injection of cells expressing the PDGF alpha receptor resulted in stage 3 or higher PVR in 8 of 10 animals. CONCLUSIONS These findings show that PDGF makes an important contribution to the development of PVR in this animal model. Furthermore, there is a marked difference between the two receptors for PDGF, and it is the PDGF alpha receptor that is capable of driving events that lead to PVR.
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hepatocyte growth factor receptor in human rpe cells implications in Proliferative Vitreoretinopathy
Investigative Ophthalmology & Visual Science, 1999Co-Authors: Kameran Lashkari, Nader Rahimi, Andrius KazlauskasAbstract:PURPOSE. To determine whether hepatocyte growth factor (HGF) receptor (HGFR) is expressed in retinal pigment epithelial (RPE) cells and to test whether RPE cells are responsive to HGF. To evaluate expression of HGFR in human donor eyes and in several epiretinal membranes associated with Proliferative Vitreoretinopathy and idiopathic epiretinal membranes. METHODS. HGF-dependent migration and proliferation in primary and simian virus (SV) 40-transformed human RPE cells was studied using a Boyden chamber and [ 3 H]thymidine uptake, respectively. The expression and tyrosine phosphorylation of HGFR protein was evaluated in RPE cells by immunoprecipitation and western blot analysis. Expression of HGFR in human donor eyes and in several epiretinal membranes associated with Proliferative Vitreoretinopathy (PVR) and idiopathic epiretinal membranes was analyzed by immunohistochemistry. RESULTS. HGFR was expressed in RPE cells and was tyrosine-phosphorylate in response to HGF. Whereas HGF was a potent motogen for RPE cells, it induced only a modest, dose-dependent uptake of [ 3 H]thymidine. Evaluation of human donor eyes showed that the RPE monolayer was the major cell type that was strongly positive for HGFR. HGFR was uniformly and readily detected in the cellular component of epiretinal membranes associated with PVR, whereas little or no HGFR was found in idiopathic epiretinal membranes. CONCLUSIONS. HGFR is expressed in cultured RPE cells, in the RPE monolayer in human donor eyes, and in epiretinal membranes obtained from patients with PVR. Furthermore, HGF is a potent chemoattractant for cultured human RPE cells. These observations suggest a role for HGF and HGFR in normal function of RPE cells and in RPE-related disease such as PVR.
David R Hinton - One of the best experts on this subject based on the ideXlab platform.
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resveratrol inhibits epithelial mesenchymal transition of retinal pigment epithelium and development of Proliferative Vitreoretinopathy
Scientific Reports, 2015Co-Authors: Keijiro Ishikawa, Hiroto Terasaki, Hossein Nazari, Huiming Zhang, Christine Spee, Ram Kannan, David R HintonAbstract:Proliferative Vitreoretinopathy (PVR) is a serious complication of retinal detachment and ocular trauma, and its recurrence may lead to irreversible vision loss. Epithelial to mesenchymal transition (EMT) of retinal pigment epithelial (RPE) cells is a critical step in the pathogenesis of PVR, which is characterized by fibrotic membrane formation and traction retinal detachment. In this study, we investigated the potential impact of resveratrol (RESV) on EMT and the fibrotic process in cultured RPE cells and further examined the preventive effect of RESV on PVR development using a rabbit model of PVR. We found that RESV induces mesenchymal to epithelial transition (MET) and inhibits transforming growth factor-β2(TGF-β2)-induced EMT of RPE cells by deacetylating SMAD4. The effect of RESV on MET was dependent on sirtuin1 activation. RESV suppressed proliferation, migration and fibronectin synthesis induced by platelet-derived growth factor-BB or TGF-β2. In vivo, RESV inhibited the progression of experimental PVR in rabbit eyes. Histological findings showed that RESV reduced fibrotic membrane formation and decreased α-SMA expression in the epiretinal membranes. These results suggest the potential use of RESV as a therapeutic agent to prevent the development of PVR by targeting EMT of RPE.
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In vivo models of Proliferative Vitreoretinopathy
Nature Protocols, 2007Co-Authors: Rajat N Agrawal, Jing Z Cui, Christine Spee, Stephen J Ryan, David R HintonAbstract:We outline current in vitro and in vivo models for experimental Proliferative Vitreoretinopathy (PVR) and provide a detailed protocol of our standardized in vivo PVR model. PVR is the leading cause of failed surgical procedures for the correction of rhegmatogenous retinal detachment. The pathogenesis of this multifactorial condition is still not completely understood. Experimental models for PVR help us understand the factors that play a role in the pathogenesis of the disease process in a controlled manner and allow for reproducible preclinical assessment of novel therapeutic interventions. We describe a cell injection model in detail that uses homologous retinal pigment epithelial (RPE) cell cultures to induce PVR over a 2–8 week period.
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novel growth factors involved in the pathogenesis of Proliferative Vitreoretinopathy
Eye, 2002Co-Authors: David R Hinton, Manlin Jin, Ernesto Barron, Stephen J RyanAbstract:Aims To determine whether hepatocyte growth factor (HGF) and connective tissue growth factor (CTGF) are expressed in human specimens of Proliferative Vitreoretinopathy (PVR) and to propose a model of PVR pathogenesis based upon the known activities of these growth factors. Methods Immunohistochemical methods (ABC Elite) were used to demonstrate the presence of HGF and CTGF in cryostat sections of five human PVR membranes. Results In each of the five PVR membranes, stromal cells were immunohistochemically positive for both HGF and CTGF. Based upon this information and the known actions of these growth factors, a model of PVR pathogenesis was developed. In this model, injury of the retina induces an inflammatory response that upregulates HGF expression inducing the formation of multilayered groups of migratory retinal pigment epithelial cells (RPE). These RPE, present in a provisional extracellular matrix, come in contact with vitreous containing TGF-β. The TGF-β is activated, upregulating expression of CTGF. Under the influence of TGF-β and CTGF, RPE become myofibroblastic and fibrosis ensues. Retinal traction induces further detachment continuing the cycle of retinal injury. Conclusions HGF and CTGF are expressed in PVR membranes and may play important roles in the pathogenesis of PVR. The expression and function of these growth factors should be critically examined in human PVR specimens, in in vitro cultures of RPE, and in animal models of PVR.
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post traumatic Proliferative Vitreoretinopathy the epidemiologic profile onset risk factors and visual outcome
Ophthalmology, 1997Co-Authors: Jose Augusto Cardillo, Jing Z Cui, David R Hinton, Timothy J Stout, Laurie Labree, Stanley P Azen, Luis Omphroy, Hideya Kimura, Stephen J RyanAbstract:Purpose: The purpose of the study was to characterize the clinical development of Proliferative Vitreoretinopathy (PVR) after trauma in the human eye. Methods: A chart review was performed on the records of 1564 patients with ocular trauma seen at a large metropolitan hospital. The frequency, type of ocular trauma, time to onset, potential risk factors, and visual outcome for PVR were evaluated. Results: Proliferative Vitreoretinopathy occurred in 71 (4%) of 1654 injured eyes. Of these 71 injured eyes, 30 (42%) resulted from rupture, 15 (21 %) from penetration, 13 (18%) from perforation, and 7 (10%) from contusion. Six (9%) were associated with an intraocular foreign body (IOFB). The frequency of PVR following perforation, rupture, penetration, IOFB, and contusion was 43%, 21%, 15%, 11 %, and 1 %, respectively. Overall, those eyes that developed PVR had a poorer visual outcome, with PVR being the primary reason for visual loss. The time from injury to onset of PVR was shortest after perforation (median, 1.3 months), followed by rupture (2.1 months), IOFB (3.1 months), penetration (3.2 months), and contusion (5.7 months). Vitreous hemorrhage was the strongest independent predictive factor for the development of PVR. A long, posteriorly located wound and persistent intraocular inflammation were also important risk factors for PVR. Conclusions: These results suggest that PVR is a common complication following a variety of ocular injuries, and that it is associated with a poor visual outcome. Its frequency, onset, and outcome are strongly dependent on the nature of the trauma. Specific high-risk groups are identified as candidates for more aggressive therapy.
Ajay E. Kuriyan - One of the best experts on this subject based on the ideXlab platform.
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salinomycin inhibits Proliferative Vitreoretinopathy formation in a mouse model
PLOS ONE, 2020Co-Authors: Alison M Heffer, Ajay E. Kuriyan, Victor Wang, Richard T Libby, Steven E Feldon, Collynn F WoellerAbstract:Proliferative Vitreoretinopathy (PVR) is a progressive disease that develops in a subset of patients who undergo surgery for retinal detachment repair, and results in significant vision loss. PVR is characterized by the migration of retinal pigment epithelial (RPE) cells into the vitreous cavity, where they undergo epithelial-to-mesenchymal transition and form contractile membranes within the vitreous and along the retina, resulting in recurrent retinal detachments. Currently, surgical intervention is the only treatment for PVR and there are no pharmacological agents that effectively inhibit or prevent PVR formation. Here, we show that a single intravitreal injection of the polyether ionophore salinomycin (SNC) effectively inhibits the formation of PVR in a mouse model with no evidence of retinal toxicity. After 4 weeks, fundus photography and optical coherence tomography (OCT) demonstrated development of mean PVR grade of 3.5 (SD: 1.3) in mouse eyes injected with RPE cells/DMSO (vehicle), compared to mean PVR grade of 1.6 (SD: 1.3) in eyes injected with RPE cells/SNC (p = 0.001). Additionally, immunohistochemistry analysis showed RPE cells/SNC treatment reduced both fibrotic (αSMA, FN1, Vim) and inflammatory (GFAP, CD3, CD20) markers compared to control RPE cells/DMSO treatment. Finally, qPCR analysis confirmed that Tgfβ, Tnfα, Mcp1 (inflammatory/cytokine markers), and Fn1, Col1a1 and Acta2 (fibrotic markers) were significantly attenuated in the RPE cells/SNC group compared to RPE/DMSO control. These results suggest that SNC is a potential pharmacologic agent for the prevention of PVR in humans and warrants further investigation.
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the polyether ionophore salinomycin targets multiple cellular pathways to block Proliferative Vitreoretinopathy pathology
PLOS ONE, 2019Co-Authors: Alison M Heffer, Richard T Libby, Steven E Feldon, Collynn F Woeller, Jacob Proano, Elisa Roztocil, Richard P Phipps, Krystel R Huxlin, Patricia J Sime, Ajay E. KuriyanAbstract:Proliferative Vitreoretinopathy (PVR) is characterized by membranes that form in the vitreous cavity and on both surfaces of the retina, which results in the formation of tractional membranes that can cause retinal detachment and intrinsic fibrosis of the retina, leading to retina foreshortening. Currently, there are no pharmacologic therapies that are effective in inhibiting or preventing PVR formation. One of the key aspects of PVR pathogenesis is retinal pigment epithelial (RPE) cell epithelial mesenchymal transition (EMT). Here we show that the polyether ionophore compound salinomycin (SNC) effectively inhibits TGFβ-induced EMT of RPE cells. SNC blocks the activation of TGFβ-induced downstream targets alpha smooth muscle actin (αSMA) and collagen 1 (Col1A1). Additionally, SNC inhibits TGFβ-induced RPE cell migration and contraction. We show that SNC functions to inhibit RPE EMT by targeting both the pTAK1/p38 and Smad2 signaling pathways upon TGFβ stimulation. Additionally, SNC is able to inhibit αSMA and Col1A1 expression in RPE cells that have already undergone TGFβ-induced EMT. Together, these results suggest that SNC could be an effective therapeutic compound in both the prevention and treatment of PVR.
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Proliferative Vitreoretinopathy: A Review
International ophthalmology clinics, 2019Co-Authors: Sana Idrees, Jayanth Sridhar, Ajay E. KuriyanAbstract:Proliferative Vitreoretinopathy (PVR) is the most common cause for failure of rhegmatogenous retinal detachment repair and is characterized by the growth and contraction of cellular membranes within the vitreous cavity and on both sides of the retinal surface as well as intraretinal fibrosis. Currently, PVR is thought to be an abnormal wound healing response that is primarily driven by inflammatory, retinal, and RPE cells. At this time, surgery is the only management option for PVR as there is no proven pharmacologic agent for the treatment or prevention of PVR. Laboratory research to better understand PVR pathophysiology and clinical trials of various agents to prevent PVR formation are ongoing.
David G Charteris - One of the best experts on this subject based on the ideXlab platform.
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classifications for Proliferative Vitreoretinopathy pvr an analysis of their use in publications over the last 15 years
Journal of Ophthalmology, 2016Co-Authors: Salvatore Di Lauro, David G Charteris, Mustafa R Kadhim, Carlos J PastorAbstract:Purpose. To evaluate the current and suitable use of current Proliferative Vitreoretinopathy (PVR) classifications in clinical publications related to treatment. Methods. A PubMed search was undertaken using the term “Proliferative Vitreoretinopathy therapy”. Outcome parameters were the reported PVR classification and PVR grades. The way the classifications were used in comparison to the original description was analyzed. Classification errors were also included. It was also noted whether classifications were used for comparison before and after pharmacological or surgical treatment. Results. 138 papers were included. 35 of them (25.4%) presented no classification reference or did not use any one. 103 publications (74.6%) used a standardized classification. The updated Retina Society Classification, the first Retina Society Classification, and the Silicone Study Classification were cited in 56.3%, 33.9%, and 3.8% papers, respectively. Furthermore, 3 authors (2.9%) used modified-customized classifications and 4 (3.8%) classification errors were identified. When the updated Retina Society Classification was used, only 10.4% of authors used a full C grade description. Finally, only 2 authors reported PVR grade before and after treatment. Conclusions. Our findings suggest that current classifications are of limited value in clinical practice due to the inconsistent and limited use and that it may be of benefit to produce a revised classification.
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ozurdex a slow release dexamethasone implant in Proliferative Vitreoretinopathy study protocol for a randomised controlled trial
Trials, 2013Co-Authors: Philip J Banerjee, Catey Bunce, David G CharterisAbstract:Background: Proliferative Vitreoretinopathy (PVR) is the commonest cause of late anatomical failure in rhegmatogenous retinal detachment. Visual and anatomical outcomes remain poor despite advances in vitreoretinal surgical techniques with reported primary failure rates of up to nearly 50%. Numerous adjunctive medications have been evaluated in clinical trials with no agent gaining widespread acceptance and use. This study was designed to investigate the benefits of using a slow-release dexamethasone implant delivered intra-operatively in patients undergoing vitrectomy surgery for retinal detachment with established PVR. Methods/design: For the study, 140 patients requiring vitrectomy surgery with silicone oil for retinal detachment with established PVR will be randomised to receive either standard treatment or study treatment in a 1:1 treatment allocation ratio. Both groups will receive the standard surgical treatment appropriate for their eye condition and routine peri-operative treatment and care, differing only in the addition of the supplementary adjunctive agent in the treatment group. The investigated primary outcome measure is stable retinal reattachment with removal of silicone oil without additional vitreoretinal surgical intervention at 6 months. Discussion: This is the first randomised controlled clinical trial to investigate the use of an adjunctive slow-release dexamethasone implant in patients undergoing vitrectomy surgery for retinal detachments with Proliferative Vitreoretinopathy.
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glial remodeling and neural plasticity in human retinal detachment with Proliferative Vitreoretinopathy
Investigative Ophthalmology & Visual Science, 2005Co-Authors: C S Sethi, Geoffrey P. Lewis, Steven K. Fisher, William P Leitner, Derrick L Mann, Philip J Luthert, David G CharterisAbstract:PURPOSE. To investigate glial remodeling and neuronal plasticity in adult human retinal detachment complicated by Proliferative Vitreoretinopathy (PVR) and to grade pathologic changes with a severity scoring system. METHODS. Sixteen full-thickness retinectomy specimens obtained at retinal relaxing surgery for PVR were fixed in 4% paraformaldehyde immediately after excision and compared to similarly processed normal donor retinas. Agarose-embedded sections (100-m-thick) were double labeled for immunohistochemistry by confocal microscopy, with antibodies against rod opsin and GFAP; vimentin and M/L-cone opsin; calbindin D and S-cone opsin; and cytochrome oxidase and synaptophysin. These staining patterns formed the basis of a retinal pathology scoring system, and immunohistochemistry was also used to detect CD68, neurofilaments, protein kinase C, growth-associated protein-43, and a pan-cone‐specific enzymatic marker. Morphology was also assessed by light microscopy of resinembedded semithin sections. RESULTS. Prolonged detachment was characterized by photoreceptor degeneration and intracellular redistribution of opsin proteins to the plasma membrane in the outer nuclear layer (ONL). Remodeling of rod synaptic terminals was characterized by terminal retraction and also by axon extension to the inner retina in most specimens. Rod bipolar cell dendrites extended into the ONL, as did fine, horizontal cell processes. Large ganglion cells showed upregulated neurofilament and GAP-43 expression, with neurites sprouting from somata and axon collaterals. Anti-cytochrome oxidase labeling of surviving inner segments was reduced but detectable in all specimens, as was anti-calbindin D labeling of horizontal and amacrine cells.
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Proliferative Vitreoretinopathy developments in adjunctive treatment and retinal pathology
Eye, 2002Co-Authors: David G Charteris, C S Sethi, G P Lewis, Steven K. FisherAbstract:Proliferative Vitreoretinopathy (PVR) remains a difficult management problem despite advances in vitreoretinal surgery. There is still a significant incidence of PVR in rhegmatogenous retinal detachment and other forms of retinal disease. Surgery for PVR now has a high anatomical success rate although visual results are often disappointing. The use of adjunctive treatments to prevent cellular proliferation holds promise for the prevention of PVR or recurrences after surgery. Control of proliferation and strategies aimed at improving visual outcome are important areas of future research in PVR and other forms of retinal disease. Studies of the intraretinal and peri-retinal pathology of PVR have demonstrated characteristic changes which may have a significant influence on visual outcome and surgical management.
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how to predict Proliferative Vitreoretinopathy a prospective study
Ophthalmology, 2001Co-Authors: Riaz H Y Asaria, Philip J Luthert, David G Charteris, Chee Hing Kon, Catey Bunce, David Wong, Peng T Khaw, G W AylwardAbstract:Abstract Purpose To determine prospectively the accuracy of a predictive risk formula for the development of postoperative Proliferative Vitreoretinopathy (PVR) when applied in a clinical setting. Design Prospective noncomparative interventional case series. Participants Two hundred nineteen subjects undergoing primary vitrectomy for rhegmatogenous retinal detachment were studied. Method By use of a formula-based discriminant rule, subjects were classified as either high or low risk for the development of PVR. All subjects were followed prospectively. Outcome measures Development of postoperative PVR as defined by the updated the Retina Society Classification. Results Complete data were available on 212 of 219 subjects. There were 130 subjects identified as low risk and 82 subjects as high risk; 9.2% of the low-risk (12 of 130) compared with 28% (23 of 82) of the high-risk subjects had postoperative PVR develop. This difference was statistically significant ( P Conclusions Our study has shown that using a clinical model it is possible to identify subjects at greater risk of PVR developing after primary vitrectomy.
Jeffrey S Heier - One of the best experts on this subject based on the ideXlab platform.
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endoscopy assisted vitrectomy and membrane dissection of anterior Proliferative Vitreoretinopathy for chronic hypotony after previous retinal detachment repair
Retina-the Journal of Retinal and Vitreous Diseases, 2016Co-Authors: Gregory D Lee, Roger A Goldberg, Jeffrey S HeierAbstract:PURPOSE To review 6-month outcomes for patients with hypotony secondary to anterior Proliferative Vitreoretinopathy after previous retinal detachment repair who were treated with endoscopic vitrectomy and anterior membrane dissection. METHODS Retrospective review. All individuals underwent endoscopic vitrectomy with removal of anterior Proliferative Vitreoretinopathy involving the ciliary body. Outcome measurements included intraocular pressure (IOP), visual acuity, and development of phthisis bulbi. RESULTS Fifteen eyes of 15 patients had an average of 4.5 previous intraocular surgeries (range 1-8). Forty Percent of eyes had silicone oil at the time of endoscopic surgery. Six months postoperatively, 4 eyes had IOP >11 mmHg while 11 had IOP <6 mmHg. The nonresponder group was older in age, had more previous intraocular surgeries, and a lower preoperative IOP. There were no differences in visual acuity or the development of prephthisis at any point. No eyes underwent enucleation or evisceration. CONCLUSION Endoscopy-assisted vitrectomy with removal of anterior Proliferative Vitreoretinopathy from the ciliary body is an effective treatment for chronic hypotony after previous retinal detachment repair in a minority of cases. The IOP improved in patients who tended to be younger and who had fewer previous intraocular surgeries. Further study is indicated to evaluate long-term outcomes and predictors of surgical success.
