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Thomas M. Aaberg - One of the best experts on this subject based on the ideXlab platform.
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Osseous metaplasia in proliferative Vitreoretinopathy.
American journal of ophthalmology, 1998Co-Authors: Young Doo Yoon, Thomas M. Aaberg, Ted H. Wojno, Hans E. GrossniklausAbstract:Purpose To report the clinicopathologic features of intraocular osseous production in association with proliferative Vitreoretinopathy. Method The clinical and histopathologic features of two patients with proliferative vitreo-retinopathy and intraocular bone formation are reviewed. Results Preretinal osseous tissue incorporated in the proliferative Vitreoretinopathy was surgically removed in one patient, and osseous tissue was present in the proliferative Vitreoretinopathy in the enucleated eye of the other patient. Conclusions Bone formation, presumably from metaplastic retinal pigment epithelium, may be present in proliferative Vitreoretinopathy tissue. The intraocular bone is present internal rather than external to the neurosensory retina.
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Pathogenetic Mechanisms in Anterior Proliferative Vitreoretinopathy
American journal of ophthalmology, 1992Co-Authors: Pedro F. Lopez, Thomas M. Aaberg, Hans E. Grossniklaus, Paul Sternberg, Antonio Capone, H. Michael LambertAbstract:A clinicopathologic study of ten consecutive patients (ten eyes) undergoing surgery for rhegmatogenous retinal detachment with anterior proliferative Vitreoretinopathy and a subsequent histopathologic, immunohisto-chemical, and ultrastructural study of ten enucleated eyes with anterior proliferative Vitreoretinopathy were performed in order to elucidate relevant pathogenetic mechanisms. Our findings suggest that the pathogenetic evolution of anterior proliferative Vitreoretinopathy occurs in three consecutive stages: (1) traction on the ciliary body and peripheral retina induced by fibrocellular contraction of the vitreous base; (2) incorporation of tractionally denuded components of the ciliary body and peripheral retina into the fibrocellular membranes overlying the vitreous base; and (3) proliferation of the incorporated components and fibrovascular ingrowth from the uvea, the retina, or both, into the fibrocellular membranes. Tractional disruption of the epithelium of the ciliary body pars plicata and breakdown of the ciliary blood-aqueous barrier are the principal pathogenetic mechanisms of chronic intractable hypotony and the postvitrectomy fibrin syndrome in anterior proliferative Vitreoretinopathy.
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Causes of Failure After Repeat Vitreoretinal Surgery for Recurrent Proliferative Vitreoretinopathy
American journal of ophthalmology, 1991Co-Authors: Hilel Lewis, Thomas M. AabergAbstract:During the last two years, we performed vitreoretinal surgery on 37 eyes with retinal detachments and recurrent severe proliferative Vitreoretinopathy in 37 patients who had had previous failed scleral buckling and vitreous surgery for proliferative Vitreoretinopathy. Anterior proliferative Vitreoretinopathy was present in 32 of 37 eyes (86%); posterior proliferative Vitreoretinopathy of fixed retinal folds in four quadrants of narrow or closed funnel shape occurred in 23 of 37 eyes (62%); and subretinal proliferation was noted in 16 of 37 eyes (43%). The retinas in 12 eyes (32%) redetached from new or recurrent anterior proliferative Vitreoretinopathy in nine eyes, reopening of pre-existing retinal breaks in two eyes, or recurrent posterior periretinal proliferation in one eye. With additional vitreoretinal procedures in six eyes and after a mean follow-up period of 11 months, 27 of 37 retinas (73%) were totally reattached, and an additional five eyes (13%) had retinal reattachment posterior to the scleral buckle. Of the 32 patients with posterior retinal reattachment, final visual acuity of 5/200 or better was attained in 19 eyes (59%).
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causes of failure after initial vitreoretinal surgery for severe proliferative Vitreoretinopathy
American Journal of Ophthalmology, 1991Co-Authors: Hilel Lewis, Thomas M. Aaberg, Gary W AbramsAbstract:We performed initial vitreoretinal surgery on 81 eyes with rhegmatogenous retinal detachments complicated by severe proliferative Vitreoretinopathy. Of 81 eyes, 68 (84%) had undergone previous scleral buckling. We performed vitreous base dissection on all 18 eyes (22%) that had anterior proliferative Vitreoretinopathy. With one vitreoretinal operation, 66 of 81 eyes (81%) remained totally reattached. The main cause of initial anatomic failure and reoperation was either new or recurrent proliferation at the vitreous base. With additional vitreoretinal surgery and after a mean follow-up period of 19 months, 73 of 81 retinas (90%) were totally reattached. The final causes of anatomic failure were anterior proliferative Vitreoretinopathy and proliferation from relaxing retinotomies. Of the 73 successfully reattached eyes, 62 (85%) had postoperative visual acuity of 5/200 or better.
Hilel Lewis - One of the best experts on this subject based on the ideXlab platform.
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Surgical treatment for chronic hypotony and anterior proliferative Vitreoretinopathy.
American journal of ophthalmology, 1996Co-Authors: Hilel Lewis, Juan VerdaguerAbstract:Purpose To determine whether vitreoretinal surgery to release anterior traction in eyes with chronic hypotony and attached posterior retinas increases the intraocular pressure and prevents atrophia bulbi. Methods In this prospective study, we operated on and followed-up postoperatively 17 eyes of 17 consecutive patients with previous vitreoretinal surgeries for retinal detachments and severe proliferative Vitreoretinopathy. These eyes had developed chronic hypotony (intraocular pressure ^5 mm Hg for at least one month) and anterior proliferative Vitreoretinopathy. Results After a minimum of six months of postoperative follow-up (mean, 10.6 months), mean intraocular pressure had increased significantly after surgery from 1.7 to 7.2 mm Hg (P Conclusions Early surgery to release traction over the anterior retina and uveal tissue in eyes with chronic hypotony and anterior proliferative Vitreoretinopathy can increase intraocular pressure and stabilize visual acuity.
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Causes of Failure After Repeat Vitreoretinal Surgery for Recurrent Proliferative Vitreoretinopathy
American journal of ophthalmology, 1991Co-Authors: Hilel Lewis, Thomas M. AabergAbstract:During the last two years, we performed vitreoretinal surgery on 37 eyes with retinal detachments and recurrent severe proliferative Vitreoretinopathy in 37 patients who had had previous failed scleral buckling and vitreous surgery for proliferative Vitreoretinopathy. Anterior proliferative Vitreoretinopathy was present in 32 of 37 eyes (86%); posterior proliferative Vitreoretinopathy of fixed retinal folds in four quadrants of narrow or closed funnel shape occurred in 23 of 37 eyes (62%); and subretinal proliferation was noted in 16 of 37 eyes (43%). The retinas in 12 eyes (32%) redetached from new or recurrent anterior proliferative Vitreoretinopathy in nine eyes, reopening of pre-existing retinal breaks in two eyes, or recurrent posterior periretinal proliferation in one eye. With additional vitreoretinal procedures in six eyes and after a mean follow-up period of 11 months, 27 of 37 retinas (73%) were totally reattached, and an additional five eyes (13%) had retinal reattachment posterior to the scleral buckle. Of the 32 patients with posterior retinal reattachment, final visual acuity of 5/200 or better was attained in 19 eyes (59%).
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causes of failure after initial vitreoretinal surgery for severe proliferative Vitreoretinopathy
American Journal of Ophthalmology, 1991Co-Authors: Hilel Lewis, Thomas M. Aaberg, Gary W AbramsAbstract:We performed initial vitreoretinal surgery on 81 eyes with rhegmatogenous retinal detachments complicated by severe proliferative Vitreoretinopathy. Of 81 eyes, 68 (84%) had undergone previous scleral buckling. We performed vitreous base dissection on all 18 eyes (22%) that had anterior proliferative Vitreoretinopathy. With one vitreoretinal operation, 66 of 81 eyes (81%) remained totally reattached. The main cause of initial anatomic failure and reoperation was either new or recurrent proliferation at the vitreous base. With additional vitreoretinal surgery and after a mean follow-up period of 19 months, 73 of 81 retinas (90%) were totally reattached. The final causes of anatomic failure were anterior proliferative Vitreoretinopathy and proliferation from relaxing retinotomies. Of the 73 successfully reattached eyes, 62 (85%) had postoperative visual acuity of 5/200 or better.
Stephen J. Ryan - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of Experimental Proliferative Vitreoretinopathy by Retroviral Vector-mediated Transfer of Suicide Gene: Can Proliferative Vitreoretinopathy be a Target of Gene Therapy?
Ophthalmology, 1995Co-Authors: Taiji Sakamoto, Hideya Kimura, Zorica Scuric, Christine Spee, Erlinda M. Gordon, David R. Hinton, W. French Anderson, Stephen J. RyanAbstract:Purpose: To determine the potential of somatic gene transfer as a treatment for proliferative Vitreoretinopathy (PVR), experimental PVR was induced in rabbits by intraocular injection of fibroblasts bearing the herpes simplex virus thymidine kinase (HStk) gene. These transduced cells should be susceptible to cytotoxicity by exposure to ganciclovir (GCV). Materials and Methods: Rabbit fibroblasts were transduced with retroviral vectors bearing an HStk gene. Proliferative Vitreoretinopathy was induced by injection of 5 × 104 normal or HStk gene-transduced fibroblasts (HStk fibroblasts) into rabbit eyes. Ganciclovir (100 µg per eye) or saline was injected into the vitreous on days 0 and 4. Experimental animals were divided into three groups: group A received HStk fibroblasts with GCV; group B, normal fibroblasts with GCV; group C, HStk fibroblasts with saline. Proliferative Vitreoretinopathy also was induced in several other groups of eyes, some receiving GCV and different proportions of HStk fibroblasts to normal fibroblasts, others receiving only normal fibroblasts and GCV. The eyes were examined by indirect ophthalmoscopy on days 4, 7, 14, and 28, and PVR was classified into six stages (0–5). Results: Proliferative Vitreoretinopathy was induced and progressed over time in each group. On day 28, PVR was most severe in animals in group B (average stage, 4.6) and group C (average stage, 4.4). Proliferative Vitreoretinopathy was inhibited in group A (average stage, 1.0). The groups that received mixed injection of HStk fibroblasts and normal fibroblasts had intermediate PVR. Results of histologic study showed no apparent toxic or pathologic reaction in the retinochoroidal tissue of group A animals. Conclusions: Severity of experimental PVR clearly was reduced by transfer of the HStk gene and administration of GCV. This inhibitory effect also was produced by a combination of 10% HStk fibroblasts and 90% normal fibroblasts, indicating a significant bystander effect. These data suggest the potential of somatic gene therapy for the treatment of PVR.
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The effects of silicone oil removal. Silicone Study Report 6
Archives of Ophthalmology, 1994Co-Authors: William L. Hutton, Mark S. Blumenkranz, Stanley P. Azen, Brooks W. Mccuen, Harry W. Flynn, Robert C. Ramsay, Stephen J. RyanAbstract:Objective: To evaluate the advisability of removing silicone oil from eyes after surgery for severe (with a classification of at least C-3) proliferative Vitreoretinopathy. Design: Subgroup analysis of the Silicone Study, a randomized, multicentered, surgical trial. Setting: Community- and university-based clinics. Patients: Two hundred twenty-two eyes with severe proliferative Vitreoretinopathy followed up in the Silicone Study. Interventions: Vitrectomy for proliferative Vitreoretinopathy with silicone oil as the intraocular tamponade. Outcome Measures: Changes in visual acuity, recurrent retinal detachment, and incidence of complications. Results: Ninety-nine (45%) of 222 eyes had surgery for silicone oil removal (oil-removed eyes). Compared with the eyes that did not undergo silicone oil removal (oil-retained eyes) evaluated at a comparable time after oil injection, oil-removed eyes at the examination prior to oil removal were more likely to be attached (85% vs 40%;P Conclusion: Removal of silicone oil in anatomically successful eyes significantly increases the likelihood of improved visual acuity with a slight increase in the likelihood of recurrent retinal redetachment. There was a trend for a reduction in the incidence of complications in the oil-removed eyes.
Mark S. Blumenkranz - One of the best experts on this subject based on the ideXlab platform.
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Improved surgical treatment of familial exudative Vitreoretinopathy in children
American journal of ophthalmology, 1995Co-Authors: Louis C. Glazer, Michael T. Trese, Albert M. Maguire, Mark S. Blumenkranz, W. Richard GreenAbstract:Purpose To evaluate current surgical results in patients with familial exudative Vitreoretinopathy and study the histologic findings of epiretinal membranes obtained at the time of surgery. Methods We performed phakic pars plana vitrectomy and membrane peeling on five patients (six eyes) with familial exudative Vitreoretinopathy, who ranged in age from 18 months to 9 years and had traction retinal detachment. Membranes from two eyes (two patients) were analyzed by light and electron microscopy. Results The macula was reattached in all six eyes. Visual acuity improved after surgery in five of the six eyes, with two eyes improving from a preoperative visual acuity of 20/400 to a postoperative visual acuity of 20/25 and 20/60. Electron microscopic analysis of the membranes from two patients disclosed thick fibrocellular fragments with vascular elements and astrocytes. Conclusion With current surgical techniques, there appears to be improvement in the anatomic reattachment rate and visual outcome in patients with familial exudative Vitreoretinopathy. Amblyopia, reproliferation, and vitreous hemorrhage may limit long-term improvement in vision.
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The effects of silicone oil removal. Silicone Study Report 6
Archives of Ophthalmology, 1994Co-Authors: William L. Hutton, Mark S. Blumenkranz, Stanley P. Azen, Brooks W. Mccuen, Harry W. Flynn, Robert C. Ramsay, Stephen J. RyanAbstract:Objective: To evaluate the advisability of removing silicone oil from eyes after surgery for severe (with a classification of at least C-3) proliferative Vitreoretinopathy. Design: Subgroup analysis of the Silicone Study, a randomized, multicentered, surgical trial. Setting: Community- and university-based clinics. Patients: Two hundred twenty-two eyes with severe proliferative Vitreoretinopathy followed up in the Silicone Study. Interventions: Vitrectomy for proliferative Vitreoretinopathy with silicone oil as the intraocular tamponade. Outcome Measures: Changes in visual acuity, recurrent retinal detachment, and incidence of complications. Results: Ninety-nine (45%) of 222 eyes had surgery for silicone oil removal (oil-removed eyes). Compared with the eyes that did not undergo silicone oil removal (oil-retained eyes) evaluated at a comparable time after oil injection, oil-removed eyes at the examination prior to oil removal were more likely to be attached (85% vs 40%;P Conclusion: Removal of silicone oil in anatomically successful eyes significantly increases the likelihood of improved visual acuity with a slight increase in the likelihood of recurrent retinal redetachment. There was a trend for a reduction in the incidence of complications in the oil-removed eyes.
Christopher M. Andreoli - One of the best experts on this subject based on the ideXlab platform.
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smoking is a risk factor for proliferative Vitreoretinopathy after traumatic retinal detachment
Retina-the Journal of Retinal and Vitreous Diseases, 2017Co-Authors: Dean Eliott, Tomasz P Stryjewski, Michael T Andreoli, Christopher M. AndreoliAbstract:PURPOSE To determine the incidence of retinal redetachment due to proliferative Vitreoretinopathy after open-globe trauma in smokers and nonsmokers. METHODS A total of 892 patients comprising 893 open-globe injuries, in whom 255 eyes were diagnosed with a retinal detachment, and 138 underwent surgical repair were analyzed in a retrospective case-control study. Time to redetachment was examined using the Kaplan-Meier method and analysis of risk factors was analyzed using Cox proportional hazards modeling. RESULTS Within one year after retinal detachment surgery, 47% (95% CI, 39-56%) of all 138 repaired retinas redetached because of proliferative Vitreoretinopathy. Being a smoker was associated with a higher rate of detachment (adjusted hazard ratio 1.96, P = 0.01). As shown in previous studies, the presence of proliferative Vitreoretinopathy at the time of surgery was also an independent risk factor for failure (adjusted hazard ratio 2.13, P = 0.005). Treatment with vitrectomy-buckle compared favorably to vitrectomy alone (adjusted hazard ratio 0.58, P = 0.04). Only 8% of eyes that redetached achieved a best-corrected visual acuity of 20/200 or better, in comparison to 44% of eyes that did not redetach (P < 0.001). CONCLUSION Proliferative Vitreoretinopathy is a common complication after the repair of retinal detachment associated with open-globe trauma, and being a smoker is a risk factor for redetachment. Further study is needed to understand the pathophysiologic mechanisms underlying this correlation.
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Inherited proliferative vitreoretinopathies of childhood.
International ophthalmology clinics, 2008Co-Authors: Christopher M. Andreoli, Scott M. Warden, Shizuo MukaiAbstract:There are a number of inherited, childhood disorders of the retinal vasculature that result in vitreoretinal proliferation. These include familial exudative Vitreoretinopathy (FEVR), Norrie disease (ND), incontinentia pigmenti (IP), autosomal dominant neovascular inflammatory Vitreoretinopathy (ADNI
