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Relevant bibliographies by topics / Proliferative vitreoretinopath

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Academic literature on the topic 'Proliferative vitreoretinopath'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 January 2023

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Journal articles on the topic "Proliferative vitreoretinopath"

1

Lewis, Hilel, Janice M. Burke, Gary W. Abrams, and Thomas M. Aaberg. "Perisilicone Proliferation after Vitrectomy for Proliferative Vitreoretinopathy." Ophthalmology 95, no. 5 (May 1988): 583–91. http://dx.doi.org/10.1016/s0161-6420(88)33136-2.

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Hatchell, D. L., T. McAdoo, S. Sheta, R. T. King, and J. V. Bartolome. "Quantification of Cellular Proliferation in Experimental Proliferative Vitreoretinopathy." Archives of Ophthalmology 106, no. 5 (May 1, 1988): 669–72. http://dx.doi.org/10.1001/archopht.1988.01060130731033.

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3

NAQVI, SYED ABID HASSAN, SOHAIL SHEHZAD, and OMAR ZAFAR. "PROLIFERATIVE VITREORETINOPATHY." Professional Medical Journal 13, no. 01 (March 6, 2006): 42–46. http://dx.doi.org/10.29309/tpmj/2006.13.01.5055.

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Objective: The objective of study to assess the success of pars planavitrectomy with use of silicone Oil for internal tamponade in traumatic rhegmatogenous R D with severe PVR. Setting& Period: This study was carried out in department of Ophthalmology Military Hospital Rawalpindi. Material &Methods: Fifteen cases with severe proliferative vitreoretinopathy (PVR Grade C, according to up dated retina SocietyClassification of 1991) was included in study. All the patients had traumatic rhegmatogenous retinal detachment withhistory of blunt ocular trauma, without globe rupture, outcome of the treatment was assessed by post operativeanatomical and physiological success. Results: Anatomical success was encouraging in-spite of advance disease andtechnically difficult and complicated intra-ocular maneuvers.

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Chaum, Edward. "Proliferative Vitreoretinopathy." International Ophthalmology Clinics 35, no. 1 (1995): 163–73. http://dx.doi.org/10.1097/00004397-199503510-00017.

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WILKES, SHELBY R., AHMAD M. MANSOUR, and W. RICHARD GREEN. "PROLIFERATIVE VITREORETINOPATHY." Retina 7, no. 2 (1987): 94–101. http://dx.doi.org/10.1097/00006982-198700720-00007.

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SCHWARTZ, DANIEL, ZENAIDA C. DE LA CRUZ, RICHARD W. GREEN, and RONALD G. MICHELS. "PROLIFERATIVE VITREORETINOPATHY." Retina 8, no. 4 (1988): 275–81. http://dx.doi.org/10.1097/00006982-198808040-00010.

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Blumenkranz, Mark S. "Proliferative Vitreoretinopathy." Retina 12, no. 1 (1992): 70. http://dx.doi.org/10.1097/00006982-199212010-00014.

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Wiedemann, Peter, and Klaus Heimann. "Proliferative vitreoretinopathy." Current Opinion in Ophthalmology 3, no. 3 (June 1992): 357–65. http://dx.doi.org/10.1097/00055735-199206000-00010.

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Coffee, Robert E., Lai Jiang, and Salman A. Rahman. "Proliferative Vitreoretinopathy." International Ophthalmology Clinics 54, no. 2 (2014): 91–109. http://dx.doi.org/10.1097/iio.0000000000000023.

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Idrees, Sana, Jayanth Sridhar, and Ajay E. Kuriyan. "Proliferative Vitreoretinopathy." International Ophthalmology Clinics 59, no. 1 (2019): 221–40. http://dx.doi.org/10.1097/iio.0000000000000258.

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Dissertations / Theses on the topic "Proliferative vitreoretinopath"

1

El-Ghrably, Ibraheem Ahmed. "Cytokine contribution to pathogenesis of proliferative vitreoretinopathy (PVR)." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367591.

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Hagan, Suzanne. "The glycoprotein SPARC (secreted protein, acidic and rich in cysteine) in proliferative retinal disease." Thesis, University of Liverpool, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250396.

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Banerjee, Philip James. "Proliferative vitreoretinopathy : strategies to improve anatomical and visual outcomes." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10024849/.

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Proliferative vitreoretinopathy (PVR) is the most common cause of late anatomical failure of retinal detachment surgery. Efforts to modify this vitreoretinal scarring response have so far proved clinically unsuccessful, with surgical and visual outcomes remaining poor. This work is aimed at identifying strategies to improve outcomes in eyes at high risk of PVR development following open globe trauma (OGT), and those with established PVR disease. Two prospective clinical trials investigating the benefit of adjunctive corticosteroids in these two populations were conducted in a total of one hundred and eighty patients. Clinical and imaging data were collected over the course of approximately 3500 hospital attendances. The Adjunct in Ocular Trauma (AOT) Trial was a two year, pilot, single-centre prospective, participant and surgeon-masked randomized-controlled-clinical trial (RCT). Forty patients requiring vitrectomy surgery following OGT were randomized to either standard (control) or study treatment (adjuncts) in a 1:1 allocation ratio. Perioperatively, the adjunct group received intravitreal and subtenons triamcinolone acetonide, oral flurbiprofen and guttae prednisolone acetate 1%. The control group received standard care. Primary outcome was anatomical success at 6 months and showed similar results in anatomical success with 50% (10/20) in the adjunct group, compared to 47% (9/19) in the standard group (Odds Ratio 1.11, 95% Confidence Interval 0.316-3.904). Secondary outcomes included final visual acuity, occurrence of PVR, intraocular pressure (IOP) rise, number of operations and recruitment rate. Final median visual acuity was 31 ETDRS letters in the adjunct group compared to 25 ETDRS letters in the standard group. Other secondary outcomes were similar between the two groups. The hypothesis that an adjunctive slow-release dexamethasone implant (Ozurdex ®) could improve the outcomes of vitreoretinal surgery for established PVR was tested in the Ozurdex® in PVR Study. In this two year, single-centre prospective, participant and surgeon-masked RCT, 140 patients requiring vitrectomy surgery with silicone oil for retinal detachment with established PVR (Grade C) were randomized to either standard (control) or study treatment (adjunct) in a 1:1 allocation ratio. Intraoperatively, the adjunct group received an injection of 0.7mg of slow-release dexamethasone (Ozurdex) at the time of (a) vitrectomy surgery and (b) at silicone oil removal. The control group received standard care. Primary outcome measure was the proportion of patients with a stable retinal reattachment with removal of silicone oil without additional vitreoretinal surgical intervention at 6 months. Secondary outcomes included i) final visual acuity (median and ETDRS of 55 letters or better), ii) cystoid macular edema (CMO), foveal thickness and macular volume iii) development of overt PVR recurrence, iv) complete and posterior retinal reattachment, vi) tractional retinal detachment, vii) hypotony/raised IOP, viii) macula pucker/epiretinal membrane, ix) cataract, x) quality of life All 140 patients were recruited within 25 months of study commencement; 138 patients had primary outcome data. Primary outcome assessment showed similar results in anatomical success between the two groups (49.3% vs 46.3%, adjunct vs control, (Odds Ratio 0.89, 95% Confidence interval 0.46 – 1.74, p= 0.733). Mean visual acuity at 6 months was 38.3 ETDRS letters and 40.2 letters in the adjunct and control group respectively. Secondary anatomical outcomes (complete/posterior reattachment rates and PVR recurrence) were comparable between the two groups. Exploratory analysis suggested that the proportion of patients with cystoid macular oedema (CMO) or a foveal thickness of >300μm was lower in steroid-treated eyes compared to controls (42.7% and 47.6% vs 67.2% and 67.7%, respectively p= 0.004, p= 0.023). Cystoid macular oedema is a secondary cause of visual loss. At 6 months following successful surgery for PVR, eyes with evidence of external limiting membrane (ELM) disruption on Spectral Domain-Optical Coherence Tomography achieve a worse visual outcome than eyes where the ELM appears preserved (p=0.006). Provisional work using retinectomy specimens retrieved at the time of surgery in sixteen patients were studied aiming to isolate a population of Müller glia with stem cell characteristics (hMSC). This suggested that it is feasible to isolate a cell population of appropriate morphology of hMSCs, from eyes with advanced PVR. These cells survived up to ten weeks in culture but eventually terminally differentiate. The work in this thesis has shown that corticosteroids do not modify the vitreoretinal scarring response sufficiently to improve anatomical outcomes at 6 months. Further work is required to improve the outcome in eyes with PVR. Adopting visual acuity as a primary outcome, may be a plausible design in future vitreoretinal trials.

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Shalaby, Usama A. "The role of matrix metallproteinases in pathogenesis of proliferative vitreoretinopathy." Thesis, University of Aberdeen, 2001. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU145724.

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Cellular migration and membrane contraction are two vital steps in pathogenesis of proliferative vitreoretinopathy (PVR). Several factors, related to cell activity, are involved in induction of cell migration and cell-induced membrane contraction. However, the roles of some of these factors in PVR pathophysiology are still to be clarified. The studies described in this thesis were undertaken to investigate the factors affecting cellular migration, mainly HRPE cells, which may modify cellular migration during proliferative vitreoretinopathy. The mechanisms of cell-induced collagen gel contraction, which resembles membrane contraction in PVR, was studied. The role of matrix metallproteinases (MMPs) in induction or inhibition of cell migration and cell-mediated gel contraction is one major goal; this study tried to clarify. In chapter III, HRPE cells were cultured from human male eyes, aged 43 years, and passed several times to create a cell line. To study the effect of different ECMs (fibronectin, laminin and different subtypes of collagen) on cell migration, I developed a cell migration assay "agarose droplet". This assay was established by incorporating HRPE cells into small amount of agarose and the solution was left to set as a gel. The drops were observed, photographed and scanned for 48 hours. The distance migrated by the cells, on plastic or substrate coated plastic, was estimated using both microscopic scale and computer analysis program (Coral Xara) by converting the pixels into metric unites. The results showed that fibronectin at a dose of 10 ,g/ml significantly enhanced cell migration in comparison with cells migrated on plastic. On the other hand, laminin at a dose of 10 g/ml markedly inhibited cell migration and this inhibition was statistically significant. These results suggest that HRPE cells require fibronecin but not laminin to migrate out of agarose droplet. This alteration in cell reaction to different ECM substrates may represent a similar phenomenon of cell-matrix interactions, which stimulate cell migration and survival in PVR environment. Cell migration assay was used again in Chapter IV to determine the role of matrix metalloproteinases (MMPs) 1, 2 9 in directing the behaviour of HRPE cells during migration from agarose droplets. Expression of MMP-1,2 9 by HRPE cells was determined by immunocytochemistry using monoclonal antibodies. In addition, expression of MMPs in cultured HRPE cells was confirmed by western blotting in the absence and in the presence of MMP synthetic inhibitor: Batimastat (BB-94). Finally, cell migration from the agarose was studied in presence of Batimastat. The results showed that MMP-2 9 were expressed by primary HRPE cell cultures and the strong expression of the duplex bands of the same enzymes were shown by western blotting technique. Expression of the MMP-2 9 bands was inhibited completely after treatment of the HRPE cells with BB-94 (500nM and 5 M). BB-94, also inhibited cellular migration from agarose droplets in a dose dependent manner. These results suggest that expression of MMP-2 9 by HRPE cells during their migration from the agarose might resemble the expression of the same enzymes during migration of the cells in the PVR and the inhibition of these enzymes by BB-94 might prevent cellular migration, a critical step in PVR pathogenesis. Therefore, we concluded that migration of HRPE cells from their resident basement membrane into periretinal surfaces requires an interplay between certain ECMs and enzymes as, MMPs to permit cellular invasion. There was an intention to use this assay to study the effect of MMPs on the cellular migration in the presence of these ECMs but because of the tiny size of the drop, it was very difficult to retrieve any materials from the drops. In chapter V, I used cell-mediated collagen gel contraction model to determine the effect of HRPE cells, seeded on the surface of 3-D collagen gels, on the integrity of the gel and to observe the behaviour of human retinal pigment epithelial (HRPE) cells during this time. A comparison between the effect of the HRPE cells on the collagen gel integrity and other cell types as human skin fibroblasts (HSF) and human monocytic cell line (THP-1) has been performed after standardisation of the HRPE cell-mediated collagen gel contraction assay. Also, the effects of coating the collagen gel with different ECM proteins on the cell-mediated collagen gel contraction were studied. The extent of cellular invasion and the degree of gel contraction were quantified for up to three days using phase contrast microscopy and digital image analysis. These experiments showed that HRPE cells mostly proliferated as sheets of cells on the surface of the collagen gel and only minimally invaded the gel, some cells were seen to invade the gel as single cells and invaded the gel to a depth of several tens of microns.

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von, Hehl Stephanie. "Vergleich der Wirkung verschiedener Wachstumsfaktoren auf physiologische Parameter kultivierter humaner retinaler Pigmentepithelzellen." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-80080.

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Bei der proliferativen Retinopathie (PVR) kommt es aufgrund einer Netzhautablösung zu einer Störung der Blut-Retina-Schranke. Durch die daraus resultierende Milieuänderung wandern retinale Zellen und Bestandteile des Blutes in den Glaskörper ein. Wachstumsfaktoren regen die mitotisch inaktiven RPE-Zellen zur Migration und Proliferation an. Im weiteren Verlauf der Erkrankung führt dies zur Ausbildung von Traktionsmembranen und zur Ablösung der Netzhaut. Die dadurch entstehenden Zugkräfte verhindern eine Wiederanlegung der Netzhaut. Ziel dieser Arbeit war es, zu untersuchen, welchen Einfluss Wachstumsfaktoren und deren Kombinationen auf die Proliferation und Migration humaner retinaler Pigmentepithelzellen, die VEGF-Sekretion durch RPE-Zellen und die mRNA-Expression von Kollagenen haben. Die beteiligten Signalwege sollten ebenfalls ermittelt werden. Im Ergebnis sollten Faktoren identifiziert werden, die die Entstehung einer PVR begünstigen. Migration, Proliferation, VEGF-Sekretion und die TGF-ß-Sekretion konnten durch den Wachstumsfaktor PDGF (Platelet-derived growth factor) gesteigert werden. Die Wirkung des PDGF-Signals wurde durch die Aktivierung verschiedener intrazellulärer Signalwege (MAPK, p38MAPK, PI3K/AKT) vermittelt. PDGF wirkte hemmend auf die Kollagen mRNA-Expression. Für TGF-ß (Transforming growth factor-ß) wurde eine hemmende Wirkung auf die Proliferation und eine induzierende Wirkung auf die Kollagensynthese nachgewiesen. Beide Faktoren – PDGF und TGF-ß – steigerten die VEGF-Sekretion. Eine additive Erhöhung der VEGF-Sekretion wurde durch die Kombination beider Faktoren nachgewiesen. Die untersuchten Wachstumsfaktoren interagieren mit den humanen retinalen Pigmentepithelzellen und tragen somit maßgeblich zur Ausbildung und auch zur Beschleunigung des Verlaufs der proliferativen Retinopathie sowie der pathologischen Gefäßneubildung bei.

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6

Zhou, Tianhong. "Multi-compartment biodegradable polymer implants for intravitreal management of proliferative vitreoretinopathy /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488186329502253.

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7

Morales, Shawn A. "Examining the role of the retinal pigment epithelium in proliferative vitreoretinopathy." Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1621832581&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.

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8

Kon, Chee Hing. "Proliferative vitreoretinopathy : a study of biological and clinical risk factors and new pharmacological therapies." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266110.

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9

Mukherjee, Sudipto. "Retinal pigment epithelial cells and the insulin-like growth factor system in proliferative vitreoretinopathy." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/mukherjee.pdf.

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10

Mazure, Ank. "Cell-mediated contraction in three-dimensional collagen matrices in relation to proliferative vitreoretinopathy and wound contraction." Thesis, Imperial College London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320529.

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Books on the topic "Proliferative vitreoretinopath"

1

1952-, Wong D., ed. Management of vitreo-retinal disease: A surgical approach. London: Springer, 1999.

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Freeman, H. MacKenzie, and Felipe I. Tolentino, eds. Proliferative Vitreoretinopathy (PVR). New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9.

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Spandau, Ulrich, Zoran Tomic, and Diego Ruiz-Casas, eds. Retinal Detachment Surgery and Proliferative Vitreoretinopathy. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-78446-5.

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Spandau, Ulrich, Zoran Tomic, and Diego Ruiz-Casas, eds. Retinal Detachment Surgery and Proliferative Vitreoretinopathy. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11946-0.

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Wong, David, and Anthony Chignell. Management of Vitreo-Retinal Disease: A Surgical Approach. Springer, 1998.

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Wong, David, Anthony Chignell, and T. R. Tarrant. Management of Vitreo-Retinal Disease: A Surgical Approach. Springer, 2014.

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Tarrant, T. R., David Wong, and Anthony Chignell. Management of Vitreo-Retinal Disease: A Surgical Approach. Springer London, Limited, 2013.

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8

Klaus, Heimann, Wiedemann P, and International Symposium on Proliferative Vitreoretinopathy. (2nd : 1988 : Köln, Germany)., eds. Proliferative vitreoretinopathy. Heidelberg: Kaden Verlag, 1989.

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1929-, Freeman H. Mackenzie, and Tolentino Felipe I, eds. Proliferative vitreoretinopathy (PVR). New York: Springer-Verlag, 1988.

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Tolentino, Felipe I., and H. MacKenzie Freeman. Proliferative Vitreoretinopathy (PVR) : (pvr). Springer London, Limited, 2012.

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Book chapters on the topic "Proliferative vitreoretinopath"

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Williamson, Thomas H. "Proliferative Vitreoretinopathy." In Vitreoretinal Surgery, 189–208. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-31872-6_8.

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Claes, Carl, and Anna Paula Lafetá. "Proliferative Vitreoretinopathy." In Microincision Vitrectomy Surgery, 188–95. Basel: S. KARGER AG, 2014. http://dx.doi.org/10.1159/000360466.

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Williamson, Thomas H. "Proliferative Vitreoretinopathy." In Vitreoretinal Surgery, 253–75. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68769-4_10.

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Zhang, Wenlan, Lejla Vajzovic, and Cynthia A. Toth. "Proliferative Vitreoretinopathy." In Albert and Jakobiec's Principles and Practice of Ophthalmology, 1–23. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-90495-5_97-1.

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Zhang, Wenlan, Lejla Vajzovic, and Cynthia A. Toth. "Proliferative Vitreoretinopathy." In Albert and Jakobiec's Principles and Practice of Ophthalmology, 3243–63. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-42634-7_97.

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Claes, Carl, H. MacKenzie Freeman, and Felipe I. Tolentino. "PVR: An Overview." In Proliferative Vitreoretinopathy (PVR), 3–11. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_1.

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Blumenkranz, Mark S., and Michael K. Hartzer. "Pharmacologic Management of PVR." In Proliferative Vitreoretinopathy (PVR), 81–87. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_10.

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Stern, Walter H., and John S. Lean. "Intraocular Silicone Oil Versus Gas in the Management of PVR: A Multicenter Clinical Study." In Proliferative Vitreoretinopathy (PVR), 88–96. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_11.

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Abrams, Gary W., Steven T. Charles, William H. Havener, Robert Machemer, Charles L. Schepens, and Walter H. Stern. "PVR: A Discussion of Common Concerns." In Proliferative Vitreoretinopathy (PVR), 97–102. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_12.

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Irvine, Alexander R., George F. Hilton, Lawrence I. Lonn, and Ariah Schwartz. "Photographic Documentation and Grading of PVR." In Proliferative Vitreoretinopathy (PVR), 105–9. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3910-9_13.

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Reports on the topic "Proliferative vitreoretinopath"

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Chen, Chen, Peng Chen, Xia Liu, and Hua Li. Combined 5-Fluorouracil and Low Molecular Weight Heparin for the Prevention of Postoperative Proliferative Vitreoretinopathy in Patients with Retinal Detachment. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0117.

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Review question / Objective: The aim of this meta-analysis is to evaluate the efficacy and safety of intraoperative infusion of combined 5-fluorouracil and low molecular weight heparin (LMWH) for the prevention of postoperative proliferative vitreoretinopathy in patients with retinal detachment. Condition being studied: Postoperative proliferative vitreoretinopathy (PVR) is the primary cause of failure of retinal reattachment surgery. 5-fluorouracil (5-FU) inhibits the proliferation of fibroblasts, and suppresses collagen contraction. On the other hand, heparin reduces fibrin exudation, and inhibits the adhesion and migration of retinal pigment epithelial cells. We conduct this comprehensive literature search and meta-analysis to address whether intraoperative infusion of combined 5-FU and LWMH improves the primary success rate of pars plana vitrectomy, as well as reduces postoperative PVR. Our study aims to provide clinical evidence for retinal surgeons concerning their choice of intraoperative medication.

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