增生性玻璃体视网膜病变的药物治疗进展

孔源性视网膜脱离并发的增生性玻璃体视网膜病变(proliferative vineoretinopathy，PVR)为一系列的细胞活动，即去分化细胞的形成、迁移、粘附及增殖，形成视网膜表面膜并收缩，导致视网膜脱离手术失败。临床上对于PVR的手术治疗效果尚不理想。药物治疗包括柔红霉素、5-氟尿嘧啶和维甲酸等的应用。文章就PVR药物治疗的种类和不同给药途径作一简要回顾。     

视网膜脱离伴有的增殖性玻璃体视网膜病变

PVR是视网膜脱离手术手术失败的主要原因。本对视网膜脱离伴有PVR的发生率、形成机制、参与的细胞类型、危险因素、最新分类及预防和治疗进行了综述。随着对该病认识的加深和治疗的进步，PVR的防治水平将会逐步提高。     

增生性玻璃体视网膜病变发病机制的研究进展

增生性玻璃体视网膜病变(proliferative vitreoretinopathy，PVR)是在孔源性视网膜脱离或视网膜脱离复位术后，由于视网膜色素上皮细胞(RPE)及神经胶质细胞的增生和收缩，造成牵拉性视网膜脱离的病变。PVR的病理特征是细胞增生，RPE一旦开始增殖，就产生细胞生长因子，而这些细胞生长因子反过来又刺激细胞增殖。PVR的过程有多种细胞及因子的参与，参与PVR增生的细胞主要是RPE和视网膜神经胶质细胞；涉及PVR的生长因子有：PDGF、EGF、VEGF、TGF、FGF、IGF、HGF等。     

增生性玻璃体视网膜病变的药物治疗

增生性玻璃体视网膜病变（PVR）常由于裂孔源性视网膜脱离、眼穿孔伤或眼内手术造成血-视网膜屏障受损,视网膜色素上皮（RPE）细胞进入玻璃体,继而引起RPE细胞、神经胶质细胞、成纤维细胞等在玻璃体内增生,形成以细胞为主的纤维膜。临床上治疗和预防PVR以手术为主,但效果不佳。近来有许多药物治疗PVR的研究报道,就PVR药物治疗研究进展进行综述。     

增生性玻璃体视网膜病变增殖膜的免疫组织化学研究

增生性玻璃体视网膜病变 (PVR)是孔源性视网膜脱离(rhegmatogenousretinaldetachment,RRD)手术失败的主要原因。增殖膜的形成、收缩 ,并牵拉视网膜导致视网膜脱离是主要病理过程 ,在以往的研究中我们已经发现PVR患者玻璃体切割液中存在细胞表型的变化[1] ,我们通过对 12例PVR患     

转化生长因子-β在增生性玻璃体视网膜病变中的作用

增生性玻璃体视网膜病变(PVR)是孔源性视网膜脱离手术失败的主要原因,其发病机制尚未完全明了。综述了转化生长因子13．(TGF—β1)的生物学特性以及它在PVR发展中的作用。探讨TGF—β1与PVR形成的关系。TGF—β在PVR的形成过程中参与了细胞的增殖、膜的收缩。TGF—β是加速PVR形成的重要生长因子之一。将来也许可以用TGF—β的拮抗剂来预防和治疗PVR。     

RPE细胞发生上皮间充质转化机制及PVR的治疗研究进展

增殖性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)是眼外伤、糖尿病性视网膜病变、血管性视网膜病变和炎症性视网膜病变等眼部疾病的严重并发症,也是孔源性视网膜脱离手术失败的最重要原因,对视功能的危害较大。大量研究已证明PVR发生的主要危险因素是视网膜损伤后血视网膜屏障受损,视网膜色素上皮(retinal pigment epithelial,RPE)细胞受到玻璃体腔内细胞因子的刺激,RPE细胞发生上皮间充质转化(epithelial-mesenchymal transition,EMT),转分化为成纤维样细胞,细胞的形态发生了变化,细胞间的紧密连接消失,细胞极性丧失,增殖、迁移、侵袭能力增强。在视网膜前表面或视网膜下形成具有收缩性的纤维增殖膜,形成的纤维增殖膜会使视网膜形成皱褶,牵拉视网膜导致视网膜脱离,最终会导致患者视力下降甚至失明。国内外对预防和治疗PVR进行了大量的研究,本文对RPE细胞发生上皮间充质转化相关信号通路及PVR的治疗进行简要综述。     

增生性玻璃体视网膜病变的动物模型

孔源性视网膜脱离并发的增生性玻璃体视网膜病变（PVR）为一系列的细胞活动导致的视网膜脱离手术失败的病变。其发生机制尚不完全清楚，药物治疗效果也不理想。为了研究PVR的发生、发展和治疗，需要首先建立PVR的动物模型。由于PVR的主要病理变化是细胞的过度增生，因而动物模型多以细胞增生模型为主，细胞种类有视网膜色素上皮（RPE）细胞、成纤维细胞、软骨细胞、血管内皮细胞等。其他的模型还包括炎症和细胞迁移模型。实验动物主要有兔、猴、猪和豚鼠等。文章就不同动物模型的制作方法和特点作一简要回顾。     

血管内皮生长因子及上皮-间充质转化在增生性玻璃体视网膜病变发病中的作用

增生性玻璃体视网膜病变(PVR)是一种发生在孔源性视网膜脱离(RRD)自然病程中或复位手术后的严重并发症,常常导致患者视力丧失。目前,临床缺乏有效的治疗方法。PVR病理特征是多种细胞在细胞因子的作用下发生的过度炎症反应和异常增生,最终在视网膜表面形成增殖膜及进一步的牵拉性视网膜脱离(TRD)。对PVR发病机制的深入研究将有助于为其治疗寻找有前景的分子靶标。近年研究发现,血管内皮生长因子(VEGF)及视网膜色素上皮(RPE)细胞的上皮-间充质转化(EMT)在PVR发病中发挥着重要作用。本文就VEGF及RPE细胞EMT在PVR发病中的作用,以及二者的相互联动机制进行了总结,以期为PVR的治疗和临床研究提供新的思路。     

增殖性玻璃体视网膜病变性视网膜脱离的手术治疗

报告189例189眼严重增殖性玻璃体视网膜病变(PVR)性视网膜脱离，单纯巩膜扣带术和玻璃体切除术的结果，平均解剖成功率63%，从C₁87.5%至D₃30.4%。术后复位成功的病例95.8%有指数以上的视力，但仅26.9%达0.1以上，且多集中于C₁和C₂组。手术失败的主要原因是新的或复发的前段PVR形成(51.4%)，其次为后部视网膜前膜增殖，将原裂孔拉开或形成新裂孔(25.7%)。就PVR性视网膜脱离的手术时机，手术方式及前段PVR的形成进行了讨论。 （中华眼底病杂志，1994，10：199-202）     

生长因子与增生性玻璃体视网膜病变相关性的研究进展

增生性玻璃体视网膜病变(PVR)是眼球穿通伤及孔源性视网膜脱离手术后的常见并发症。该病的发病机制仍未明确,但研究表明,视网膜色素上皮(RPE)细胞具有自分泌细胞因子的能力,许多生长因子在PVR患者的玻璃体或者视网膜下积液中过度表达,这些生长因子及其受体在PVR的发生发展中扮演了重要角色,血-视网膜屏障被破坏后,生长因子的生理平衡即被打破,RPE细胞受到生长因子的刺激发生上皮-间质转化(EMT)、迁移及增殖,进而与其他细胞及细胞外基质形成视网膜前膜,牵拉视网膜造成视网膜脱离。近年来学者们对生长因子在PVR的形成中所涉及的信号通路、促EMT进程及细胞增殖做了大量研究,本文将对近年来促PVR发展的生长因子及拮抗生长因子治疗PVR的研究结果作一综述。     

玻璃体切割手术116例临床分析

目的 通过评价玻璃体切割对玻璃体积血及复杂性视网膜脱离的手术效果,分析产生手术并发症的原因。方法1995-06/2000-06行玻璃体切割术116例(118眼)进行回顾性分析。结果 视力提高者76.4％;术前存在视网膜脱离者,术后视网膜脱离复发31.7％;术前无视网膜脱离者,术后发生视网膜脱离14.5％。结论 术前存在PVR是术后出现视网膜脱离的重要危险因素,合理选择手术适应症,结束手术前仔细检查可能存在的视网膜医源性损伤和潜在病灶,防止玻璃体嵌塞,能有效减少并发症。     

Risk factors for proliferative vitreoretinopathy

Despite the recent progress in vitreous surgery, treatment of proliferative vitreoretinopathy (PVR) is still difficult. Even if the reattachment of the retina is successful, visual prognosis is often unsatisfactory. Identification of clinical risk factors for PVR provides useful guidelines for planning the management of rhegmatogeneous retinal detachment. This review summarized the current concept for pathogenesis, clinical risk factors, and medical treatment for PVR. The presence of retinal breaks and the breakdown of the blood-retinal barrier are prerequisite to development of PVR. Almost all risk factors for PVR are associated with intravitreal dispersion of retinal pigment epithelial cells or the breakdown of the blood-retinal barrier.     

上皮-间充质转化在增生性玻璃体视网膜病变发病机制中的作用

增生性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)是孔源性视网膜脱离及玻璃体视网膜手术后的常见并发症,其主要特征是在视网膜前形成无血管的纤维细胞膜.超微结构和免疫病理研究表明,多种细胞参与PVR的发生与发展,如视网膜色素上皮细胞、神经胶质细胞、巨噬细胞、玻璃体细胞、成纤维细胞和肌成纤维细胞等.其中,肌成纤维细胞是引起PVR增生膜收缩导致视网膜复位手术失败的主要细胞,主要来自于视网膜色素上皮细胞的上皮-间充质转化(epithelial-mesenchymal transition,EMT),在PVR的发生发展中具有重要作用.因此,阻断视网膜色素上皮细胞转分化为肌成纤维细胞可能成为预防和治疗PVR的一种有效的方法.     

Proliferative vitreoretinopathy and chemotherapeutic agents

Proliferative vitreoretinopathy (PVR) is a disease process that occurs in eyes with rhegmatogenous retinal detachments and accounts for the majority of failures following retinal detachment surgery. PVR involves the uncontrolled proliferation of non-neoplastic cells capable of forming membranes, which may occur on either surface of the retina or along the detached surface of the vitreous gel. Contraction of these membranes creates tractional forces that can distort or detach the retina. Various surgical procedures have been used to repair retinal detachments associated with PVR. The results have not been encouraging in many instances. Recent efforts have been directed toward the chemical inhibition of cellular proliferation in PVR. The majority of drugs used in these studies have been antineoplastic agents that affect various phases in the cycle of cell growth.     

Demonstration of mononuclear phagocytes in a human epiretinal membrane using a monoclonal anti-human macrophage antibody

Proliferative vitreoretinopathy (PVR), the major complication of rhegmatogenous retinal detachment and posterior segment ocular trauma, is a multistage disease process eventually resulting in traction retinal detachment. The migration of macrophages to a site of disrupted barriers between the vitreous, retina, and choroidea, respectively, is considered to be an important step in the early pathogenesis of PVR. In this study, we demonstrate the presence of numerous mononuclear phagocytes in a human PVR membrane by an APAAP (alkaline phosphatase — anti-alkaline phosphatase) immunostain using a monoclonal mouse anti-human macrophage antibody. This finding correlates with a highly positive fibronectin immunostain in the same specimen. Our results warrant further investigation of the involvement of mononuclear phagocytes in vitreoretinal proliferative disorders.This study was supported by the Retinovit Foundation and the Forschungsförderung Nordrhein-Westfalen     

Primary vitrectomy for pseudophakic retinal detachment.

AIM/BACKGROUND: Viewing the peripheral retina is the major problem in the repair of pseudophakic retinal detachments. Conventional buckling procedures in pseudophakic eyes are complicated by persistent retinal (re-) detachment and proliferative vitreoretinopathy (PVR) more often than in phakic eyes. METHODS: Primary vitrectomy was performed in 33 consecutive cases for pseudophakic retinal detachment with the help of liquid perfluorocarbons and a wide angle viewing system, following a standardised procedure. All eyes have passed the 12 month follow up examination. RESULTS: The primary reattachment rate was 94%. PVR was observed in one case (3%). Seventy nine per cent (26 eyes) regained vision of 20/50 or better, with a median visual acuity of 20/30. The most frequent complication was transient glaucoma during the early postoperative period in 48% (16 eyes) requiring carboanhydrase inhibitors. CONCLUSION: The main advantage of primary vitrectomy over conventional buckling seems to be the better intraoperative sight to the most peripheral retinal holes, controlled removal of vitreous traction, and focused endolaser coagulation. This may explain the low rate of PVR after primary vitrectomy. Also, visual results tended to be better compared with conventional surgical techniques possibly because of removed vitreous opacities, and because of a superior retinal reattachment rate as well as the reduced rate of PVR.     

Surgery of retinal detachment with proliferative vitreoretinopathy

Surgical treatment of retinal detachment complicated by proliferative vitreoretinopathy (PVR) depends on understanding both the pathoanatomy of the structural changes and the biologic time course of the intraocular proliferative process. Successful surgery is dependent on treating both the traction and rhegmatogenous components. Vitreous surgery is used to relieve the transvitreal traction and to remove epiretinal membranes causing fixed folding of the posterior retina. A broad and high scleral buckle is used to close all retinal breaks and to relieve remaining anteroperipheral vitreous and epiretinal membrane traction that cannot be relieved by vitrectomy. Vitreous surgery is best done after the proliferative process has run its biologic time course to minimize recurrence of epiretinal membranes. Therefore, staged procedures may be used in selected cases by first modifying the scleral buckle to treat the rhegmatogenous component followed later by definitive vitreous surgery. The principles and techniques of managing retinal detachment with PVR are described.     

增生性玻璃体视网膜病变炎性细胞增殖过程的实验研究

目的观察实验性增生性玻璃体视网膜病变（ＰＶＲ）形成过程中炎性细胞的增殖过程。方法通过眼球穿孔伤和玻璃体内注入自家血诱发大鼠ＰＶＲ模型,分别在处理后第１,３,７,１４,２１和２８天取模型眼行细胞学和免疫组化方法检测玻璃体和视网膜的增殖细胞。结果炎症反应在处理后第五天就开始,细胞增殖在第７天达高峰,１４天后以单核细胞,淋巴细胞和成纤维细胞增殖为主。后期玻璃体纤维化,视网膜脱离,结构不清。结论实验性ＰＶＲ形成过程中,炎性细胞的增殖规律与创伤后伤口愈合过程相一致。