脉络膜新生血管患者房水中血管内皮生长因子和色素上皮衍生因子的浓度

目的:研究血管内皮生长因子(VEGF)和色素上皮衍生因子(PEDF)在活动性脉络膜新生血管膜(CNV)患者房水中的表达。方法:应用酶联免疫吸附测定法对32例活动性CNV患者和10例白内障患者(对照组)的房水标本进行VEGF和PEDF检测。结果:CNV患者房水中的VEGF为(523.0±273.7)pg/m l,PEDF为(16.58.±13.11)ng/m l;对照组患者房水中的VEGF为(108.3±72.3)pg/m l,PEDF为(0.35±0.57)ng/m l。两组间的VEGF和PEDF均有显著性差异(均P=0.000)。结论:活动性CNV患者房水中VEGF和PEDF增高,可能与脉络膜新生血管的形成有关。     

渗出型老年性黄斑变性与息肉状脉络膜血管病变眼底造影的对比分析

目的对比分析渗出型老年性黄斑变性（AMD）与息肉状脉络膜血管病变（PCV）眼底造影表现的异同。方法回顾性分析渗出型AMD患者98例119只眼及PCV患者61例68只眼的荧光素眼底血管造影（FFA）和吲哚青绿血管造影（ICGA）检查资料。结果 119只渗出型AMD患眼中,眼底彩照和FFA显示21只眼为经典型脉络膜新生血管（CNV）,占17.6%;29眼为微小经典型CNV,占24.4%;69眼诊断为隐匿型CNV,占58%;6只眼CNV与PCV共存,占5%。68只PCV眼中,54只眼荧光素眼底ICGA显示有异常分支的脉络膜血管网及其末梢的息肉状扩张、膨隆灶,占79.4%;14只眼见多个息肉状脉络膜血管扩张灶但无明显的分支状脉络膜血管网与之相连,占20.6%。造影后期部分息肉状病灶染料渗漏或染色,部分呈息肉状病灶中心为弱荧光,周围环状染色的＂冲刷现象＂。在疑似PCV的患者中,有90例行ICGA,确诊PCV 61例,占67.8%;PCV约占渗出性AMD的36.36%。结论渗出型AMD与PCV不同的ICGA表现,有助于两者的诊断与鉴别诊断。     

光动力学疗法治疗脉络膜新生血管的护理配合

脉络膜新生血管病因不明,常继发于年龄相关性黄斑变性（AMD）、中心性渗出性脉络膜视网膜病变（CEC）、病理性近视（PM）等眼底病变。CNV通常位于黄斑中心凹下或中心凹旁,反复出血,渗出、最终形成疤痕中心视力丧失,     

脉络膜新生血管的药物治疗

脉络膜新生血管(CNV)是一种严重影响视力的难治性疾病,目前抗VEGF药物、糖皮质激素及非甾体类抗炎药等已广泛应用于渗出性AMD、病理性近视等脉络膜新生血管性疾病的治疗并取得了一定的临床效果。1抗VEGF类药物1.1黄斑变性的治疗目前,常用的抗VEGF药主要是重组人VEGF单克隆抗体Bevacizumab(倍伐单抗)和Ranibizumab(雷珠单抗),通过抑制VEGF达到抑制新生血管生成的作用。美国国立     

病理性近视伴脉络膜新生血管的特点及其抗VEGF药物治疗

脉络膜新生血管是病理性近视患者常见的视力下降的重要原因之一,常引起不可逆的中心视力丧失.该文主要对病理性近视的流行病学、继发于病理性近视的脉络膜新生血管的病理机制、临床表现及其抗VEGF药物的治疗进行综述.     

病理性近视伴脉络膜新生血管的特点及其抗VEGF药物治疗

脉络膜新生血管是病理性近视患者常见的视力下降的重要原因之一,常引起不可逆的中心视力丧失。该文主要对病理性近视的流行病学、继发于病理性近视的脉络膜新生血管的病理机制、临床表现及其抗VEGF药物的治疗进行综述。     

光动力疗法治疗病理性近视脉络膜新生血管的临床观察

目的 探讨病理性近视脉络膜新生血管采用光动力疗法（PDT）治疗的临床效果.方法 选择病理性近视脉络膜新生血管患者20例（20眼）,均采用PDT治疗,回顾性分析治疗前后临床资料.结果 末次随访时,检测视力呈＞2行提高者3眼,占15％;保持稳定者16眼,占80％;视力下降1眼,占5％.眼底检查示视网膜神经感觉层缩小或脱离,黄斑渗出、水肿、出血均有程度不等的吸收.视网膜出血在治疗6个月后基本吸收.眼底荧光血管造影（FFA）/吲哚青绿血管造影（ICGA）在治疗后3个月检查显示,12只眼黄斑下脉络膜新生血管（CNV）荧光素渗漏静止,CNV闭合占60％,9只眼CNV渗漏好转,占45％.结论 CNV采用PDT治疗可获得理想效果,因为短期观察,选取的病例数相对较少,而从根本上,PDT无法杜绝CNV发生,故存在未彻底治疗的情况,长时间不能完全消失,也不能改善远期视力,若需客观评价PDT疗法,需行远期观察.     

色素上皮衍生因子在大鼠脉络膜新生血管中的表达

目的：探讨激光诱导BN大鼠脉络膜新生血管（choroidal neovascularization，CNV）中色素上皮衍生因子（pigment epithelium—derived factor，PEDF）的表达及意义。方法：对3组18只BN大鼠行单眼视网膜氩绿激光光凝，诱导脉络膜新生血管形成。分别在光凝后1周、2周、3周摘除眼球，对光凝区进行病理学检查、Ⅷ因子相关抗原（FⅧR：Ag）的免疫组织化学检查。应用免疫组织化学检测CNV形成过程中PEDF的表达及变化。结果：病理学检查及FⅧR：如免疫组织化学检查显示，光凝后1周开始形成CNV，3周达到高峰。正常BN大鼠PEDF在视网膜神经节细胞、内核层部分细胞、视网膜色素上皮层表达。视网膜光凝后，PEDF阳性染色信号可见于视网膜神经节细胞层、内核层、视网膜色素上皮层、外核层和脉络膜的损伤区；光斑边缘近脉络膜侧PEDF阳性表达信号明显高于光斑内部。光凝后1周至3周，光斑区内FⅧR：Ag阳性染色密度逐渐增加（P〈0．05），PEDF阳性染色密度逐渐下降（P〈0．05），PEDF与FⅧR：Ag阳性染色密度呈负相关（r=-0．832，P〈0．05）。结论：CNV形成与PEDF表达量负相关，提示PEDF表达不足可能是CNV形成和增生的素因之一。     

息肉状脉络膜血管病变

目的 观察息肉状脉络膜血管病变（polypoidal choroidal vasculopathy，PCV）的发病率及其临床特征。方法 回顾性分析1997～2003年诊断为渗出型AMD163例157眼脉络膜新生血管（choroidal neovascu larization，CNV）的眼底血管造影资料。结果 54例55眼符合PCV，分别占本组CNV患者163例157眼的33％和35％。除1例为双眼发病外，其余均为单眼。男性36例36眼、女性18例19眼，经统计学分析男女发病率无明显差别（t=1．847，P〉0．05）。年龄47～75岁，平均61．8岁。网膜下出血部位主要位于后极部，39眼可见橘红色病灶，其中34眼合并黄白色脂质渗出，13眼合并玻璃体积血。荧光素眼底血管造影（fundus fluorescein angiographv，FFA）显示：22眼出血性色素上皮脱离，12眼网膜下出血联合浆液性色素上皮脱离，9眼出血性色素上皮脱离联合浆液性神经上皮脱离。2眼浆液性色素上皮脱离。8眼仅表现为网膜下出血遮蔽伴息肉状斑点样高荧光而无色素上皮和或神经上皮脱离；息肉状斑点样高荧光位置：黄斑区32眼，混合区（黄斑区＋血管弓区、黄斑＋乳头旁、视盘旁＋血管弓区）7眼，血管弓区5眼，视盘旁区3眼，中周区1眼，7眼未显现斑点样高荧光。结论 PCV多见于老年病人，大部分为单眼发病，男女发病率差异不明显，通过临床上见到的后极部大片网膜下出血性合并橘红色病灶和（或）黄白色脂质渗出以及FFA所显示的脉络膜斑点状或花簇状高荧光及其位置，可作出初步诊断。     

维替泊芬光动力治疗后脉络膜新生血管膜VEGF和PEDF的表达

目的:检测光动力治疗(PDT)后人脉络膜新生血管(CNV)膜中色素上皮衍生因子(PEDF)和血管内皮细胞生长因子(VEGF)的表达。设计:干预性病例序列。方法:回顾性分析42例(42眼)进行CNV切除术的病例。所有的CNV继发于老年性黄斑变性(AM D)。15例患者于手术前3～246d使用PDT治疗。将CNV进行CD34、CD105、细胞角蛋白18、VEGF和PEDF染色。27例在手术前未进行任何治疗的CNV作为对照组。结果:手术前未进行过任何治疗的标本显示不同程度的血管化,不同的细胞表达VEGF和PEDF。3d前经过PDT治疗的标本,显示大部分阻塞血管沿损伤的内皮细…     

脉络膜黑色素瘤及脉络膜转移癌的临床影像学分析

目的观察脉络膜黑色素瘤及脉络膜转移癌的临床影像学特征,提高两种肿瘤的诊断率。方法回顾性分析21只眼的临床资料,患者行直接检眼镜、FFA、B超、CT等检查。结果B超、CT、MRI在脉络膜肿瘤诊断方面无明显差异,但CT、MRI定位诊断优于B超;B超、MRI对脉络膜黑色素瘤的诊断优于CT;MRI对肿瘤眼外侵犯显示更为清晰;而CT对肿瘤密度的诊断则明显优于B超、MRI。FFA对脉络膜肿瘤的诊断有一定意义,但对临床表现不典型的病例,FFA仍有局限性。结论脉络膜黑色素瘤及脉络膜转移癌的影像学特征,有助于临床上发现和鉴别脉络膜原发肿瘤。     

Ultrasound-mediated microbubble delivery of pigment epithelium-derived factor gene into retina inhibits choroidal neovascularization

Background Many studies have suggested that the imbalance of angiogenic factor and anti-angiogenic factor expression contributes significantly to the development of choroidal neovascularization （CNV）, and ultrasound microbubble combination system can increase the gene transfection efficiency successfully. This study was designed to investigate whether ultrasound-mediated microbubble destruction could effectively deliver therapeutic plasmid into the retina of rat, and whether gene transfer of pigment epithelium-derived factor （PEDF） could inhibit CNV.
Methods Human retinal pigment epithelial cells were isolated and treated either with ultrasound or plasmid alone, or with a combination of plasmid, ultrasound and microbubbles to approach feasibility of microbubble-enhanced ultrasound enhance PEDFgene expression; For in vivo animal studies, CNV was induced by argon lasgon laser in rats. These rats were randomly assigned to five groups and were treated by infusing microbubbles attached with the naked plasmid DNA of PEDF into the vitreous of rats followed by immediate ultrasound exposure （intravitreal injection）; infusing liposomes with the naked plasmid DNA of PEDF into the vitreous （lipofectamine ＋ PEDF）; infusing microbubbles attached with PEDF into the orbit of rats with ultrasound irradiation immediately （retrobular injection）; infusing microbubbles attached with PEDF into the femoral vein of rats with exposed to ultrasound immediately （vein injection）. The CNV rats without any treatment served as control. Rats were sacrificed and eyes were enucleated at 7, 14, and 28 days after treatment. Gene and protein expression of PEDF was detected by quantitative real-time RT-PCR, Western blotting and immunofluorescence staining, respectively. The effect of PEDF gene transfer on CNV was examined by fluorescein fundus angiography.
Results In vitro cell experiments showed that microbubbles with ultrasound irradiation could significantly enhance PEDF delivery as compared with microbubbles or ultrasound alone. In the rat CNV model, transfection efficiency mediated by ultrasound/microbubbles was significantly higher than that by lipofectamine-mediated gene transfer at 28 days after treatment. The study also showed that with the administration of ultrasound-mediated microbubbles destruction, the CNV of rats was inhibited effectively.
Conclusions Ultrasound-microbubble technique could increase PEDF gene transfer into rats＇ retina and chorioid, in association with a significant inhibition of the development of CNV, suggesting that this noninvasive gene transfer method may provide a useful tool for clinical gene therapy.     

Role of pigment epithelium-derived factor on proliferation and migration of choroidal capillary endothelium induced by vascular endothelial growth factor in vitro

Background Pigment epithelium-derived factor （PEDF） is expressed in several normal organs and identified as an inhibitor of neovascularization. In the present study, we investigated the effect of PEDF in an in vitro model of ocular choroidal neovascularization. Methods Microdissection was used to isolate the human choroidal endothelial cells （CECs）, followed by the use of superparamagnetic beads （Dynabeads） coated with the CD31 antibody, which selectively binds to the endothelial cell surface. The mitogenic and motogenic effects of vascular endothelial growth factor （VEGF） on cultured choroidal capillary endothelial cells were examined in the presence or absence of PEDF （1, 10, 100, and 1000 ng/ml） using cell counts and migration assays. Results Cells bound to the beads were isolated using a magnetic particle concentrator and they were successfully cultured and characterized to be endothelial cells that possessed greater than 95% immunoreactivity to von Willebrand factor. PEDF suppressed the proliferation and migration of VEGF-induced choroidal capillary endothelial cells. However, the concentration of PEDF which we used has little effect on normal CECs. Conclusions PEDF played an important role on the growth and migration of VEGF-stimulated choroidal endothelial cell These findings suggest that PEDF may be an effective approach to the treatment of choroidal neovascular disorders.     

Annexin A2 promotes choroidal neovascularization by increasing vascular endothelial growth factor expression in a rat model of argon laser coagulation-induced choroidal neovascularization

Background Choroidal neovascularization （CNV） is a common cause of visual loss in the elderly patients with age-related macular degeneration and represents the growth of subretinal new vessels in the macular region. This study aimed to investigate the relationship between annexin A2 （ANXA2） and vascular endothelial growth factor （VEGF） in CNV.Methods In a rat model of argon laser coagulation-induced CNV, the mRNA expressions of the annexins and VEGF protein expression in the retina were detected using fluorescent real-time polymerase chain reaction （PCR） and immunohistochemistry, respectively. The interactions between ANXA2 and VEGF in both a retinal pigment epithelial cell line RPE-J and the rat model of CNV were examined by means of RNA interference, real-time PCR, Western blotting, enzyme-linked immunosorbent assay （ELISA） and histopathological examinations. Results Fundus fluorescein angiography （FFA） showed that argon laser coagulation of the retina induced stable CNV models in the rats. Two to three weeks after the coagulation, ANXA2. and VEGF expressions in the coagulated area in the retina and choroid increased to the peak level, while the other annexin members （ANXA4, ANXA5, ANXA7 and ANXA11） showed no obvious changes. In RPE-J cells and the CNV model, RNA interference of ANXA2 gene significantly lowered the VEGF protein and mRNA expressions, and application of an adenoviral vector containing ANXA2 gene markedly increased VEGF expressions in the rat model of CNV, but produced no significant effects on the expressions of the kinase insert domain-containing receptor （KDR） or the fms-like tyrosine kinase （Fit-l）. The expression of KDR inhibited the increment in ANXA2 expression, but VEGF and Rt-1 did not directly affect ANXA2 expression. Conclusion Besides the role as a plasminogen and the receptor of tissue plasminogen activator, ANXA2, which is under regulation of KDR via a negative feedback mechanism, also participates in neovascularization by regulating VEGF expression through a positive feedback mechanism.     

内皮抑素抑制脉络膜新生血管及VEGF和bFGF表达的研究

目的 研究内皮抑素对实验性脉络膜新生血管的抑制作用。方法 50只雄性BN大鼠，40只为实验组，10只为空白对照组。用半导体激光光凝实验组BN大鼠的视网膜，随机分为4组，内皮抑素Ⅱ组、内皮抑素Ⅰ组、生理盐水组和激光损伤组，每组10只；由光凝后当天开始，至光凝后13d，每天分别给予腹腔注射内皮抑素20mg／kg、10mg／kg和生理盐水1.2mL，激光损伤组光凝后不做任何处理。空白对照组为未行激光光凝和给药处理的BN大鼠。于光凝后第7天及第14天行眼底血管荧光素造影检查、组织病理学检查、VEGF免疫组化检测和bFGF mRNA的原住杂交检测。结果随着内皮抑素剂量增加，荧光素渗漏率和渗漏强度减弱；激光光凝后7d，内皮抑素Ⅱ组与其他组相比，渗漏强度的差异有显著性；光凝后14d，两个内皮抑素组与生理盐水组和激光损伤组比较，荧光素渗漏强度差异均有显著性；生理盐水组和激光损伤组差异无显著性。激光光凝后7dVEGF和bFGFmRNA表达达高峰，光凝后14d下降，内皮抑素组vEGF和bFGFmRNA表达较激光损伤组减弱，并呈剂量依赖性趋势。结论 内皮抑素可以有效地抑制实验性CNV的形成。下调VEGF和bFGF的表扶可能是肉皮抑素抑制CNV的作用机制之一．     

玻璃体腔注射雷珠单抗对息肉状脉络膜血管病变中心凹下脉络膜厚度的影响

目的:观察玻璃体腔注射雷珠单抗对息肉状脉络膜血管病变(PCV)中心凹下脉络膜厚度的影响。方法:回顾性分析2015年1月-2016年6月于武汉大学人民医院确诊为PCV患者32例(32只眼)。所有患者行视力、眼底荧光造影(FFA)、吲哚青绿血管造影(ICGA)和频域相干断层成像(SD-OCT)检查。抗血管内皮生长因子(VEGF)治疗患者玻璃体腔注射10 mg/mL雷珠单抗0.05 ml(含雷珠单抗0.5 mg),注射方案为3+PRN。治疗后随访时间至少6个月,观察患者治疗前后视力、中心视网膜厚度(CRT)和黄斑中心凹下脉络膜厚度(SFCT)的变化。结果:抗VEGF治疗前平均视力为logMAR(0.84±0.26),治疗后6个月为logMAR(0.56±0.30),较治疗前提高logMAR(0.28±0.36);CRT治疗前为(354.32±107.64)μm,治疗后6个月为(253.47±79.56)μm,厚度明显变薄(P<0.01);SFCT从治疗前(285.09±75.93)μm变为治疗后(249.76±69.05)μm,厚度明显变薄(P<0.05)。结论:玻璃体腔注射雷珠单抗能够降低中心凹下脉络膜厚度,脉络膜厚度的基线水平可能是影响PCV患者预后的重要因素之一。     

Atypical presentations of choroidal melanocytoma

Melanocytoma is a specific variant of melanocytic nevus, located in the optic disk or anywhere in the uveal tract, characterized clinically by a dark-brown to black color, and composed histopathologically of deeply pigmented round to oval cells with small, round, uniform nuclei. In this report, we described a case of large juxtapapillary melanocytoma with atypical presentations.