抗血管内皮生长因子药物治疗渗出型老年性黄斑变性的局限性研究现状

渗出型老年性黄斑变性(wAMD)是由于脉络膜新生毛细血管通过破裂的Bruch膜到达RPE层和光感受器细胞层形成脉络膜新生血管(CNV),继而导致新生血管出血、渗漏以及瘢痕形成。鉴于VEGF在CNV发生发展过程中具有重要作用,各种眼内抗VEGF药物靶向治疗是目前wAMD治疗的一线选择。但抗VEGF药物治疗wAMD的疗效受多种因素影响,仍有部分患者存在治疗无应答、药物耐受、需要长期反复注射以及严重副作用等问题。深入探究wAMD发病的生理病理过程,寻找导致CNV形成的最根本原因,从病因出发探寻更优的治疗方案是未来研究的方向。     

细胞因子在渗出性年龄相关性黄斑变性中的表达及靶向治疗

渗出性年龄相关性黄斑变性(AMD)是导致老年人中心视力丧失的重要原因之一,其病理机制为脉络膜新生血管(CNV)的形成.近年来研究者发现,促血管生成因子与抗血管生成因子的平衡在CNV的形成中起重要作用,其中血管内皮生长因子(VEGF)与色素上皮衍生因子(PEDF)分别为促血管生成因子与抗血管生成因子的代表性因子.针对这些细胞因子的靶向治疗为渗出性AMD的药物治疗提供了新的方向,目前广泛应用于临床,抗VEGF药物在控制CNV并提高患者视力方面具有重要意义.本文就与渗出性AMD发病相关的多种细胞因子的作用机制及渗出性AMD的靶向治疗研究进展进行综述.     

光动力疗法治疗渗出型老年性黄斑变性

光动力疗法(PDT)是目前治疗老年性黄斑变性(AMD)的脉络膜新生血管(CNV)较为安全有效的方法。本文综述了适于PDT治疗的CNV的特点和PDT的并发症。其中CNV的类型、病灶大小、位置及活动性对治疗效果影响较大,而对于AMD特殊类型如息肉状脉络膜血管病变和视网膜血管瘤样增生症的治疗方案尚需进一步探索。     

光动力疗法联合抗血管内皮生长因子药物治疗脉络膜新生血管的进展

脉络膜新生血管( choroidal neovascularization, CNV)是多种眼底病致盲的主要原因,好发于黄斑区,严重影响中心视力。 CNV常用治疗包括相对选择性治疗———光动力疗法( photodynamic therapy, PDT)、选择性治疗———抗血管内皮生长因子( anti-vascular endothelial growth factor, VEGF)药物。但PDT治疗后视力不提高,还可上调VEGF的表达、继发炎症反应;抗VEGF药物需多次注射以维持疗效,进而带来不良反应的风险和经济负担。目前, PDT联合抗VEGF药物治疗CNV在基础与临床研究方面均取得一定进展,使得联合疗法成为 CNV 治疗的选择之一。为了减少治疗后的不良反应,实施联合疗法时是否变更PDT治疗参数需要进一步研究。     

年龄相关性黄斑变性脉络膜新生血管的抗VEGF治疗

血管内皮生长因子(VEGF)是最重要的影响新生血管形成的因子,在年龄相关性黄斑变性的脉络膜新生血管形成中有重要作用。抗VEGF药物可抑制CNV的产生,从而起治疗作用。本文就VEGF及其受体的生理及病理作用,以及近两年来出现的抗VEGF治疗AMD的进展做一综述。     

成纤维细胞生长因子与脉络膜新生血管关系的研究进展

脉络膜新生血管(choroidal neovascularization,CNV)可见于年龄相关性黄斑变性(age-related macular degeneration,AMD)和病理性近视等眼科疾病,是许多眼底疾病发展、恶化以及引起视力障碍的重要原因。促进CNV发生发展的生长因子有很多,包括血管内皮生长因子(vascular endothelial growth factor,VEGF)、成纤维细胞生长因子(fibroblast growth factor,FGF)、转化生长因子(transforming growth factor,TGF)、胰岛素生长因子(insulin like growth factor,IGF)和结缔组织生长因子(connective tissue growth factor,CTGF)等。其中VEGF是最重要的促进新生血管生成的因子。近年来,激光治疗、抗VEGF药物等抗CNV的措施已广泛应用于临床,并在大部分情况下取得了良好的效果。然而,抗VEGF药存在药物抵抗和一定不良反应,且CNV的发病机制尚未完全阐明。FGF可以同时对成纤维细胞、内皮细胞产生直接和间接作用,促进新生血管形成。FGF家族的相关因子可能成为CNV治疗的新靶点,或可以对目前的单纯抗VEGF治疗进行补充。     

本期导读

本期以眼底疾病的诊治为重点报道内容。国内采用光动力疗法(PDT)治疗年龄相关性黄斑变性(AMD)等脉络膜新生血管形成(CNV)性疾病已有十年的历程,为了使PDT疗法更健康稳定地发展,本期请王雨生、王海燕撰写了PDT治疗脉络膜新生血管疾病的历程和现状的述评,作者回顾     

曲安奈德玻璃体内注射联合PDT治疗AMD患者中心凹下脉络膜新生血管[英]Rechtman E…／／Br J Ophthalmol

目前，对年龄相关性黄斑变性(AMD)患者中心凹下脉络膜新生血管(CNV)的治疗，仅维替泊芬(verteporfin)的光动力学疗法(PDT)和激光凝固治疗有确实效果。曲安奈德作为常用类固醇药物，是已知的最具潜力的抗新生血管药物。目前尚鲜见有关曲安奈德玻璃体内注射(intravitreal triamcinolone acetonide，iTAAC)联合PDT治疗AMD患者CNV的报道。     

年龄相关性黄斑变性脉络膜新生血管的抗VEGF治疗

血管内皮生长因子(VEGF)是最重要的影响新生血管形成的因子，在年龄相关性黄斑变性的脉络膜新生血管形成中有重要作用。抗VEGF药物可抑制CNV的产生，从而起治疗作用。本文就VEGF及其受体的生理及病理作用，以及近两年来出现的抗VGF治疗AMD的进展做一综述。     

血管内皮生长因子抑制剂在角膜新生血管治疗中的研究进展

正常角膜是无血管、完全透明的组织,是眼部重要的屈光介质,但许多眼部疾病均可破坏抗血管生成因子与促血管生成因子之间的平衡,导致病理性角膜新生血管(CNV)的形成.大量研究表明,CNV的形成与血管内皮生长因子(VEGF)信号通路的激活密切相关.通过多靶点多途径阻断该信号通路可以有效抑制新生血管的形成,为CNV的治疗带来了希望.目前,针对新生血管性眼病的新型靶向治疗策略主要包括VEGF抑制剂和以微小RNA(miRNA)为核心的基因治疗,前者主要包括抗VEGF单克隆抗体、核酸适体、VEGFtrap、VEGF受体(VEGFR)酪氨酸激酶抑制剂等.本文将对具有代表性的抗VEGF药物和基因治疗的作用机制、用药疗效、药物安全性及研究现状进行综述.     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.