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本文引用的文献

1
Neuroprotection: extrapolating from neurologic diseases to the eye.神经保护:从神经系统疾病推断至眼部疾病
Am J Ophthalmol. 2009 Aug;148(2):186-191.e2. doi: 10.1016/j.ajo.2009.03.029. Epub 2009 May 23.
2
Potential benefit of intraocular pressure reduction in normal-tension glaucoma in South Korea.韩国正常眼压性青光眼中降低眼压的潜在益处。
J Ocul Pharmacol Ther. 2009 Feb;25(1):91-6. doi: 10.1089/jop.2008.0056.
3
Recent clinical findings with memantine should not mean that the idea of neuroprotection in glaucoma is abandoned.美金刚最近的临床研究结果并不意味着青光眼神经保护的理念被摒弃。
Acta Ophthalmol. 2009 Jun;87(4):450-4. doi: 10.1111/j.1755-3768.2008.01459.x. Epub 2009 Jan 9.
4
Experimental glutamatergic excitotoxicity in rabbit retinal ganglion cells: block by memantine.兔视网膜神经节细胞实验性谷氨酸能兴奋性毒性:美金刚的阻断作用
Invest Ophthalmol Vis Sci. 2009 Jun;50(6):2940-8. doi: 10.1167/iovs.08-2103. Epub 2009 Jan 10.
5
Memantine blocks mitochondrial OPA1 and cytochrome c release and subsequent apoptotic cell death in glaucomatous retina.美金刚可阻断青光眼视网膜中线粒体OPA1和细胞色素c的释放以及随后的细胞凋亡性死亡。
Invest Ophthalmol Vis Sci. 2009 Feb;50(2):707-16. doi: 10.1167/iovs.08-2499. Epub 2008 Oct 20.
6
Neuroprotection in glaucoma: drug-based approaches.青光眼的神经保护:基于药物的方法。
Optom Vis Sci. 2008 Jun;85(6):406-16. doi: 10.1097/OPX.0b013e31817841e5.
7
Current management of glaucoma and the need for complete therapy.青光眼的当前治疗方法及全面治疗的必要性。
Am J Manag Care. 2008 Feb;14(1 Suppl):S20-7.
8
History of neuroprotection and rationale as a therapy for glaucoma.神经保护的历史以及作为青光眼治疗方法的基本原理。
Am J Manag Care. 2008 Feb;14(1 Suppl):S11-4.
9
Report from the NEI/FDA Ophthalmic Clinical Trial Design and Endpoints Symposium.美国国立眼科研究所/美国食品药品监督管理局眼科临床试验设计与终点研讨会报告。
Invest Ophthalmol Vis Sci. 2008 Feb;49(2):479-89. doi: 10.1167/iovs.07-1132.
10
Medical interventions for primary open angle glaucoma and ocular hypertension.原发性开角型青光眼和高眼压症的医学干预措施。
Cochrane Database Syst Rev. 2007 Oct 17;2007(4):CD003167. doi: 10.1002/14651858.CD003167.pub3.

用于治疗成人青光眼的神经保护。

Neuroprotection for treatment of glaucoma in adults.

作者信息

Sena Dayse F, Ramchand Kanchan, Lindsley Kristina

机构信息

Massachusetts Eye and Ear Infirmary, 243 Charles St, Connecting Building 703, Boston, Massachusetts, USA, 02114.

出版信息

Cochrane Database Syst Rev. 2010 Feb 17(2):CD006539. doi: 10.1002/14651858.CD006539.pub2.

DOI:10.1002/14651858.CD006539.pub2
PMID:20166085
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3478138/
Abstract

BACKGROUND

Glaucoma is a heterogeneous group of conditions involving progressive damage to the optic nerve, deterioration of retinal ganglion cells and ultimately visual field loss. It is a leading cause of blindness worldwide. Open angle glaucoma (OAG), the commonest form of glaucoma, is a chronic condition that may or may not present with increased intraocular pressure (IOP). Neuroprotection for glaucoma refers to any intervention intended to prevent optic nerve damage or cell death. The treatment can target extracellular factors such as reducing IOP, or cellular factors derived from the optic nerve itself such as blocking intracellular death signals.

OBJECTIVES

The objective of this review was to systematically examine the evidence regarding the effectiveness of neuroprotective agents, either topical or oral, for slowing the progression of OAG in adults.

SEARCH STRATEGY

We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library, Issue 4, 2009), MEDLINE (January 1960 to January 2010), EMBASE (January 1980 to January 2010), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to January 2010) and ClinicalTrials.gov (http://clinicaltrials.gov). (5 January 2010). There were no language or date restrictions in the search for trials. The electronic databases were last searched on 5 January 2010.

SELECTION CRITERIA

This review was limited to randomized controlled trials (RCTs) in which topical or oral treatments were used to prevent retinal ganglion cell death. Our population of interest was adults with OAG. As the primary outcome for this review was the proportion of participants who developed any progression of visual field loss at five years post intervention, only trials with at least five years of follow-up were included.

DATA COLLECTION AND ANALYSIS

Two review authors independently reviewed titles and abstracts from the literature searches. Full text copies of relevant or potentially relevant studies were obtained and re-evaluated for inclusion. There were no trials identified for this review, thus we performed no data extraction or meta-analysis. Two studies comparing memantine to placebo are currently awaiting classification until additional study details are provided. Reasons for excluding studies from the review were documented.

MAIN RESULTS

In accordance with the selection criteria for inclusion, we identified no studies relevant for this review. The results of short-term trials and other studies are discussed in this review.

AUTHORS' CONCLUSIONS: Although neuroprotective agents are intended to act as pharmacological antagonists to prevent cell death, the evidence that they are effective in preventing retinal ganglion cell death, and thus preserving vision in patients with OAG, has not been demonstrated. Long-term RCTs are needed to determine whether or not neuroprotective agents may be beneficial for individuals with OAG.

摘要

背景

青光眼是一组异质性疾病,涉及视神经的进行性损伤、视网膜神经节细胞的退化,最终导致视野丧失。它是全球失明的主要原因。开角型青光眼(OAG)是最常见的青光眼类型,是一种慢性疾病,眼压(IOP)可能升高,也可能不升高。青光眼的神经保护是指任何旨在预防视神经损伤或细胞死亡的干预措施。治疗可以针对细胞外因素,如降低眼压,或针对源自视神经本身的细胞因素,如阻断细胞内死亡信号。

目的

本综述的目的是系统地研究局部或口服神经保护剂延缓成人OAG进展有效性的证据。

检索策略

我们检索了Cochrane对照试验中心注册库(CENTRAL)(其中包含Cochrane眼科和视觉组试验注册库)(《Cochrane图书馆》,2009年第4期)、MEDLINE(1960年1月至2010年1月)、EMBASE(1980年1月至2010年1月)、拉丁美洲和加勒比地区健康科学文献数据库(LILACS)(1982年1月至2010年1月)以及ClinicalTrials.gov(http://clinicaltrials.gov)。(2010年1月5日)。检索试验时没有语言或日期限制。电子数据库最后一次检索时间为2010年1月5日。

选择标准

本综述仅限于随机对照试验(RCT),其中使用局部或口服治疗来预防视网膜神经节细胞死亡。我们感兴趣的人群是患有OAG的成年人。由于本综述的主要结局是干预后五年出现任何视野丧失进展的参与者比例,因此仅纳入了至少有五年随访的试验。

数据收集与分析

两位综述作者独立审查了文献检索中的标题和摘要。获取了相关或潜在相关研究的全文副本,并重新评估以确定是否纳入。本次综述未识别出任何试验,因此我们未进行数据提取或荟萃分析。两项比较美金刚与安慰剂的研究目前正在等待分类,直到提供更多研究细节。记录了将研究排除在综述之外的原因。

主要结果

根据纳入选择标准,我们未识别出与本综述相关的研究。本综述讨论了短期试验和其他研究的结果。

作者结论

尽管神经保护剂旨在作为药理学拮抗剂来预防细胞死亡,但它们在预防视网膜神经节细胞死亡从而保护OAG患者视力方面有效的证据尚未得到证实。需要进行长期RCT来确定神经保护剂对OAG患者是否有益。