Pathogenesis of lesions in late age-related macular disease

Pathogenesis of lesions in late age-related macular disease
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DOI:
10.1016/j.ajo.2003.11.026
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发表时间:
2004-03-01
影响因子:
4.2
通讯作者:
Bird, AC
Bird, AC
中科院分区:
医学1区
文献类型:
--
作者:
Holz, FG;Pauleikhoff, D;Bird, AC

文献摘要

被引文献

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目得:回顾关于晚期年龄相关性黄斑病变(AMD)发病机制的现有证据。设计:文献回顾。方法:回顾解决这些问题的实验证据和临床观察。结果:有充分的证据表明,脉络膜新生血管(CNV)是由于来自视网膜色素上皮基底外侧质膜域的生长因子平衡的变化(视网膜色素上皮)。视网膜血管瘤性增生也可能有类似的发病机制,涉及顶端领域。视网膜色素上皮的脱落可能是由于脂质沉积导致布鲁赫膜对水流的阻力增加的结果。地图萎缩之前的视网膜色素上皮细胞中的自体荧光物质的积累和两者之间可能的因果关系已被证明centered.CONCLUSION:有越来越多的了解有关的事件,导致这些病变的顺序造成中央视力丧失的AMD。解决潜在机制的治疗方法比目前的治疗方案更有可能成功。这种方法已经开始在脉络膜新生血管的管理。(C)2004年,Elsevier Inc. All rights reserved.
PURPOSE: To review the evidence that exists concerning the pathogenesis of lesions in late age-related macular disease (AMD).DESIGN: Review of the literature.METHODS: A review of both experimental evidence and clinical observations that address these problems.RESULTS: There is good evidence that choroidal neovascularization (CNV) is due to a change in the balance of growth factors derived from the retinal pigment epithelial basolateral plasma membrane domain (retinal pigment epithelium). Retinal angiomatous proliferation may also have a similar pathogenesis involving the apical domain. Detachment of the retinal pigment epithelium is likely to be a consequence of increased resistance of the Bruch membrane to water flow due to deposition of lipids. Geographic atrophy is preceded by accumulation of autofluorescent material in the retinal pigment epithelium and possible causal relationships between the two have been demonstrated.CONCLUSION: There is increasing understanding concerning the sequence of events that lead to those lesions causing loss of central vision in AMD. Therapeutic approaches that address the underlying mechanisms are more likely to succeed than current treatment options. Such an approach has already been initiated in the management of choroidal neovascularization. (C) 2004 by Elsevier Inc. All rights reserved.