David R
Allergan, 2525 Dupont Drive, PO Box 19534, Irvine, CA 92623-9534, USA.
Expert Opin Investig Drugs. 1998 Jul;7(7):1063-86. doi: 10.1517/13543784.7.7.1063.
Glaucoma is a family of diseases commonly characterised by progressive optic neuropathy with associated visual field deficits for which elevated intraocular pressure (IOP) is one of the primary risk factors. For more than a century the main goal of glaucoma management has been to eliminate the risk associated with elevated IOP. In recent years, accumulating evidence of pressure-independent causes of glaucomatous optic neuropathy has led to the recognition that lowering IOP alone may often be insufficient for the long-term preservation of visual function. An innovative therapeutic approach is now emerging to prevent progression of glaucomatous optic neuropathy and preserve vision, irrespective of disease aetiology: direct protection of the optic nerve. In addition to reducing the risk associated with elevated IOP, this neuroprotective approach will augment the overall goal of preserving the optic nerve through direct promotion of retinal ganglion cell (RGC) survival and/or prevention of RGC death. Although no currently available compounds have been clinically demonstrated to provide neuroprotective benefit in glaucoma, recent preclinical studies have shown that alpha-adrenergic agonists, such as brimonidine, provide neuroprotective benefits, as well as excellent IOP lowering efficacy. In addition, new agents with promising neuroprotective utility that are emerging from other studies are now being investigated for efficacy in glaucoma. The review discusses recently introduced compounds and new drugs in development with regard to their potential value in conventional and/or neuroprotective strategies for vision sparing in glaucoma.
青光眼是一类疾病,其共同特征是进行性视神经病变并伴有视野缺损,而眼内压升高是主要危险因素之一。一个多世纪以来,青光眼治疗的主要目标一直是消除与眼内压升高相关的风险。近年来,越来越多的证据表明青光眼性视神经病变存在与眼压无关的病因,这使得人们认识到仅降低眼压往往不足以长期保护视功能。一种创新的治疗方法正在兴起,旨在预防青光眼性视神经病变的进展并保护视力,而不论疾病的病因如何:直接保护视神经。除了降低与眼内压升高相关的风险外,这种神经保护方法还将通过直接促进视网膜神经节细胞(RGC)存活和/或预防RGC死亡来增强保护视神经的总体目标。尽管目前尚无临床证据表明现有化合物能在青光眼中提供神经保护益处,但最近的临床前研究表明,α-肾上腺素能激动剂,如溴莫尼定,具有神经保护作用,同时降低眼压的效果也非常好。此外,其他研究中出现的具有潜在神经保护作用的新药正在进行青光眼疗效研究。本文综述了最近引入的化合物和正在研发的新药在青光眼传统和/或神经保护策略中对视功能保护的潜在价值。