老年性黄斑变性的发病机制及治疗

Medvedeva L.M
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摘要

老年性黄斑变性(AMD)导致中央视力明显下降,扰乱了一个人的社会和工作活动。这种病理与年龄有关,其临床显著表现见于66岁至74岁年龄组,占人口的15%,75岁至84岁年龄组占25%,85岁及以上年龄组占30%。这种疾病的发病机制尚不完全清楚。但某些基因在老年性黄斑变性发生中的作用已经得到证实:PLEKHA1、HTRA1、CFH、CFB / C2、CRP、补体C3、ARMS2、HMCN1 / FBLN6、FBLN5、TLR3、ApoE、VEGF A等。可能与AMD相关的新基因仍在继续研究,例如编码磷脂酶c的PLCG 2。目前,新血管性AMD唯一有效的致病治疗方法是玻璃体内注射抗vegf治疗。新的有希望的治疗领域出现了:长效药物(brolucizumab),联合治疗(补体系统成分抑制剂和抗vegf治疗),其中许多正处于临床试验的不同阶段。进一步研究AMD的发病机制旨在开发一种新的、更有效的治疗方法。
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SOME ASPECTS OF PATHOGENESIS AND TREATMENT OF AGE-RELATED MACULAR DEGENERATION
Age-related macular degeneration (AMD) leads to a marked decrease in central vision and disrupts social and work activities of a person. This pathology is associated with age, and its clinically significant manifestations are determined in the age group from 66 to 74 years in 15% of the population, from 75 to 84 years - in 25%, from 85 years and older - in 30%. The pathogenesis of this disease is not fully understood. But the role of certain genes in the development of age-related macular degeneration has already been proved: PLEKHA1, HTRA1, CFH, CFB / C2, CRP, complement C3, ARMS2, HMCN1 / FBLN6, FBLN5, TLR3, ApoE, VEGF A and others. New genes, presumably related to AMD, continue to be investigated, for example, PLCG 2, which codes the enzyme phospholipase C. The only effective pathogenetic treatment of neovascular AMD nowadays is anti-VEGF therapy in the form of intravitreal injections. New promising areas of treatment appear: prolonged drugs (brolucizumab), combination therapy (inhibitors of the components of the complement system and anti-VEGF therapy), many of them being at various stages of clinical trials. Further study of the pathogenesis of AMD is aimed at the development of a new, more effective treatment.
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