中华眼底病杂志

中华眼底病杂志

反复抗血管内皮生长因子药物治疗对渗出型老年性黄斑变性患者玻璃体黄斑界面的影响

查看全文

目的观察反复玻璃体腔注射抗血管内皮生长因子(VEGF)药物对渗出型老年性黄斑变性(AMD)患者玻璃体黄斑界面(VMI)的影响。方法回顾性研究。临床确诊为渗出型AMD并接受玻璃体腔抗VEGF药物治疗的34例患者纳入研究。其中,男性26例,女性8例。年龄50~80岁,平均年龄(62.8±8.35)岁。取其1年随访期间最少抗VEGF药物治疗6次的眼为研究眼,未接受抗VEGF药物治疗的对侧眼为对照眼。治疗前采用光相干断层扫描(OCT)检查观察双眼VMI状态。将存在玻璃体黄斑粘连(VMA)、黄斑前膜(MEM)、完全性玻璃体后脱离(C-PVD)定义为VMI异常。根据OCT图像上玻璃体与黄斑部粘附的直径大小将VMA分为局灶型(≤1500 μm)和广泛型(>1500 μm)。治疗前研究眼中存在VMI异常12只眼,包括广泛型VMA 8只眼、局灶型VMA 3只眼、MEM 1只眼;对照眼中存在VMI异常12只眼,包括广泛型VMA 7只眼、局灶型VMA 2只眼、C-PVD 2只眼、MEM 1只眼。治疗后平均随访时间16.4个月。随访期间每月用随访模式进行双眼OCT检查。对比分析患者双眼治疗前后VMI的变化情况。使用χ2检验比较研究眼及对照眼治疗前及末次随访时VMI的差异,由于样本数<40,进行Fisher确切概率法进行分析。结果末次随访时,研究眼中VMI异常12只眼,包括广泛型VMA 5只眼、局灶型VMA 2只眼、C-PVD 3只眼、MEM 2只眼;与治疗前比较,共有6只眼VMI发生变化。对照眼中VMI异常13只眼,包括广泛型VMA 5只眼、C-PVD 7只眼、MEM 1只眼。与治疗前比较,共有6只眼VMI发生变化。末次随访时,研究眼及其相应对照眼VMI变化情况比较,差异无统计学意义(P=0.053)。所有研究眼及对照眼中共有4只眼在末次随访时由局灶型VMA变为C-PVD,占总局灶型VMA的80.0%;共有3只眼由广泛型VMA变为C-PVD,占总广泛型VMA的21.4%。结论反复抗VEGF药物治疗对渗出型AMD患者VMI无明显影响。无论是否反复抗VEGF药物治疗,局灶型VMA较广泛型VMA更容易发生C-PVD。

ObjectiveTo observe the effects of repeated intravitreal injections of anti-vascular endothelial growth factor (VEGF) drugs on vitreous macular interface (VMI) in patients with exudative age-related macular degeneration (AMD).MethodsRetrospective study. Thirty-four exudative AMD patients who treated with intravitreal anti-VEGF drugs were included in this study. There were 26 males and 8 females. The age ranged from 50 to 80 years, with the average of (62.8±8.35) years. The eyes with at least 6 treatments during the 1-year follow-up were taken as the study eyes, and the eyes with no anti-VEGF drug treatment were the control eyes. Optical coherence tomography (OCT) examination was used to observe the VMI status of both eyes before treatment. Vitreous macular adhesion (VMA), macular epiretinal membrane (MEM), and complete vitreous detachment (C-PVD) were defined as abnormalities in VMI. The VMA was classified as focal (≤1500 μm) and broad (>1500 μm) depending on the diameter of the vitreous and macular adhesions on the OCT images. Before treatment, there were 12 eyes with abnormal VMI in study eyes, including 8 eyes with broad VMA, 3 eyes with focal VMA, and 1 eye with MEM; 12 eyes with abnormal VMI in control eyes: broad VMA in 7 eyes, focal VMA in 2 eyes, C-PVD in 2 eyes, and MEM in 1 eye. The average follow-up time after treatment was 16.4 months. During the follow-up period, OCT was performed monthly in a follow-up mode. Comparing the changes on VMI between before and after treatment in both eyes of patients, respectively. The chi-square test was used to compare the difference on VMI. Because the number of samples was <40, Fisher's exact test was used for the analysis.ResultsAt the final follow-up, 12 eyes with abnormal VMI in the study eyes, including 5 eyes with broad VMA, 2 eyes with focal VMA, 3 eyes with C-PVD, and 2 eyes with MEM. There were 6 eyes altered comparing with baseline. In the control eyes, there were 13 eyes with abnormal VMI, including 5 eyes with broad VMA, 7 eyes with C-PVD, and 1 eye with MEM. A total of 6 eyes changed on VMI comparing with baseline. At the final follow-up, there was no significant difference on VMI changes between the study eyes and its corresponding control eyes (P=0.053). In all eyes, a total of 4 eyes changed from focal VMA to C-PVD at the final follow-up, accounting for 80.0% of the total focal VMA; 3 eyes changed from broad VMA to C-PVD, accounting for 21.4% of the total broad VMA.ConclusionsRepeated anti-VEGF treatment has little effect on VMI. Regardless of anti-VEGF therapy, eyes with focal VMA appears to be more prone to C-PVD than the broad one.

关键词: 血管生成抑制剂/副作用; 湿性黄斑变性; 玻璃体黄斑界面

Key words: Angiogenesis inhibitors/adverse effects; Wet macular degeneration; Vitreomacular interface

引用本文: 董琪, 华英彬, 徐海峰. 反复抗血管内皮生长因子药物治疗对渗出型老年性黄斑变性患者玻璃体黄斑界面的影响. 中华眼底病杂志, 2018, 34(3): 263-267. doi: 10.3760/cma.j.issn.1005-1015.2018.03.013 复制

登录后 ,请手动点击刷新查看全文内容。 没有账号,
登录后 ,请手动点击刷新查看图表内容。 没有账号,
1. Rosenfeld PJ, Brown DM, Heier JS, et al. Ranibizumab for neovascular age-related macular degeneration [J]. N Engl J Med, 2006, 355(14): 1419-1431. DOI: 10.1056/NEJMoa054481.
2. Brown DM, Michels M, Kaiser PK, et al. Ranibizumab versus verteporfin photodynamic therapy for neovascular age-related macular degeneration: two-year results of the ANCHOR study [J]. Ophthalmology, 2009, 116(1): 57-65. DOI: 10.1016/j.ophtha.2008.10.018.
3. Kaiser PK, Blodi BA, Shapiro H, et al. Angiographic and optical coherence tomographic results of the MARINA study of ranibizumab in neovascular age-related macular degeneration [J]. Ophthalmology, 2007, 114(10): 1868-1875. DOI: 10.1016/j.ophtha.2007.04.030.
4. Comparison of Age-Related Macular Degeneration Treatments Trials Research G, Martin DF, Maguire MG, et al. Ranibizumab and bevacizumab for treatment of neovascular age-related macular degeneration: two-year results [J]. Ophthalmology, 2012, 119(7): 1388-1398. DOI: 10.1016/j.ophtha.2012.03.053.
5. Lalwani GA, Rosenfeld PJ, Fung AE, et al. A variable-dosing regimen with intravitreal ranibizumab for neovascular age-related macular degeneration: year 2 of the PrONTO Study [J]. Am J Ophthalmol, 2009, 148(1): 43-58. DOI: 10.1016/j.ajo.2009.01.024.
6. Ho AC, Busbee BG, Regillo CD, et al. Twenty-four-month efficacy and safety of 0.5 mg or 2.0 mg ranibizumab in patients with subfoveal neovascular age-related macular degeneration [J]. Ophthalmology, 2014, 121(11): 2181-2192. DOI: 10.1016/j.ophtha.2014.05.009.
7. Zhu M, Chew JK, Broadhead GK, et al. Intravitreal ranibizumab for neovascular age-related macular degeneration in clinical practice: five-year treatment outcomes [J]. Graefe's Arch Clin Exp Ophthalmol, 2015, 253(8): 1217-1225. DOI: 10.1007/s00417-014-2799-8.
8. Boyer DS, Heier JS, Brown DM, et al. A Phase Ⅲb study to evaluate the safety of ranibizumab in subjects with neovascular age-related macular degeneration [J]. Ophthalmology, 2009, 116(9): 1731-1739. DOI: 10.1016/j.ophtha.2009.05.024.
9. Chavan R, Panneerselvam S, Adhana P, et al. Bilateral visual outcomes and service utilization of patients treated for 3 years with ranibizumab for neovascular age-related macular degeneration [J]. Clin Ophthalmol, 2014, 8: 717-723. DOI: 10.2147/OPTH.S60763.
10. Holz FG, Tadayoni R, Beatty S, et al. Multi-country real-life experience of anti-vascular endothelial growth factor therapy for wet age-related macular degeneration [J]. Br J Ophthalmol, 2015, 99(2): 220-226. DOI: 10.1136/bjophthalmol-2014-305327.
11. Mojana F, Cheng L, Bartsch DU, et al. The role of abnormal vitreomacular adhesion in age-related macular degeneration: spectral optical coherence tomography and surgical results [J]. Am J Ophthalmology, 2008, 146(2): 218-227. DOI: 10.1016/j.ajo.2008.04.027.
12. Nomura Y, Takahashi H, Tan X, et al. Effects of vitreomacular adhesion on ranibizumab treatment in Japanese patients with age-related macular degeneration [J]. Jpn J Ophthalmol, 2014, 58(5): 443-447. DOI: 10.1007/s10384-014-0333-5.
13. Lee SJ, Lee CS, Koh HJ. Posterior vitreomacular adhesion and risk of exudative age-related macular degeneration: paired eye study [J]. Am J Ophthalmol, 2009, 147(4): 621-626 e1. DOI: 10.1016/j.ajo.2008.10.003.
14. Schulze S, Hoerle S, Mennel S, et al. Vitreomacular traction and exudative age-related macular degeneration[J]. Acta Ophthalmol, 2008, 86(5): 470-481. DOI: 10.1111/j.1755-3768. 2008.01210.x.
15. Krebs I, Brannath W, Glittenberg C, et al. Posterior vitreomacular adhesion: a potential risk factor for exudative age-related macular degeneration? [J]. Am J Ophthalmol, 2007, 144(5): 741-746. DOI: 10.1016/j.ajo.2007.07.024.
16. Robison CD, Krebs I, Binder S, et al. Vitreomacular adhesion in active and end-stage age-related macular degeneration [J]. Am J Ophthalmol, 2009, 148(1): 79-82. DOI: 10.1016/j.ajo.2009.01.014.
17. Duker JS, Kaiser PK, Binder S, et al. The international vitreomacular traction study group classification of vitreomacular adhesion, traction, and macular hole [J]. Ophthalmology, 2013, 120(12): 2611-2619. DOI: 10.1016/j.ophtha.2013.07.042.
18. Suh MH, Seo JM, Park KH, et al. Associations between macular findings by optical coherence tomography and visual outcomes after epiretinal membrane removal [J]. Am J Ophthalmol, 2009, 147(3): 473-480. DOI: 10.1016/j.ajo.2008.09.020.
19. Kakehashi A, Takezawa M, Akiba J. Classification of posterior vitreous detachment [J]. Clini Ophthalmol, 2014, 8: 1-10. DOI: 10.2147/OPTH.S54021.
20. Uchino E, Uemura A, Ohba N. Initial stages of posterior vitreous detachment in healthy eyes of older persons evaluated by optical coherence tomography [J]. Arch Ophthalmol, 2001, 119(10): 1475-1479. DOI: 10.1001/archopht.119.10.1475.
21. Johnson MW. Perifoveal vitreous detachment and its macular complications [J]. Trans Am Ophthalmol Soc, 2005, 103: 537-567.
22. Veloso CE, Kanadani TM, Pereira FB, et al. Vitreomacular interface after anti-vascular endothelial growth factor injections in neovascular age-related macular degeneration [J]. Ophthalmology, 2015, 122(8): 1569-1572. DOI: 10.1016/j.ophtha.2015.04.028.
23. Stalmans P, Benz MS, Gandorfer A, et al. Enzymatic vitreolysis with ocriplasmin for vitreomacular traction and macular holes [J]. N Engl J Med, 2012, 367(7): 606-615. DOI: 10.1056/NEJMoa1110823.