Department of Ophthalmology at Shiley Eye Center and Institute for Genomic Medicine, University of California-San Diego, 9415 Campus Point Drive #0946, La Jolla, CA 92093-0838, USA.
Curr Mol Med. 2013 Jul;13(6):929-34. doi: 10.2174/15665240113139990048.
Age-related macular degeneration (AMD) is a leading cause of visual impairment in aging populations in industrialized countries. Here we investigated whether the genotype of vascular endothelial growth factor A (VEGFA) gene is associated with response to anti-VEGF therapy. 223 eyes with neovascular AMD were treated with intravitreal anti-VEGF therapy. Responders were defined as patients who had an improvement in best corrected visual acuity (BCVA) of at least 5 letters or one line on the EDTRS visual acuity chart along with resolution of intraretinal or subretinal fluid over 12 months. Patients who did not meet the definition of responders were classified as poor-responders. The vision of responders (n = 148) improved while the vision of poor-responders (n = 75) worsened (P<0.001). Responders on average had a decrease in central foveal thickness (CFT), while poor-responders had an increase in CFT (P <0.001). Compared with the responder group, the poor-responder group had a higher frequency of the risk (T) allele (Allelic P = 0.019) and TT genotype (P = 0.002 under a recessive model) for the VEGFA-rs943080 polymorphism. VEGFA expression was 1.8-fold higher in cells with the VEGFA rs943080 TT genotype than in cells with the VEGFA rs943080 CC genotype (P = 0.012). Age, gender, smoking, diabetes mellitus, and hypertension did not play a significant role in treatment response, but BMI was found to be significantly different between responders and poorresponders (P = 0.033). In conclusion, we demonstrated a potential pharmacogenetic relationship between the VEGFA gene and treatment response to anti-VEGF therapy.The studies are registered at ClinicalTrials.gov under the identifiers NCT00474695 (http://clinicaltrials. gov/ct2/show/NCT00474695) and NCT01464723 (http://clinicaltrials.gov/ct2/show/NCT01464723).
年龄相关性黄斑变性(AMD)是工业化国家老年人群视力损害的主要原因。在这里,我们研究了血管内皮生长因子 A(VEGFA)基因的基因型是否与抗 VEGF 治疗的反应相关。223 只患有新生血管性 AMD 的眼睛接受了玻璃体内抗 VEGF 治疗。反应者定义为最佳矫正视力(BCVA)至少提高 5 个字母或 EDTRS 视力表上提高一行,同时在 12 个月内视网膜内或视网膜下液体消退的患者。不符合反应者定义的患者被归类为治疗效果差的患者。反应者(n=148)的视力有所提高,而治疗效果差的患者(n=75)的视力则恶化(P<0.001)。反应者的平均中央视网膜厚度(CFT)减少,而治疗效果差的患者的 CFT 增加(P<0.001)。与反应者组相比,治疗效果差的患者组中 VEGFA-rs943080 多态性的风险(T)等位基因(等位基因 P=0.019)和 TT 基因型(隐性模型下 P=0.002)的频率更高。VEGFA 表达在携带 VEGFA rs943080 TT 基因型的细胞中比在携带 VEGFA rs943080 CC 基因型的细胞中高 1.8 倍(P=0.012)。年龄、性别、吸烟、糖尿病和高血压在治疗反应中没有起到显著作用,但发现 BMI 在反应者和治疗效果差的患者之间存在显著差异(P=0.033)。总之,我们证明了 VEGFA 基因与抗 VEGF 治疗反应之间存在潜在的药物遗传学关系。这些研究在 ClinicalTrials.gov 注册,标识符为 NCT00474695(http://clinicaltrials.gov/ct2/show/NCT00474695)和 NCT01464723(http://clinicaltrials.gov/ct2/show/NCT01464723)。