2013OphthalmologicaRequires access

Genetic Association with Response to Intravitreal Ranibizumab for Neovascular Age-Related Macular Degeneration in the Han Chinese Population

Dongqing Yuan, Donglan Yuan, Xiaoyi Liu, Songtao Yuan, Ping Xie, Qinghuai Liu

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Abstract

PURPOSE: To investigate a possible association between gene variants and patient response to treatment with intravitreal ranibizumab for neovascular age-related macular degeneration (AMD). METHODS: Visual acuity score (VAS) was recorded at baseline and a subsequent visit at 6 months. Genotypes of 3 polymorphisms in known AMD susceptibility loci (rs1061170 in complement factor H (CFH), rs11200638 in HTRA1 and rs1413711 in VEGF) were determined. Central retinal thickness and maximum thickness of the lesion were also measured. RESULTS: A total of 168 neovascular AMD patients treated with intravitreal ranibizumab were included in our study. For HTRA1 rs11200638, mean VAS changes were 3.5, 9.4 and 10.6 letters for the AA, AG and GG genotypes, respectively (p = 0.022). In contrast, for CFH rs1061170 and VEGF rs1413711, mean VAS changes were not significant. However, there was no significant difference in the changes in central retinal thickness and maximum lesion thickness among the genotypes of the tested single-nucleotide polymorphisms. CONCLUSIONS: HTRA1 gene polymorphism may influence patient response to treatment with intravitreal ranibizumab for neovascular AMD.

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PURPOSE: To investigate a possible association between gene variants and patient response to treatment with intravitreal ranibizumab for neovascular age-related macular degeneration (AMD). METHODS: Visual acuity score (VAS) was recorded at baseline and a subsequent visit at 6 months. Genotypes of 3 polymorphisms in known AMD susceptibility loci (rs1061170 in complement factor H (CFH), rs11200638 in HTRA1 and rs1413711 in VEGF) were determined. Central retinal thickness and maximum thickness of the lesion were also measured. RESULTS: A total of 168 neovascular AMD patients treated with intravitreal ranibizumab were included in our study. For HTRA1 rs11200638, mean VAS changes were 3.5, 9.4 and 10.6 letters for the AA, AG and GG genotypes, respectively (p = 0.022). In contrast, for CFH rs1061170 and VEGF rs1413711, mean VAS changes were not significant. However, there was no significant difference in the changes in central retinal thickness and maximum lesion thickness among the genotypes of the tested single-nucleotide polymorphisms. CONCLUSIONS: HTRA1 gene polymorphism may influence patient response to treatment with intravitreal ranibizumab for neovascular AMD.

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Available abstract

PURPOSE: To investigate a possible association between gene variants and patient response to treatment with intravitreal ranibizumab for neovascular age-related macular degeneration (AMD). METHODS: Visual acuity score (VAS) was recorded at baseline and a subsequent visit at 6 months. Genotypes of 3 polymorphisms in known AMD susceptibility loci (rs1061170 in complement factor H (CFH), rs11200638 in HTRA1 and rs1413711 in VEGF) were determined. Central retinal thickness and maximum thickness of the lesion were also measured. RESULTS: A total of 168 neovascular AMD patients treated with intravitreal ranibizumab were included in our study. For HTRA1 rs11200638, mean VAS changes were 3.5, 9.4 and 10.6 letters for the AA, AG and GG genotypes, respectively (p = 0.022). In contrast, for CFH rs1061170 and VEGF rs1413711, mean VAS changes were not significant. However, there was no significant difference in the changes in central retinal thickness and maximum lesion thickness among the genotypes of the tested single-nucleotide polymorphisms. CONCLUSIONS: HTRA1 gene polymorphism may influence patient response to treatment with intravitreal ranibizumab for neovascular AMD.

Key concepts: Macular degeneration, Ranibizumab, Medicine, Ophthalmology, Visual acuity, Retinal, Choroidal neovascularization, Factor H

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