In Brief Purpose: To study the association of single-nucleotide polymorphisms of interleukin 8, vascular endothelial growth factor, erythropoietin, complement factor H, complement component C3, and LOC387715 genes with the response to bevacizumab treatment in exudative age-related macular degeneration. Methods: Clinical records, smoking history, optical coherence tomography, and angiographies of 96 bevacizumab-treated exudative age-related macular degeneration patients were analyzed retrospectively. Blood DNA was collected. Based on the disappearance of intra- or subretinal fluid in optical coherence tomography, patients were graded as responders, partial responders, or nonresponders after 3 initial treatment visits and a median time of 3.5 months. Results: Interleukin 8 promoter polymorphism −251A/T was significantly associated with persisting fluid in optical coherence tomography. The A allele was more frequent in nonresponders than in responders (P = 0.033). In multivariate modeling, the AA genotype of −251A/T (P = 0.043) and occult (P = 0.042) or predominantly classic (P = 0.040) lesions predicted poorer outcome. Visual acuity change was better in responders than in nonresponders (P = 0.006). Baseline lesion size (P = 0.006) and retinal cysts after the treatment (P < 0.001) correlated with less visual acuity gain. Conclusion: The A allele and the homozygous AA genotype of interleukin 8 −251A/T were associated with anatomical nonresponse to bevacizumab treatment. The genotype AA of interleukin 8 promoter polymorphism −251A/T was associated with persisting intra- or subretinal fluid in exudative age-related macular degeneration patients after the initial treatment with intravitreal bevacizumab. Interleukin 8 seems to modulate the response to anti–vascular endothelial growth factor therapy at least during the first months of the .treatment
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Hautamäki et al. (2013) studied this question.
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