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Interleukin‐8 promoter polymorphism is associated with the initial repose to bevacizumab in AMD treatment
Author(s) -
IMMONEN I,
HAUTAMÄKI A,
KIVIOJA J,
VAVULI S,
KAKKO S,
SAVOLAINEN ER,
SAVOLAINEN M,
LIINAMAA J,
SEITSONEN S,
ONKAMO P,
JÄRVELÄ I
Publication year - 2013
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2013.t077.x
Subject(s) - bevacizumab , macular degeneration , medicine , single nucleotide polymorphism , genotype , gastroenterology , interleukin , vascular endothelial growth factor , factor h , ophthalmology , immunology , complement system , vegf receptors , gene , antibody , cytokine , genetics , biology , chemotherapy
Purpose To study the association of potential key single‐nucleotide polymorphisms with the short‐term anatomic response to bevacizumab treatment in exudative age‐related macular degeneration (AMD). Methods Clinical data 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. Representative single‐nucleotide polymorphisms of interleukin 8, vascular endothelial growth factor, erythropoietin, complement factor H, complement component C3, and LOC387715 genes were analysed. Results Interleukin 8 promoter polymorphism −251A/T,conferring a more acitve interleuking‐8 system, 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 a poorer outcome. Conclusion The interleukin ‐8 pathway may modulate the early anatomic response to anti‐VEGF treatment in AMD. A possible activation of interleukin ‐8 production in patients may represent a compensatory mechanism to chronic blockade of VEGF signalling in AMD lesions