Abstract

Objective. To prospectively evaluate the effect of intravitreal bevacizumab on aqueous levels of interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF) in patients with exudative age-related macular degeneration (AMD) and correlate clinical outcomes with cytokine levels. Methods. 30 eyes of 30 patients with exudative AMD underwent intravitreal injection of bevacizumab three times at monthly intervals. The aqueous samples prior to the 1st injection (baseline) and 3rd injection were analyzed for VEGF and IL-6 levels. Subjects were subgrouped based upon change in the central subfield (CSF) macular thickness on SD-OCT at 8 weeks. Group 1 included patients (n = 14) with a decrease in CSF thickness greater than 10% from the baseline (improved group). Group 2 included patients (n = 16) who had a decrease in CSF thickness 10% or less (treatment-resistant). Results. In subgroup analysis, in both groups 1 and 2 patients, compared to aqueous VEGF, aqueous IL-6 levels showed a better correlation with CSF thickness on SD-OCT (r = 0.72 and 0.71, resp.). Conclusions. Aqueous IL-6 may be an important marker of treatment response or resistance in wet macular degeneration. Future therapeutic strategies may include targeted treatment against both VEGF and IL-6, in patients who do not respond to anti-VEGF treatment alone.

Highlights

  • Age-related macular degeneration (AMD) is the leading cause of irreversible blindness among patients over the age of 55 years in the western world [1, 2]

  • We investigated the correlation between Vascular endothelial growth factor (VEGF) and IL-6 levels in the aqueous with the treatment response after intravitreal bevacizumab for exudative AMD

  • Aqueous IL-6 levels showed a better correlation than aqueous VEGF levels in predicting treatment response in exudative AMD after bevacizumab treatment

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Summary

Introduction

Age-related macular degeneration (AMD) is the leading cause of irreversible blindness among patients over the age of 55 years in the western world [1, 2]. Exudative AMD, a less common form, is characterized by the formation of a choroidal neovascular membrane that emanates from the choriocapillaris through defective Bruch’s membrane [3]. Inhibition of VEGF has become a widely accepted treatment modality of exudative AMD [6, 7]. Bevacizumab, an anti-VEGF agent, binds and inhibits VEGF related cellular effects [8]. In addition to VEGF, choroidal neovascularization (CNV) involves a number of angiogenic molecules and inflammatory cytokines: interleukin-6 (IL-6), interleukin-8 (IL8), intercellular adhesion molecule-1 (ICAM-1), and monocyte chemoattractant protein-1 (MCP-1) [9, 10]

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