Abstract
BackgroundNumerous cytokines have been proven to participate in the pathogenesis of neovascular age-related macular degeneration (nAMD). The present study aimed to investigate the aqueous humor cytokine expression profile in nAMD patients before and after ranibizumab treatments in comparison to cataract patients.MethodsThis prospective study included 20 treatment-naïve nAMD eyes of 20 patients who received three consecutive monthly injections of ranibizumab. Aqueous humor samples were collected before the first (baseline), second (1 month later), and third (2 months later) injections. Controls were 20 age- and gender-matched cataract patients without any other ocular disease. The aqueous concentrations of 28 cytokines were measured using a multiplex bead assay. Central macular thickness (CMT) and maximum retinal thickness (MRT)-3 mm were measured by spectral domain optical coherence tomography (SD-OCT). The greatest linear diameter (GLD) was measured by fundus fluorescein angiography (FA).ResultsThree cytokines in aqueous humor, including angiogenin, interleukin-36β (IL-36β), and fibroblast growth factor-acidic (FGF-α) were significantly higher in nAMD patients in comparison to cataract patients, both before and after two consecutive monthly ranibizumab injections. Compared with the nAMD patients’ basal levels, two consecutive monthly ranibizumab injections effectively reduced the aqueous concentrations of VEGF-A and placental growth factor (PlGF), as well as the values of CMT, MRT-3 mm, and GLD.ConclusionsAngiogenin, IL-36β, and FGF-α have higher expression levels in nAMD patients in comparison to cataract patients, both before and after 2 months of ranibizumab therapy. These cytokines may have correlations with the pathogenesis of nAMD.
Highlights
Numerous cytokines have been proven to participate in the pathogenesis of neovascular age-related macular degeneration
All patients with neovascular age-related macular degeneration (nAMD) or cataract were examined in a full ophthalmological examination, including bestcorrected visual acuity (BCVA) determined as the logarithm of the minimum angle of resolution, slit-lamp biomicroscopy, intraocular pressure (IOP) measurement, dilated fundus examination, color fundus photography, and spectral domain optical coherence tomography (SD-OCT)
In the nAMD group, Polypoidal choroidal vasculopathy (PCV) was found in 4 eyes (20%), type I choroidal neovascularization (CNV) was found in 6 eyes (30%), type II CNV was found in 10 eyes (50%), and there was no retinal angiomatous proliferation
Summary
Numerous cytokines have been proven to participate in the pathogenesis of neovascular age-related macular degeneration (nAMD). Age-related macular degeneration (AMD) is a leading cause of blindness in the elderly population. Subfoveal geographic atrophy and choroidal neovascularization (CNV) cause severe visual loss in AMD patients [1]. CNV is the main feature of neovascular AMD (nAMD), in which the formation of new aberrant blood vessels leads to macular edema, hemorrhage, fibrosis, and visual impairment [2]. NAMD accounts for only approximately 20% of the overall incidence of AMD, this subtype of patients is most likely to have severe visual loss among AMD patients [3]. Vascular endothelial growth factor (VEGF) and many other cytokines are important mediators of inflammatory responses in nAMD patients [2, 7]. Recurrent or persistent CNV is still very common, despite repeated application of anti-VEGF agents, and the efficacy of only using anti-VEGF drugs is still debatable [9, 10]
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