Inflammatory changes in aqueous induced by diabetes in open angle glaucoma patients

Abstract

PurposeComparative changes of inflammatory cytokines expression in open angle glaucoma and diabetes.MethodsA cross‐sectional study: 87 eyes, from 87 patients, distributed in 4 groups: 24 eyes from healthy subjects, 26 eyes from diabetic patients, 16 POAG eyes and 21 eyes from diabetic glaucoma patients. Aqueous was collected during conventional cataract surgery. 21 inflammatory markers were quantified and compared between groups using a Luminex® Performance Assay multiplex kit based on flowcytometric methods. Data on patient demographics, duration of glaucoma/diabetes, intraocular pressure as well as duration of anti‐glaucoma therapy were collected for correlations and prediction models.ResultsMolecules like CXCL5 (p = 0.008), CXCL8 (p = 0.048), IL‐1α (p = 0.005), IL‐2 (p = 0.015) and TNFα (p = 0.041) were found significantly higher if diabetes was present in POAG patients. Based on the same pathogenic pathway (TNFα stimmulation, Th1 lymfocytes), a prediction model was created for each glaucoma group. As such, levels of CXCL5, CXCL8, IL‐1α and IL‐2 could highly predict TNFα level for the POAG patients (r2 = 0.842, p = 0.000), whereas for the diabetic glaucomatous patients the prediction level was inferior (r2 = 0.618, p = 0.034). Therefore, we tested a second inflammatory model for this category. Presence of diabetes induced collateral stimmulation of TNFα via elevated GM‐CSF expression (stimmulation via Th2 lymfocytes). Molecules like TNFα, G‐CSF and VEGF were significant predictors for a GM‐CSF augmented expression (r2 = 0.758, p = 0.018) in this group; moreover a lineary dependence between GM‐CSF and TNFα was noted. No other parameter was signifficant in these models.ConclusionsInflammatory reaction in glaucoma patients was based on TNFα overexpression, induced either directly (POAG) or indirectly via collateral pathways GM‐CSF mediated (diabetic POAG).