Aims Fluocinolone acetonide (FAc) is an intravitreal corticosteroid implant approved for the second-line treatment of diabetic macular edema (DME). This study compared outcomes of patients with DME switched directly to an FAc implant, versus indirectly via dexamethasone, after anti-VEGF therapy failure. Methods This is a retrospective, single-center chart review. Patients were assigned to Group A (switched to FAc after anti-VEGF) or Group B (switched to dexamethasone and then to FAc after > 4 months). Charts were reviewed for best-corrected visual acuity (BCVA), central macular thickness (CMT), intraocular pressure (IOP) and cataract development. Results Forty-nine eyes were included. BCVA increased and CMT decreased with anti-VEGF (both groups), and dexamethasone (Group B only), but regressed after stopping treatment. With FAc, BCVA increased rapidly and significantly: increases were maintained up to 36 months (P < 0.001), except at 18 and 9 months in Groups A and B, respectively. Significant CMT reductions (P < 0.001) were evident after 3 months and maintained up to 36 months in both groups. IOP increase > 21 mmHg occurred in 14 patients (nine in Group A, five in Group B): all were sufficiently treated with IOP-lowering drops. Nineteen phakic eyes (73.1%) developed cataract: seven underwent phaco-emulsification (two in Group A, five in Group B). Conclusions Similar functional and anatomical improvements occurred in FAc-treated eyes, regardless of whether they first received dexamethasone or switched directly to FAc after anti-VEGF. Safety signals were consistent with corticosteroid class effects. Early switch to FAc could benefit patients who respond insufficiently to anti-VEGF. Keywords Diabetic macular edema • Fluocinolone acetonide • Dexamethasone • Second-line treatment • Best-corrected visual acuity • Central macular thickness This article belongs to the topical collection Eye Complications of Diabetes managed by Giuseppe Querques.

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Background/Aims: By the release of antiangiogenic factors, Müller glial cells provide an angiostatic environment in the normal and ischemic retina. We determined whether Müller cells produce thrombospondin-1 (TSP-1), a known inhibitor of angiogenesis. Methods: Secretion of TSP-1 by cultured Müller cells was determined with ELISA. Slices of rat retinas and surgically excised retinal membranes of human subjects were immunostained against TSP-1 and the glial marker vimentin. The effects of TSP-1 on the growth of bovine retinal endothelial cells (BRECs) and activation of ERK1/2 were determined with DNA synthesis and migration assays, and Western blotting, respectively. Results: Cultured Müller cells secrete TSP-1 under normoxic and hypoxic (0.2% O₂) conditions. Secretion of TSP-1 was increased in hypoxia compared to normoxia. In rat retinal slices, glial, retinal ganglion, and possibly horizontal cells were stained for TSP-1. Retinal glial cells in preretinal membranes from human subjects with nonhypoxic epiretinal gliosis (macular pucker) and proliferative diabetic retinopathy, respectively, were immunopositive for TSP-1. Exogenous TSP-1 reduced the VEGF-induced proliferation and migration of BRECs and decreased the phosphorylation level of ERK1/2 in BRECs. Conclusion: The data suggest that Müller cells are one major source of TSP-1 in the normal and ischemic retina. Glia-derived TSP1 may inhibit angiogenic responses in the ischemic retina.