The purpose of this retrospective study was to examine the efficacy of dexamethasone implant in refractory diabetic macular oedema (DMO) in real life settings. Methods: In all, 24 eyes of 22 patients that required treatment with single or multiple intravitreal dexamethasone implants for refractory DMO were included in the study. Patients having macular oedema for another retinal disease were excluded from the study. The patient data were collected and analyzed retrospectively. As a demographic data age, gender, the type of diabetes and the duration of DMO were collected. Changes in central foveal thickness and the number of hyper reflective spots (HRS) were analyzed with Heidelberg SD-OCT. Furthermore, the best-corrected visual acuity (BCVA) and changes in the intraocular pressure (IOP) were measured. Results: In all, 50.0% of the eyes with baseline BCVA 0.45 (±2.4) lines in ETDRS LogMAR scale received only one implant during the follow-up of 332 (±79) days. At the end of the follow-up, BCVA was 0.26 (±2.0) lines. The other 50.0% of the eyes with baseline BCVA 0.64 (±3.0) lines received the second implant in 156 (±38) days. Central retinal thickness (CRT) at baseline was 333 (±44) μm in the eyes with only one implant and 497 (±125) μm in the eyes with 2 or more implants. IOP lowering medication was needed for 8.3% of the eyes. The decrease in the number of HRS was significant (8±17, p=0.048) in response to dexamethasone implantation. Conclusion: The dexamethasone implant is a useful treatment in refractory DMO and HRS seen in the OCT might indicate inflammation in the retina.

Vascular endothelial growth factor (VEGF) expression induces age-related macular degeneration (AMD), which is a common vision-threatening disease due to choroidal neovascularization and a fibrovascular membrane. We describe a mouse model of neovascular AMD with the local expression of human VEGF-A165 in the eye. We use a transgenic mouse in which human VEGF-A165 has been silenced with the loxP-STOP fragment. The choroidal neovascularization and human VEGF-A165 expression in the mouse are induced by subretinal adenoviral Cre gene delivery. Cre gene transfer is compared with adenoviral LacZ gene transfer control. We characterize the AMD phenotype and changes in the vasculature by using fluorescein angiography, optical coherence tomography, and immunohistochemistry. At early time points, mice exhibit increases in retinal thickness (348 ± 114 µm vs. 231 ± 32 µm) and choroidal neovascularization area (12000 ± 15174 µm2 vs. 2169 ± 3495 µm2) compared with the control. At later time points, choroidal neovascularization develops into subretinal fibrovascular membrane. Human VEGF-A165 expression lasts several weeks. In conclusion, the retinas display vascular abnormalities consistent with choroidal neovascularization. Together with immunohistochemical findings, these changes resemble clinical AMD-like ocular pathologies. We conclude that this mouse model of Cre-induced choroidal neovascularization is useful for mimicking the pathogenesis of AMD, studying the effects of human VEGF-A165 in the retina, and evaluating anti-VEGF treatments for choroidal neovascularization.

Aim: Transgenic mice with an elastic fiber mutation (C1039G+/-) in the fibrillin-1 gene and apolipoprotein E deficiency express vulnerable atherosclerotic plaque formation in the aorta and coronary and carotid arteries. The fibrillin-1 gene mutation alone leads to impaired fibrillin-1 function common to Marfan syndrome. The aim was to study for the first time the potential effects of atherosclerosis and vulnerable plaques in mouse eye and spontaneous retinal vessel occlusions in these mice.Methods: Apolipoprotein E-deficient and fibrillin-1 mutated mice (ApoE-/-/Fbn1C1039G+/-) were used for the study. ApoE-/- littermates served as controls. Optical coherence tomography and fluorescein angiography were used to study the retina and retinal vessels before and after the 12-week high-fat diet. Series of staining were performed to study morphology, apoptosis, glial fibrillary acidic protein activation, collagen formation, inflammatory cell infiltration and drusen formation.Results: No pathological changes were found in hypercholesterolemic ApoE-/-/Fbn1C1039G+/- mice in imaging studies nor in the histological stainings. There was neither abnormality in the retinal morphology nor any detectable biomarkers.Conclusion: ApoE-/-/Fbn1C1039G+/- mice did not present the ocular signs of Marfan syndrome.12-week high-fat diet is not sufficient to induce retinal vessel occlusion on 20 to 23 weeks old mice. This indicates that the mechanistic background of retinal vessel occlusion is more complex.

Purpose The efficacy of dexamethasone implant in refractory diabetic macular oedema (DMO). Methods 24 eyes of 22 patients having single dexamethasone implant for refractory DMO were included in the study. Patients with another retinal disease causing macular oedema were excluded. The patient data was collected and analyzed retrospectively. As a demographic data, age, gender and the type of diabetes and duration of DMO were collected. Morphology of the retina and changes in foveal thickness were analyzed with Heidelberg SD‐OCT. Furthermore improvement in the best‐corrected visual acuity (BCVA) and changes in the intraocular pressure (IOP) were observed. Results The mean age of patients was 65,6 (±10,6) years. 36,4% were female and 63,6% were male. 22,7% had type 1 (DM1) and 77,3% had type 2 diabetes (DM2). The mean duration of DMO was 26,1 (±23,8) months. 90,9% of the eyes had had previous argon laser treatment to macula and/or periphery. Panphotocoagulation was made in 29,2% of the eyes, 87,5% of the eyes were treated with intravitreal bevacizumab (4,3 ±3,0 injections) and 37,5% were treated with triamcinolone before. The mean BCVA at baseline was 0,34 (±0,17) in Snellen. Best improvement in visual acuity was seen 120,5 (±78,8) days after dexamethasone implant. Best achieved VA was 0,53 (±0,19). Baseline foveal thickness was 413,4 (±120,2) μm and at the point of best achieved VA 333,5 (±46,5) μm. Vitrectomy was performed in 20,8% before. 45,8% of the eyes were phakic and cataract developed in 72,7% of these eyes. The highest increase in IOP was 4,9 (±6,5) mmHg. 8,3% of the eyes needed IOP lowering medication. Conclusion We suggest that dexamethasone implant is a useful treatment in DMO even in relatively poor eyes. Commercial interest