In diabetic eyes, there is an overall thinning of the choroid on EDI OCT. A decreased choroidal thickness may lead to tissue hypoxia and consequently increase the level of VEGF, resulting in the breakdown of the blood-retinal barrier and development of macular edema.

In the past years, the management of diabetic retinopathy (DR) relied primarily on a good systemic control of diabetes mellitus, and as soon as the severity of the vascular lesions required further treatment, laser photocoagulation or vitreoretinal surgery was done to the patient. Currently, even if the intensive metabolic control is still mandatory, a variety of different clinical strategies could be offered to the patient. The recent advances in understanding the complex pathophysiology of DR allowed the physician to identify many cell types involved in the pathogenesis of DR and thus to develop new treatment approaches. Vasoactive and proinflammatory molecules, such as vascular endothelial growth factor (VEGF), play a key role in this multifactorial disease. Current properly designed trials, evaluating agents targeting VEGF or other mediators, showed benefits in the management of DR, especially when metabolic control is lacking. Other agents, directing to the processes of vasopermeability and angiogenesis, are under investigations, giving more hope in the future management of this still sight-threatening disease.

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This cross-sectional study evaluated the relationship between ) functional and structural measurements of neurodegeneration in the initial stages of diabetic retinopathy (DR) and) the presence of neurodegeneration and early microvascular impairment. We analyzed baseline data of 449 patients with type 2 diabetes enrolled in the European Consortium for the Early Treatment of Diabetic Retinopathy (EUROCONDOR) study (NCT01726075). Functional studies by multifocal electroretinography (mfERG) evaluated neurodysfunction, and structural measurements using spectral domain optical coherence tomography (SD-OCT) evaluated neurodegeneration. The mfERG P1 amplitude was more sensitive than the P1 implicit time and was lower in patients with Early Treatment of Diabetic Retinopathy Study (ETDRS) level 20-35 than in patients with ETDRS level <20 ( = 0.005). In 58% of patients, mfERG abnormalities were present in the absence of visible retinopathy. Correspondence between SD-OCT thinning and mfERG abnormalities was shown in 67% of the eyes with ETDRS <20 and in 83% of the eyes with ETDRS level 20-35. Notably, 32% of patients with ETDRS 20-35 presented no abnormalities in mfERG or SD-OCT. We conclude that there is a link between mfERG and SD-OCT measurements that increases with the presence of microvascular impairment. However, a significant proportion of patients in our particular study population (ETDRS ≤35) had normal ganglion cell-inner plexiform layer thickness and normal mfERG findings. We raise the hypothesis that neurodegeneration may play a role in the pathogenesis of DR in many but not in all patients with type 2 diabetes.

MT was greater in diabetics than controls and tended to increase with DR and ME severity. OCT is a sensitive technique for detecting early diabetic macular abnormalities and quantifying their reduction after laser treatment.

Purpose: To evaluate the effects of repeated intravitreal dexamethasone implant (IDI) (Ozurdex®) in eyes with macular edema (ME) due to retinal vein occlusion (RVO). Methods: We reviewed the charts of patients with RVO-related ME, who received repeated Ozurdex IDI (0.7 mg) on an ‘as-needed’ basis. Main outcome measures included changes in best-corrected visual acuity (BCVA), central macular thickness (CMT), retreatment interval, and incidence of side effects. Results: A total of 33 eyes were included for analysis. Retreatment with Ozurdex was judged necessary after 4.7 ± 1.1 months from the first IDI (1st IDI) and 5.1 ± 1.5 months from the second IDI (2nd IDI). Baseline BCVA was 0.65 ± 0.43 logMAR; it significantly improved to 0.50 ± 0.42 logMAR after 1.4 ± 0.7 months from the 1st IDI (peaking efficacy) (p < 0.001) and to 0.48 ± 0.44 logMAR after 1.8 ± 0.8 months from the 2nd IDI (peaking efficacy) (p < 0.001). CMT decreased from 636 ± 217 µm (baseline) to 300 ± 114 µm, 1.4 ± 0.7 months after the 1st IDI (p < 0.001), and to 298 ± 91 µm, 1.8 ± 0.8 months after the 2nd IDI (p < 0.001). A rebound effect was recorded in 7 eyes after the 1st IDI (mean 168 ± 158 µm) and in 4 eyes after the 2nd IDI (mean 215 ± 199 µm). All eyes with a rebound effect improved again after a 2nd intravitreal Ozurdex injection. No serious adverse events were observed; 12 eyes developed a transient IOP increase, and cataracts were extracted in 2 eyes. Conclusion: Repeated intravitreal Ozurdex on an ‘as-needed’ basis, with a retreatment interval <6 months, may produce long-term clinically meaningful benefits in the treatment of ME due to RVO, without other significant side effects than expected after intraocular corticosteroid treatment.

Clinical trial reg. no. NCT01726075, clinicaltrials.gov This article contains Supplementary Data online at http://diabetes .diabetesjournals.org/lookup/suppl/

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