The aim of this pilot study was to investigate the effect of intravitreal administration of etanercept in refractory diabetic macular edema. Seven patients diagnosed with diabetic macular edema, refractory to previous treatment, were enrolled. They all received 2 consecutive intravitreal injections of 2.5 mg (0, 1 ml) of Etanercept (Enbrel), with a two-week interval. In all patients visual acuity assessment, fundoscopy and fluorescein angiography were performed prior to the first injection, weekly for the first month, as well as 2 and 3 months following the first injection. No adverse reactions or adverse events were noticed in any patient. Analysis of the data indicates a trend for improvement of visual acuity, a slight worsening of hard exudates and fluorescein leakage, while hemorrhages remained stable, 3 months after initiation of therapy. However, no statistical significance has been reached. This small pilot study did not reveal any improvement in the clinical course of patients with refractory diabetic macular edema after the intravitreal injection of etanercept. Further research is warranted in order to obtain conclusive results concerning the role of anti-TNF therapy in diabetic macular edema.
Oral atorvastatin therapy in patients with diabetes mellitus and dyslipidemia seems to reduce the severity of hard exudates and fluorescein leakage in diabetic maculopathy and could be useful as an adjuvant therapy in the management of diabetic macular edema.
Purpose. To compare ocular rigidity (OR) and outflow facility (C) in patients with nonproliferative diabetic retinopathy (NPDR) and control subjects. Methods. Twenty-four patients with NPDR (NPDR group) and 24 controls (control group) undergoing cataract surgery were enrolled. NPDR group was further divided into patients with mild NPDR (NPDR1-group) and patients with moderate and/or severe NPDR (NPDR2-group). After cannulation of the anterior chamber, a computer-controlled device was used to infuse saline and increase the intraocular pressure (IOP) in a stepping procedure from 15 to 40 mmHg. Ocular rigidity and outflow facility coefficients were estimated from IOP and volume recordings. Results. Ocular rigidity was 0.0205 μL−1 in NPDR group and 0.0202 μL−1 in control group (P = 0.942). In NPDR1-group, OR was 0.017 μL−1 and in NPDR2-group it was 0.025 μL−1 (P = 0.192). Outflow facility was 0.120 μL/min/mmHg in NPDR-group compared to 0.153 μL/min/mmHg in the control group at an IOP of 35 mmHg (P = 0.151). There was no difference in C between NPDR1-group and NPDR2-group (P = 0.709). Conclusions. No statistically significant differences in ocular rigidity and outflow facility could be documented between diabetic patients and controls. No difference in OR and C was detected between mild NPDR and severe NPDR.
Purpose To investigate the effect of intravitreal ketorolac tromethamine in chronic post‐operative cystoid macular edema.
Methods Six patients diagnosed with chronic post‐operative CME non responsive in conventional therapies, were enrolled. 2 patients received 2 intravitreal injections of 300 μg (0.05ml) of ketorolac tromethamine (Toradol) with a 3‐week interval, three patients received 4 consecutive injections of 500 μg (0.05ml) weekly and 3 patients received 4 consecutive injections of 500 μg (0.05ml) daily. Patients were followed by means of biomicroscopy, fluorescein angiography and optical coherent tomography. Follow‐up lasted up to six months.
Results No adverse effect was noticed in any of the patients. A trend for visual acuity improvement and macular edema regression was noticed after initiation of the therapy. A rebound of the edema happened usually a week after the last injection. In the long follow‐up regression of the macular edema was noticed in three out of six patients.
Conclusion This pilot study indicates a possible role of intravitreal injection of ketorolac tromethamine in patients with chronic postoperative cystoid macular edema. Further research is warranted in order to obtain conclusive results concerning doses and timing of injections.
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