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Results from the consecutive treatment of refractory diabetic macular edema with bevacizumab and ranibizumab in a clinical setting

Poster Details

First Author: I.Papandreou UK

Co Author(s):    C. Leak   M. Ting   E. Mensah            0   0 0   0 0   0 0   0 0

Abstract Details


To evaluate and compare the outcome of intravitreal treatment with bevacizumab (Avastin) and consecutive ranibizumab (Lucentis) in patients with refractory diabetic macular oedema (DMO).


In the UK, licensing of ranibizumab by the national institute for clinical health and excellence (NICE) for the management of DMO patients has allowed the transition of patients that had been treated with bevacizumab and have a central retinal thickness (CRT) of more than 400μm to a treatment with Lucentis.


Prospective data was entered into an in-house database of all patients receiving treatment for refractory DMO at the Ophthalmology Department of Central Middlesex Hospital, London, UK. Prior to June 2010, treatment involved argon macular laser. Subsequent to June 2010 treatment included bevacizumab, with consecutive ranibizumab from September 2013. Best corrected visual acuity (BCVA) on the logMAR chart was recorded at each visit as well as CRT with optical coherence tomography (OCT). OCT was performed with the Spectralis OCT device (Heidelberg Engineering, Heidelberg, Germany) using the standard protocol of the clinic. Statistical analysis involved the Wilcoxon signed rank test and Spearman correlation test. Results with p<0.05 and a correlation coefficient >0.6 were considered statistically significant.


32 eyes of 25 patients were included in this study. The mean age was 68 years (range 43 - 83 years). Patients received a mean of 3 bevacizumab (range 1 - 10) and 3 ranibizumab (range 1 - 5) injections. The follow-up time was up to 16 and 5 months for bevacizumab and ranibizumab respectively. The mean logMAR BCVA at baseline for bevacizumab was 0.68. At 3, 5 and 7 months mean BCVA was 0.66, 0.59 and 0.66 respectively (p=0.04, 0.025, 0.06). There was no significant difference in BCVA between baseline and any period thereafter. Mean CRT at baseline was 546μm. The mean CRT at months 1 and 2 were 494μm and 550μm respectively and were significantly different for baseline, (p= 0.009, 0.03). CRT for months 3 to 15 were not significantly different from baseline. The mean logMAR BCVA at baseline for ranibizumab was 0.62. BCVA at months 1, 2, 3 and 4 was 0.50, 0.48, 0.51 and 0.48 respectively; this was statistically significant (p= 0.002, <0.001, 0.009, 0.04). The mean CRT at baseline was 546μm. CRT at months 1, 2, 3 and 4 was 436μm, 382μm, 379μm and 321μm; this change was statistically significant (p<0.001, <0.001, 0.001, 0.02).


The treatment of refractory DMO with intravitreal bevacizumab made little difference to improving the BCVA and CRT of our patients. Consecutive treatment with ranibizumab resulted in a significant improvement in BCVA and CRT, which was preserved in the subsequent four months of treatment. Although the follow-up time for Lucentis was limited, data suggests that it may be a better option for the management of diabetic macula oedema that does not respond to argon laser treatment.

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