Diffuse diabetic macular oedema treated with intravitreal bevacizumab or triamcinolone acetonide

Editor, O ne of the most frequent complications of diabetic retinopathy is diabetic macular oedema (DMO) (Klein et al. 1984). Therapeutic recommendations for the therapy of DMO usually include intensive glycaemic control (Diabetes Control and Complication Trial Research Group 1993; UK Prospective Diabetes Study [UKPDS] Group 1998), arterial blood pressure control (Gray et al. 2002) and focal or grid retinal photocoagulation, as demonstrated by the Early Treatment Diabetic Retinopathy Study [ETDRS] Research Group (1985). During the last 10 years, additional therapeutic modalities have been proposed, such as pars plana vitrectomy (Lewis et al. 1992) and intravitreal injections of anti-vascular endothelial growth factor (VEGF) agents such as pegabtanib (Macugen Diabetic Retinopathy Study Group 2005) and bevacizumab (Browning et al. 2006; Haritoglou et al. 2006; Arevalo et al. 2007; Fang et al. 2008; Soliman et al. 2008a, 2008b) or triamcinolone acetonide (Jonas & Söfker 2001; Audren et al. 2006; LecleireCollet et al. 2007; Vinten et al. 2007; Margolis et al. 2008). As the effects of intravitreal bevacizumab and intravitreal triamcinolone on visual acuity (VA) and macular thickness have not been compared, it was the purpose of the present pilot study to compare the drugs. The study included 27 patients (27 eyes) with DMO, who received either two intravitreal injections of 1.5 mg bevacizumab with an interval of 6 weeks between them (n = 12 patients) or one intravitreal injection of about 25 mg triamcinolone acetonide (n = 15 patients). Inclusion criteria were clinically significant macular oedema as shown by loss of VA and macular thickening as imaged by optical coherence tomography (OCT), and leakage in fluorescence angiography. The decision to inject triamcinolone or bevacizumab depended on the ophthalmologist examining the patient (UHMS for bevacizumab, JBJ for triamcinolone). Each patient was examined at baseline, and at 1, 3 and 6 months after the first injection. Follow-up examinations included VA measured by Snellen charts, intraocular pressure (IOP) measured by applanation tonometry and central retinal thickness (CRT) measured by OCT. All patients were fully informed about the experimental character of the treatment and gave signed informed consent. All patients in both groups attended all four examinations. At baseline, the bevacizumab and triamcinolone study groups did not vary significantly in age (58.2 ± 6.8 years [mean ± standard deviation] and 57.3 ± 8.6 years, respectively; p = 0.76), VA (1.00 ± 0.44 logMAR and 0.85 ± 0.24 logMAR, respectively; p = 0.29), macular thickness (469 ± 126 lm and 379 ± 154 lm, respectively; p = 0.12) or length of follow-up (6.2 ± 0.2 months and 6.1 ± 0.2 months, respectively). In the bevacizumab group, mean VA increased from 1.00 ± 0.44 logMAR at baseline to 0.84 ± 0.50 logMAR at 1 month after the first injection, 0.71 ± 0.30 logMAR at 3 months after the first injection (reflecting a significant increase: p = 0.03) and 0.69 ± 0.26 logMAR at 6 months after the first injection (p = 0.02). In the triamcinolone acetonide group, VA increased significantly from 0.85 ± 0.24 logMAR at baseline to 0.60 ± 0.11 logMAR (p = 0.001) at 1 month, 0.64 ± 0.13 logMAR (p = 0.004) at 3 months and 0.64 ± 0.15 logMAR (p = 0.004) at 6 months after injection. The increase in VA measured at 1 month (p = 0.48), 3 months (p = 0.57) and 6 months (p = 0.43) after baseline did not vary significantly between the two study groups. Mean CRT in the bevacizumab group was 469 ± 126 lm at baseline and decreased significantly to 331 ± 94 lm (p = 0.004) at 1 month after the first injection, 361 ± 157 lm (p = 0.05) at 3 months and 361 ± 125 lm (p = 0.005) at 6 months. In the triamcinolone group, mean CRT was 380 ± 155 lm at baseline and decreased significantly to 262 ± 83 lm (p = 0.006) at 1 month, 277 ± 98 lm (p = 0.003) at 3 months and 321 ± 129 lm (p = 0.009) at 6 months. The decrease in macular thickness measured at 1 month (p = 0.71), 3 months (p = 0.93) and 6 months (p = 0.22) did not vary significantly between the two study groups. The decrease in macular thickness was significantly correlated with the increase in VA at 1 month (p = 0.003), 3 months (p = 0.05) and 6 months (p = 0.004). No systemic or intraocular side-effects were observed in either group. Mean IOP in the bevacizumab group was 15.0 ± 2.4 mmHg at baseline, 15.8 ± 2.0 mmHg at 1 month after injection (non-significant: p = 0.13), 15.3 ± 1.9 mmHg (p = 0.70) at 3 months and 14.8 ± 2.1 mmHg (p = 0.69) at 6 months. In the triamcinolone group, IOP increased slightly, but not statistically significantly, from 15.0 ± 2.2 mmHg at baseline to 17.1 ± 5.0 mmHg (p = 0.13) at 1 month, 15.7 ± 3.3 mmHg (p = 0.45) at 3 months and 15.7 ± 3.5 mmHg (p = 0.40) at 6 months. The results suggest that, in the patients with diffuse DMO included in the present study, both intravitreal bevacizumab and intravitreal triamcinolone significantly improved VA and reduced macular thickness. There were no major differences between the study groups. These findings agree with the results of a recent study by the Diabetic Retinopathy Clinical Research Network (2008) (DRCR.net) in which mean VA had significantly improved at 4 months after baseline. In the DRCR.net study, the visual improvement was significantly better in the study group that received 4 mg triamcinolone than in the study groups that received macular laser therapy (p < 0.001) or an intravitreal injection of 1 mg triamcinolone (p = 0.001) (Diabetic Retinopathy Clinical Research Network 2008). The results of the present study also agree with previous studies in terms of showing a significant improvement in Acta Ophthalmologica 2010