Introduction

Diabetic retinopathy (DR), branch retinal vein occlusion (BRVO) and central retinal vein occlusion (CRVO) are frequently complicated by macular oedema (MO), a condition that arises as a direct consequence of blood–retinal barrier (BRB) breakdown and the subsequent increase in vascular permeability. Accumulating evidence suggests that the upregulation of inflammatory factors or the downregulation of anti-inflammatory factors and a subsequent increase in leucocyte–endothelial interactions contribute to disruption of tight junctions and BRB breakdown.1 2

Recently, clinical treatment has become available to reduce the ocular expression of inflammatory cytokines. Intravitreal injection of triamcinolone acetonide (TA) is effective for reducing macular thickness in patients with diabetic macular oedema (DMO) and those with MO due to BRVO or CRVO.3 4 In addition, the intravitreal injection of antivascular endothelial growth factor (VEGF) antibody has been reported to be effective for reducing MO.5 6 At the usual concentration, intravitreal injection of TA is more effective for reducing DMO and improving the visual acuity than anti-VEGF antibody, suggesting that the pathogenesis of DMO is attributable not only to VEGF, but also to other mechanisms that are suppressed by the corticosteroid.7 Furthermore, the therapeutic effect of TA for MO due to BRVO and CRVO shows similarities.8 9 It has been unclear whether there is any difference in therapeutic effect and which inflammatory cytokines are increased or decreased in the clinical setting.

In this study, we measured the vitreous levels of VEGF and interleukin-6 (IL-6) in patients who had MO associated with DMO or MO due to BRVO and CRVO. The vitreous levels of VEGF and IL-6 were compared among patients with DMO, MO due to BRVO and MO due to CRVO in order to clarify the influence of these molecules on the response to treatment.