Abstract
To investigate the influence of the epiretinal membrane (ERM) on intravitreal ranibizumab (IVR) therapy for diabetic macular edema (DME). This retrospective study included 56 eyes of 48 patients with DME divided into two groups: the DME with ERM (study) and only DME (control) groups. Changes in the central macular thickness (CMT) and best-corrected visual acuity (BCVA) were evaluated. In the study group, although the CMT was significantly reduced following the first injection (p<0.001), BCVA did not improve significantly (p=0.296). However, after the first injection, the control group exhibited both a significant decrease in CMT (p<0.001) and improvement in BCVA (p<0.001). However, the improvement in BCVA in the control group was not significantly different from the outcome of the study group. We observed a negative short-term influence of the ERM on IVR treatment for DME.
Highlights
Diabetic macular edema (DME) is the most common cause of decreased visual acuity (VA) in patients with diabetes mellitus[1], and has been associated with vitreomacular interface abnormality (VMIA) incidence rates of 7%-16%(2,3)
The present study investigated the effects of epiretinal membrane (ERM) on visual acuity and morphological changes in patients with DME who are receiving intravitreal ranibizumab (IVR) therapy
Changes in the logMar best-corrected visual acuity (BCVA) and central macular thickness (CMT) from baseline after the first injection are shown in table 2
Summary
Diabetic macular edema (DME) is the most common cause of decreased visual acuity (VA) in patients with diabetes mellitus[1], and has been associated with vitreomacular interface abnormality (VMIA) incidence rates of 7%-16%(2,3). Anti-vascular endothelial growth factor (VEGF) agents are considered gold-standard agents in the management of DME and have been shown to improve clini cal outcomes[4]. Vitreomacular traction (VMT) may cause low-grade inflammation and stimulate the induction or progression of DME by inducing the continued release of VEGF, a powerful angiogenic and vascular permeability factor[7,8]. VEGF and its receptors, as well as IL-6, localize to cells in the vascular and avascular epiretinal membranes (ERMs) of patients with diabetic retinopathy, further increasing inflammation[12,13] and possibly promoting persistent DME. Patients with ERM likely require more frequent injections for inflammation, ERMs may act as a physical barrier and decrease drug penetration
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