Evaluation of the effect of vitreomacular interface disorders on anti-VEGF treatment in patients with diabetic macular edema in real life: MARMASIA study group report No. 10.

Purpose: The aim of this study is to investigate the effect of vitreomacular interface disorders (VMID) on treatment response in patients treated with anti-vascular endothelial growth factor (anti-VEGF) due to diabetic macular edema (DME).

Methods: Three hundred seventy-seven eyes of 239 patients in the MARMASIA Study Group who received intravitreal anti-VEGF treatment (IVT) due to DME were included in the study. The group 1 consisted of 44 eyes of the patients who had not received any treatment before, were followed up regularly for 24 months after at least a 3-month loading dose, and suffered from VMID such as epiretinal membrane, vitreomacular adhesion or traction, and lamellar hole. The group 2 consisted of 333 eyes of the patients without VMID. Best-corrected visual acuity (BCVA) and central macular thickness (CMT) of the patients at baseline, 3rd month, 6th month, 1st year and 2nd year follow-ups were measured.

Results: The mean age of the Groups 1 and 2 was 67.1 ± 11.3 and 61.9 ± 10.2 years, respectively. 61.3% of the group 1 and 58.8% of the group 2 were female (p > 0.05). The duration of diabetes was 19.2 ± 3.7 and 15.8 ± 3.2 years, respectively, and the number of follow-ups was 16.09 ± 4.68 and 12.06 ± 4.58, respectively in the groups (p < 0.001, 0.001, respectively). The number of IVT was 7.13 ± 2.71 and 7.20 ± 2.22, respectively in the groups 1 and 2 and no statistically significant difference was observed between them (p = 0.860). According to logMAR, BCVA values at baseline were 0.63 ± 0.24 and 0.59 ± 0.26 (p = 0.29), respectively, in the groups and the amount of change in BCVA at the end of the 2nd year was - 0.02 ± 0.48 in the group 1 and - 0.12 ± 0.48 in the group 2. It was observed as 0.48 (p = 0.13). Although the increase in BCVA was greater at all follow-ups in the group 2 compared to their initial examination, no significant difference was observed between the groups in terms of BCVA change. The CMT values of the groups at baseline were 442.5 ± 131.3 µm and 590.9 ± 170.6 µm, respectively (p = 0.03) The decrease in CMT after IVT was significantly greater in the group 2 at all follow-ups when compared to the first group (p < 0.05).

Conclusion: While the presence of VMID in DME patients receiving IVT did not affect visual results, it negatively affected the anatomical response and macular edema morphology. The presence of VMID at baseline affected the success of IVT. It should be taken into consideration that VMID may resolve spontaneously or with IVT, and new cases of VMID may occur in patients during the treatment process.