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Abstract
Diabetic macular edema (DME) is a common cause of visual impairment in patients with diabetes. Although intravitreal anti-vascular endothelial growth factor (VEGF) injections were efficacious in clinical trials, several patients exhibited a poor response. This study aimed to compare clinical features between patients who were susceptible to intravitreal anti-VEGF injections for DME and those who were not. A single-center, retrospective study of 102 such patients was conducted (123 eyes; mean ± standard deviation age, 63.4 ± 10.8 years; 57.8% males). Systemic and ocular data, assessed at baseline and after a month, were compared between good (>20% decrease in central macular thickness (CMT)) and poor (≤20% decrease in CMT) responders using the Mann–Whitney U test/Fisher’s exact test. Eighty-one eyes (65.9%) were good responders. The glycosylated hemoglobin level was higher (p = 0.011) in poor (7.5% ± 0.94%) than in good (7.04% ± 1.19%) responders. The foveal avascular zone was larger (p = 0.0003) in poor (0.67 ± 0.33 μm2) than in good (0.47 ± 0.23 μm2) responders. The number of microaneurysms in the pericapillary network was higher (p = 0.0007) in poor (2.7 ± 2.2) than in good (1.4 ± 2.0) responders. Baseline glycemic control and macular ischemia may be associated with the short-term response to intravitreal anti-VEGF injections.
Highlights
The purpose of this study was to elucidate which clinical features affect the anatomical response to intravitreal anti-vascular endothelial growth factor (VEGF) therapy in patients with Diabetic macular edema (DME); we discovered that fluorescein angiography (FA) findings were highly associated with that response
We investigated the factors affecting the anatomical outcome in patients with DME
We discovered that a high baseline HbA1c level, a large baseline foveal avascular zone (FAZ), and a high baseline number of MAs in the PCN were associated with a poor response to anti-VEGF injections
Summary
Intravitreal anti-VEGF injections are recognized to improve visual outcomes and decrease macular fluid in patients with DME [4,5]. The pathogenesis of DME is complex, with multiple factors contributing to its pathophysiology, including angiogenic, inflammatory, hypoxic, and hemodynamic processes that lead to the breakdown of the blood-retinal barrier and leakage of the intraretinal fluid [7]. This may be why certain patients respond moderately or even poorly to anti-VEGF therapy. In two landmark clinical trials, 14.4% (RIDE) and 15.2% (RISE) of patients experienced no improvement or decreased visual acuity at the primary endpoint, even though patients with DME in clinical trials receive far more injections than patients in clinical practice [5,8]
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