Objective To compare the thickness of the macular ganglion cell inner plexiform layer (mGCIPL) in patients with a history of laser photocoagulation (LP) versus intravitreal injection of ranibizumab (IVR) for retinopathy of prematurity (ROP). MethodsA retrospective clinical study. From June 2020 to January 2021, 70 eyes of 35 children with a history of surgery for ROP in Shenzhen Eye Hospital were included in the study. Among them, 18 males had 36 eyes, and 17 females had 34 eyes. The average age was 5.54±1.04 years. There were 18 patients (36 eyes) in LP group and 17 patients (34 eyes) in IVR group. There was no significant difference in age (t=－1.956), sexual composition ratio (χ2=0.030), birth gestational age (t=－1.316) and birth weight (t=－1.060) between the two groups (P=0.059, 0.862, 0.197, 0.297). All the eyes underwent the examination of optical coherence tomography (OCT). An elliptical region of 14.13 mm2 centered on macular fovea was scanned according to the macular cube 512×128 model of the Cirrus HD-OCT 5000. The software was used to automatically divide macular fovea into six sectors (superior, inferior, temporal-superior, temporal-inferior, nasal-superior and nasal-inferior) and the average and minimum thickness of mGCIPL. t test was used to compared mGCIPL thickness between two groups using independent samples. Pearson correlation analysis was used to evaluate the correlation between mGCIPL thickness and age, birth gestational age, birth weight. ResultsPatients in IVR group had significantly decreased mGCIPL thickness than that in LP group in the six sectors (superior, inferior, temporal-superior, temporal-inferior, nasal-superior and nasal-inferior) and the average and minimum (t=6.484, 6.719, 7.682, 7.697, 5.151, 5.008, 7.148, 6.581; P＜0.05). The thickness of mGCIPL was not significantly correlated with age, birth gestational age, birth weight (P＞0.05). ConclusionThe thickness of mGCIPL in patients with IVR treatment history is thinner than that in LP treatment.
Fundus neovascularization is a significant cause of ocular diseases, mainly including retinal neovascularization and choroidal neovascularization. Anti-vascular endothelial growth factor therapy, though effective, has limitations such as a short half-life, non-responsiveness, and drug resistance. 6-Phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (PFKFB3), a key regulator of glycolysis, affects the generation of pathological blood vessels by modulating the metabolism of vascular endothelial cells. Small molecule inhibitors targeting PFKFB3 protein have been confirmed in animal and cell models to significantly inhibit pathological angiogenesis, showing good therapeutic potential. However, most of them are still in the preclinical research stage. In the future, it is necessary to further investigate the mechanism of PFKFB3, optimize the specificity and safety of the inhibitors, and explore the effects of combining them with existing therapies, so as to provide new strategies for the treatment of fundus neovascular diseases.