ROP: Consensus of Pediatric Retina Group

賴佐庭 Tso-Ting LaiTaiwan Speaker ROP: Consensus of Pediatric Retina GroupOBJECTIVE: Retinopathy of prematurity (ROP) is the leading cause of childhood blindness, particularly in preterm infants. In Taiwan, the absence of national guidelines and the variability in clinical practice have highlighted the need for locally adapted consensus recommendations. METHODS: An expert panel of eleven ophthalmologists from eight tertiary centers in Taiwan convened to develop a consensus on ROP management. Through a structured process that included key question formulation, systematic literature review, iterative discussion, and voting, the panel established consensus statements. Agreement was defined as >/=75% of panelists voting "agree" or "strongly agree" using a five-point Likert scale. RESULTS: Consensus recommendations were developed across three major domains: screening, treatment, and follow-up. For screening, the panel endorsed criteria commonly used in Taiwan-gestational age <32 weeks or birth weight <1500 g-but emphasized the need for population-based validation. Both anti-vascular endothelial growth factor (VEGF) agents and laser photocoagulation were recognized as acceptable first-line treatments for type 1 ROP, with individualized treatment decisions based on disease characteristics, anesthesia risk, and follow-up capacity. Guidelines were also established for the management of ROP reactivation, procedural protocols, and agent selection. For follow-up, the panel recommended extended surveillance after anti-VEGF therapy and outlined the criteria for identifying and monitoring persistent avascular retina. Follow-up schedules were proposed to detect long-term ocular and neurodevelopmental complications. CONCLUSIONS: This consensus provides updated evidence-based guidance for ROP care in Taiwan, addressing both traditional and emerging clinical challenges. These recommendations aim to standardize care practices while remaining adaptable to future research and evolving clinical needs.What Else Behind Diabetic Retinopathy Beside Anti-VEGF?Diabetic retinopathy (DR) has long been characterized as a microvascular disease, and anti-VEGF therapy remains one of the standard treatments for its sight-threatening complications. However, accumulating evidence demonstrates that DR is a complex neurovascular disorder in which neurodegeneration, oxidative stress, chronic inflammation, dysregulated cell death pathways, and impaired autophagy play central roles. Preclinical studies highlight early retinal neurodegeneration, glial dysfunction, and microglia-mediated inflammation as substantial contributors to DR development and progression, which might precede clinically visible vascular changes. Oxidative stress is another major driver, triggering mitochondrial injury, endothelial dysfunction, and aberrant programmed cell death—including apoptosis, pyroptosis, and necroptosis—which further accelerates neurovascular impairment. A growing body of experimental work has explored therapeutic strategies beyond VEGF suppression. Antioxidants such as astaxanthin have been shown to restore autophagy and enhance Nrf2-mediated defense mechanisms in photoreceptors under high-glucose stress—findings demonstrated in our own studies. Similarly, targeting inflammatory pathways with agents such as fenofibrate or cilostazol has been shown to reduce inflammatory mediators, oxidative damage, and retinal apoptosis in diabetic models. Additional approaches, including fibroblast growth factor 1 treatment and interventions aimed at preventing high-glucose-induced cellular senescence, further underscore the multifaceted nature of DR pathophysiology. Together, these insights suggest that DR extends far beyond vascular endothelial dysfunction, and effective long-term management may require therapies targeting oxidative stress, inflammation, neuroprotection, autophagy regulation, and metabolic resilience. This talk will review these emerging mechanisms and discuss future therapeutic perspectives that complement, rather than replace, anti-VEGF therapy.