International Journal of Retina and Vitreous最新文献

Purpose: To evaluate the clinical outcomes of the switch to faricimab in a treat-and-extend (T&E) regimen patients with neovascular age-related macular degeneration (nAMD).

Methods: This prospective cohort study included consecutive patients with nAMD who had previously been treated with anti-VEGF agents in a T&E regimen, with treatment intervals (TI) that could not be extended beyond 12 weeks, and a minimum follow-up of 24 weeks. These patients were switched to faricimab therapy in a T&E regimen for at least 6 months. The primary endpoint was the TI between intravitreal injections (IVIs), and the secondary endpoint was the mean change in best-corrected visual acuity (BCVA) from baseline to the last follow-up visit (LFUV).

Results: A total of 225 eyes from 188 patients were included, with a mean age of 79.6 ± 7.4 years. Previous anti-VEGF treatments included ranibizumab (n = 34), aflibercept (n = 144), brolucizumab (n = 6), and bevacizumab (n = 41). TI1 (5.9 ± 2.0 weeks) matched the prior treatment interval. Significant increases in treatment intervals were observed at subsequent time points (TI2: 8.2 ± 3.2 weeks, TI3: 10.1 ± 3.9 weeks, TI4: 10.7 ± 4.3 weeks, TI5: 9.9 ± 4.0 weeks, and TI6: 8.5 ± 4.4 weeks; p < 0.001). BCVA remained stable, going from 0.41 ± 0.23 to 0.43 ± 0.24 (p = 0.0112). The mean number of injections was 5.9 ± 1.9, with a mean follow-up duration of 51.4 ± 11.8 weeks.

Conclusions: The switch to faricimab in a T&E regimen significantly increased treatment intervals maintaining BCVA in patients with nAMD under other anti-VEGF treatments. No serious adverse events were reported. Longer follow-up is needed to confirm these results.

Background: To describe a case of inadvertent methylene blue use during pars plana vitrectomy (PPV) for an epiretinal membrane (ERM).

Case: A 69-year-old man presented with 1 day of severe vision loss in his left eye. Two days prior to presentation, he had undergone PPV that was complicated by accidental methylene blue use. Visual acuity (VA) at presentation to our institution was CF from his baseline VA of 20/60. Optical coherence tomography (OCT) demonstrated diffuse hyperreflectivity and thickening of the inner retinal layers. The patient was started on oral prednisone with no improvement. On postoperative month 1, VA was HM. OCT showed disruption of the inner retinal architecture, inner retinal layer thinning and focal disruption of the outer retina layers superiorly.

Conclusion: Methylene blue may be associated with severe retinal toxicity. Given its similarity to other vital dyes in ophthalmology, care must be taken to avoid its inadvertent administration.

Background: Retinal vein occlusion (RVO) is a leading cause of vision loss, yet there are inconsistent risk estimates related to risk factors. Mendelian randomization (MR) uses genetic variants as proxies for lifelong exposure and can clarify causal pathways for RVO. We aimed to systematically review MR studies to identify causally supported systemic and ocular risk factors for RVO.

Methods: Four databases (PubMed, Embase, Scopus, and Web of Science) were searched from inception to June 2025 for peer-reviewed MR studies evaluating modifiable systemic or ocular risk factors in relation to any form of RVO utilizing GWAS data. Narrative synthesis was undertaken as methodological heterogeneity precluded meta-analysis. All effect estimates (ORs) were extracted directly from individual studies and robustness of evidence for each exposure across studies was assessed as robust, probable, suggestive, insufficient, and non-evaluable based on significance and direction of evidence.

Results: Twelve two-sample MR studies, all conducted in European cohorts, met inclusion criteria. Ocular traits showed the most consistent signals: higher intraocular pressure (RVO (OR = 1.53, 95% CI: 1.0402.26) and glaucoma liability (OR = 1.31, 95% CI: 1.18-1.45) were robustly associated with greater risk of RVO. Among cardiovascular factors, elevated blood pressure/hypertension liability demonstrated probable evidence of increased RVO risk (OR = 1.58, 95% CI: 1.34-1.85), whereas lipid profiles yielded mixed signals, with some support for higher LDL (OR = 1.23, 95% CI: 1.05-1.44) and total cholesterol (OR = 1.44, 95% CI: 1.08-1.92) effects. For metabolic factors, glycemic traits showed probable to robust evidence with fasting glucose (OR = 5.01, 95% CI: 2.00-12.55) and two-hour glucose (OR = 3.17, 95% CI: 1.63-6.18) associated with higher RVO risk. Similarly, type 2 diabetes liability showed probable evidence (OR = 2.82, 95% CI: 2.07-3.85); anthropometric measures offered probable to robust support with body mass index (OR = 1.94, 95% CI: 1.23-3.08) and waist circumference (OR = 2.40, 95% CI: 1.36-4.24) associated with RVO. In other domains, selected coagulation and platelet traits showed probable-robust signals, vitamin D evidence was insufficient, and gut microbiota instruments provided preliminary robust evidence for Bacilli and Family XIII AD3011 association with RVO.

Conclusion: Genetic evidence supports a multifactorial vascular-metabolic model for RVO in which elevated IOP, glaucoma, hypertension, adiposity, and acute hyperglycemia are genetically supported risk factors. These findings highlight blood-pressure control, weight management, and glycemic regulation as important prevention targets and underscore the need for ancestry-diverse MR studies with refined phenotyping.

Objectives: Age-related macular degeneration (AMD), in which oxidative stress, inflammation and metabolic imbalances play a role in its pathogenesis, is one of the leading causes of irreversible vision loss. The kynurenine (KYN) pathway, one of the principal routes of tryptophan (TRP) metabolism, constitutes an important mechanism in retinal neurodegeneration. Based on this information, our study aimed to compare the serum TRP, KYN, kynurenic acid (KYNA), 3-hydroxykynurenine (3HK), 3-hydroxyanthranilic acid (3HAA) and, quinolinic acid (QA) levels of AMD patients and to investigate the diagnostic values ​​of these biomarkers.

Methods: Serum samples were collected from AMD patients and control groups. TRP, KYN, KYNA, 3HK, 3HAA, and QA levels were measured using a commercial ELISA method. KYN pathway activity, KYN/TRP and, KYNA/3HK ratios were also assessed. Mann-Whitney U test, ROC analysis, Spearman correlation were applied for statistical comparisons.

Results: According to our results, 3HK was significantly higher in the AMD group, while TRP, KYN, QA, and KYNA/3HK ratio were higher in the control. ROC analysis revealed 3HK to be the strongest discriminatory marker. The KYNA/3HK ratio also provided significant diagnostic value. Correlation analysis revealed strong negative correlations between 3HK and KYN, QA, and especially KYNA/3HK. Conversely, strong positive correlations were found between KYN and KYNA/3HK, and between TRP, KYN, QA, and KYNA.

Conclusion: KYN pathway metabolites exhibit significant alterations in patients with AMD. 3HK levels and the reduction of the KYNA/3HK ratio suggest a disruption of the neurotoxic-neuroprotective balance and imply that KYN pathway dysfunction may play a role in the pathogenesis of AMD. Among the biomarkers examined, 3HK displayed the highest diagnostic performance, while the KYNA/3HK ratio emerged as an additional biological indicator. These findings indicate that 3HK and the KYNA/3HK ratio may serve as potential biomarker candidates for the early diagnosis and monitoring of AMD.