■息肉状脉络膜血管病变(PCV)是一种不可逆的视网膜脉络膜疾病。PCV个体表现出不同的基线特征,包括系统特征,眼部特征,代谢因子水平,以及对玻璃体内抗VEGF治疗的不同反应。本研究通过分析PCV的全身特点,探讨PCV的发病机制,眼部特征,以及一组对抗VEGF治疗表现出不同反应的患者中基线时的细胞因子水平。
■我们进行了一项包括80只诊断为PCV的眼睛的回顾性分析。基于对次优玻璃体内雷珠单抗注射治疗的反应,将患者分为两组:具有次优反应和最佳反应的那些。从实验眼睛收集房水样本,使用细胞计数珠阵列分析评估细胞因子表达水平。根据中位脉络膜厚度将所有受试者进一步分层为两组。随后,logistic回归分析和ROC曲线检测细胞因子表达水平之间的关系,脉络膜厚度,和抗VEGF反应。
■结果显示,与最佳抗VEGF反应组相比,次优反应组的脉络膜厚度明显更大。此外,与次优抗VEGF反应组相比,在最佳抗VEGF反应组中,VEGF和VCAM-1的表达水平明显降低,而TNF-α则表现出相反的趋势。Logistic回归分析显示VEGF、房水中的VCAM-1和TNF-α是次优抗VEGF反应的独立危险因素。调整其他风险因素后,次优抗VEGF反应的风险降低到0.998倍,0.997倍,和1.294倍。VEGF的AUC值,VCAM-1和TNF-α分别测定为0.805、0.846和0.897。此外,VEGF的风险,在厚脉络膜组校正危险因素后,VCAM-1和TNF-α与次优抗VEGF反应风险增加显著相关。
■我们的研究表明,基于不同的抗VEGF反应,PCV表现出全身和眼部特征变化。发现房水中细胞因子的水平与PCV中的抗VEGF反应具有显着相关性。VEGF,VCAM-1和TNF-α是评估厚脉络膜PCV治疗反应的潜在目标。
Polypoidal choroidal vasculopathy (PCV) is an irreversible retinal choroidal disease. Individuals with PCV exhibit diverse baseline characteristics, including systemic characteristics, ocular traits, metabolic factor levels, and different responses to intravitreal anti-VEGF therapy. This
study aims to investigate the pathogenesis of PCV by analyzing the systemic characteristics, ocular traits, and cytokine levels at baseline within a cohort of patients who exhibit different responses to anti-VEGF treatment.
We conducted a retrospective analysis involving 80 eyes diagnosed with PCV. Patients were categorized into two groups based on responses to suboptimal intravitreal ranibizumab injection therapy: those with suboptimal responses and optimal responses. Aqueous humor samples were collected from the experimental eyes, and cytokine expression levels were assessed using cytometric bead array analysis. All subjects were further stratified into two groups according to the median choroidal thickness. Subsequently, logistic regression analysis and the ROC curve were employed to examine the relationship between cytokine expression levels, choroidal thickness, and anti-VEGF response.
The results revealed that compared to the group of optimal anti-VEGF response, the choroid in the suboptimal response group exhibited a significantly greater thickness. Additionally, compared to the suboptimal anti-VEGF response group, the expression levels of VEGF and VCAM-1 were markedly lower observed in the optimal anti-VEGF response group, while TNF-α showed the opposite trend. Logistic regression analysis indicated that VEGF, VCAM-1, and TNF-α in the aqueous humor were independent risk factors for a suboptimal anti-VEGF response. After adjusting other risk factors, the risk of suboptimal anti-VEGF response decreased to 0.998-fold, 0.997-fold, and 1.294-fold. The AUC values for VEGF, VCAM-1, and TNF-α were determined to be 0.805, 0.846, and 0.897, respectively. Furthermore, the risk of VEGF, VCAM-1, and TNF-α were significantly associated with an increased risk of suboptimal anti-VEGF response after correction for risk factors in the thick choroid group.
Our
study demonstrated that PCV exhibits systemic and ocular characteristics variations based on different anti-VEGF responses. The levels of cytokines in aqueous humor were found to have a significant correlation with the anti-VEGF response in PCV. VEGF, VCAM-1, and TNF-α are potential targets for assessing treatment response in thick choroidal PCV.