Department of Ophthalmology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Front Endocrinol (Lausanne). 2024 Jan 3;14:1307337. doi: 10.3389/fendo.2023.1307337. eCollection 2023.
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.
息肉样脉络膜血管病变（PCV）是一种不可逆转的视网膜脉络膜疾病。PCV 患者表现出不同的基线特征，包括全身特征、眼部特征、代谢因子水平以及对玻璃体内抗血管内皮生长因子（VEGF）治疗的不同反应。本研究旨在通过分析不同抗 VEGF 治疗反应患者队列中的基线全身特征、眼部特征和细胞因子水平，探讨 PCV 的发病机制。
我们进行了一项回顾性分析，纳入了 80 只诊断为 PCV 的眼。根据玻璃体内雷珠单抗注射治疗效果不佳的情况，将患者分为两组：治疗反应不佳组和治疗反应良好组。从实验组眼采集房水样本，并采用流式细胞术微珠阵列分析评估细胞因子表达水平。所有患者均根据脉络膜厚度中位数进一步分为两组。随后，采用逻辑回归分析和 ROC 曲线分析，研究细胞因子表达水平、脉络膜厚度与抗 VEGF 反应之间的关系。
结果显示，与抗 VEGF 治疗反应良好组相比，治疗反应不佳组的脉络膜厚度显著增加。此外，与治疗反应不佳组相比，治疗反应良好组房水中 VEGF 和 VCAM-1 的表达水平明显降低，而 TNF-α 的表达水平则相反。逻辑回归分析表明，房水中的 VEGF、VCAM-1 和 TNF-α 是抗 VEGF 治疗反应不佳的独立危险因素。调整其他危险因素后，抗 VEGF 治疗反应不佳的风险降低至 0.998 倍、0.997 倍和 1.294 倍。VEGF、VCAM-1 和 TNF-α 的 AUC 值分别为 0.805、0.846 和 0.897。此外，在对厚脉络膜组中校正危险因素后，VEGF、VCAM-1 和 TNF-α 的风险与抗 VEGF 治疗反应不佳的风险显著相关。
本研究表明，PCV 表现出基于不同抗 VEGF 反应的全身和眼部特征变化。房水中细胞因子的水平与 PCV 中的抗 VEGF 反应具有显著相关性。VEGF、VCAM-1 和 TNF-α 可能是评估厚脉络膜 PCV 治疗反应的潜在靶点。
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