Background Intravitreal ranibizumab injection (IRI) is effective for patients with exudative age-related macular degeneration (AMD) and decreases intraocular levels of vascular endothelial growth factor (VEGF), but VEGF receptor intraocular dynamics after IRI are unclear. Therefore, we evaluated changes in the aqueous humor levels of soluble vascular endothelial growth factor receptor (sVEGFR)-1, sVEGFR-2, and their ligands for these receptors (VEGF) patients with AMD receiving IRI. Methods The subjects were 24 patients with AMD (24 eyes) who received 3 doses of IRI at monthly intervals. Aqueous humor samples were obtained when each IRI dose was given (visits 0, 1, and 2 at 4-week intervals). Then the suspension array method was employed to measure sVEGFR-1, sVEGFR-2, VEGF, and placental growth factor (PlGF) in aqueous humor samples from the 24 AMD patients and 13 cataract patients (as controls). Best corrected visual acuity (BCVA; logMAR) chart and central macular thickness (CMT; optical coherence tomography) were also assessed over time. Results At baseline, the aqueous humor levels of sVEGFR-1, sVEGFR-2, VEGF, and PlGF were significantly higher in the AMD group than in the control group. There was a significant correlation between VEGF and PlGF or between sVEGFR-1 and sVEGFR-2. BCVA and CMT both improved significantly after IRI, and the aqueous humor levels of VEGF, PlGF, and sVEGFR-1 also decreased significantly. Conclusions VEGFRs may be involved in the pathogenesis of AMD. IRI improves clinical parameters in AMD patients by suppressing intraocular levels of VEGF, PlGF, and sVEGFR-1.

中文翻译：

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雷珠单抗治疗年龄相关性黄斑变性期间房水中可溶性血管内皮生长因子受体及其配体的动力学。

背景玻璃体内雷珠单抗注射液 (IRI) 对渗出性年龄相关性黄斑变性 (AMD) 患者有效，可降低眼内血管内皮生长因子 (VEGF) 水平，但 IRI 后 VEGF 受体眼内动力学尚不清楚。因此，我们评估了接受 IRI 的 AMD 患者可溶性血管内皮生长因子受体 (sVEGFR)-1、sVEGFR-2 及其配体的房水水平变化。方法 受试者为 24 名 AMD 患者（24 只眼），每月接受 3 剂 IRI。在给予每个 IRI 剂量时获得房水样本（以 4 周的间隔访问 0、1 和 2 次）。然后采用悬浮阵列法测定sVEGFR-1、sVEGFR-2、VEGF、和来自 24 名 AMD 患者和 13 名白内障患者（作为对照）的房水样品中的胎盘生长因子 (PlGF)。随着时间的推移，还评估了最佳矫正视力（BCVA；logMAR）图表和中央黄斑厚度（CMT；光学相干断层扫描）。结果基线时，AMD组房水中sVEGFR-1、sVEGFR-2、VEGF和PlGF水平显着高于对照组。VEGF与PlGF之间或sVEGFR-1与sVEGFR-2之间存在显着相关性。IRI 后 BCVA 和 CMT 均显着改善，房水中 VEGF、PlGF 和 sVEGFR-1 水平也显着下降。结论 VEGFRs可能参与了AMD的发病机制。IRI 通过抑制 VEGF、PlGF 和 sVEGFR-1 的眼内水平来改善 AMD 患者的临床参数。