第一部分  SS-OCT观察息肉状脉络膜血管病变及湿性老年性黄斑变性抗血管内皮生长因子治疗前后的脉络膜形态学改变的研究

    第一节  SS-OCT观察息肉状脉络膜血管病变及湿性老年性黄斑变性抗血管内皮生长因子治疗前后脉络膜形态学改变

 目的：用SS-OCT观察PCV和wAMD的脉络膜形态学特征以及抗血管内皮生长因子治疗前后的变化。

方法：前瞻性病例对照试验。本研究实验组纳入从2016年8月至2017年4月，未经过治疗的wAMD 11例11只眼和PCV 24例24只眼，对照组纳入50岁以上健康人11例22只眼。实验组经FFA和ICGA确诊后，每4~6周行玻璃体腔注射雷珠单抗1次，连续3次。实验组及对照组治疗前及随访时均行SS-OCT横断面影像扫描，用SS-OCT电子卡尺测量黄斑中心凹下视网膜厚度（central retina thickness，CRT）、SFCT和脉络膜最大血管直径（choroidal maximal vessel diameter，MVD）。分析各组患者治疗前后对数最小分辨角（logarithm of the minimum angle of resolution，logMAR）视力（visual acuity，VA）、CRT、SFCT、MVD的异同和变化趋势。

结果：治疗前wAMD患者logMAR VA为0.94±0.59，PCV患者为0.73±0.40，对照组为0.06±0.10，PCV组的logMAR视力与wAMD组无明显差异；wAMD组的CRT为318.73±101.83μm，PCV组为421.38±164.19μm，对照组为185.48±20.30μm，PCV组的CRT明显大于 wAMD组； wAMD组的SFCT为155.45±62.22μm，PCV为305.23±98.51μm，对照组为246.27±62.78μm，PCV组的SFCT明显大于对照组和wAMD组，wAMD组的SFCT明显小于对照组；wAMD组的MVD为139.55±48.96μm，PCV组为209.09±68.91μm，对照组为180.82±47.16μm，PCV组的MVD明显大于wAMD组；三组中，SFCT与MVD均呈明显正相关。

治疗后，PCV组的logMAR视力为0.47±0.28，较前明显改善，wAMD组的logMAR视力为0.75±0.42，较前无明显改善；PCV组的CRT为268.06±129.31μm，wAMD组为169.05±90.36μm，均较前明显降低；PCV组的SFCT 为269.77±93.38μm，wAMD组为120.36±63.33μm，均较前明显降低；PCV组的MVD 为184.68±63.95μm，wAMD组为120.91±53.50μm，均较前明显降低。

结论：PCV患眼的SFCT较健康人眼和wAMD患眼厚，而wAMD患眼SFCT较健康人眼薄。PCV患眼的MVD明显大于wAMD患眼。可见，PCV和wAMD的视网膜脉络膜形态学有明显差异，SFCT、MVD可以用于两种疾病的鉴别。wAMD、PCV及健康人的SFCT与MVD呈明显正相关。治疗后，wAMD和PCV的SFCT、MVD均明显下降，SFCT、MVD可作为评估疗效的指标。

   第二节 息肉状脉络膜血管病变及湿性老年性黄斑变性抗血管内皮生长因子治疗前后脉络膜形态学变化的亚组分析

 目的：探究脉络膜增厚型息肉状脉络膜血管病变（thick type of polypoidal choroidal vasculopathy，Thick-PCV）、脉络膜变薄型息肉状脉络膜血管病变（thin type of polypoidal choroidal vasculopathy，Thin-PCV）与wAMD脉络膜形态学和对抗血管内皮生长因子治疗反应的异同，以进一步揭示PCV是一种独立的疾病还是PCV的亚型属于wAMD的一种表现。

方法：将第一节的PCV患者按SFCT大于等于或小于300μm，分为Thick-PCV组和Thin-PCV组，各12例12只眼，比较两亚组与wAMD组患者治疗前后logMAR VA、CRT、SFCT、MVD的异同和变化趋势。

结果：治疗前，wAMD组的logMAR VA为0.94±0.59，Thick-PCV组为0.73±0.41，Thin-PCV组为0.73±0.41，三组间视力无明显统计学差异；wAMD组的CRT为318.73±101.83μm，Thick-PCV组为338.96±105.81μm，Thin-PCV组为503.79±174.21μm，Thin-PCV组的CRT明显大于wAMD组和Thick-PCV组，而wAMD组和Thick-PCV组无明显差异；wAMD组的SFCT为155.45±62.22μm，Thick-PCV组为369.00±87.73μm，Thin-PCV组为212.50±50.25μm，Thick-PCV组的SFCT明显大于wAMD组和Thin-PCV组，而wAMD组和Thin-PCV组无明显差异；wAMD组的MVD为139.55±48.96μm，Thick-PCV组为247.42±62.61μm，Thin-PCV组为153.00±47.32μm，Thick-PCV组的MVD明显大于wAMD组和Thin-PCV组，而wAMD组和Thin-PCV组间无明显差异。

治疗后，wAMD组的logMAR VA为0.75±0.42，较前无明显改善，Thick-PCV组为0.43±0.31，较前明显改善，Thin-PCV组为0.50±0.26，较前明显改善；wAMD组的CRT为169.05±90.36μm，Thick-PCV组为203.12±69.73μm，Thin-PCV组为333.00±144.57μm，均较前明显降低；wAMD组的SFCT 为120.36±63.33μm，Thick-PCV组为337.17±67.61μm，Thin-PCV组为176.00±45.81μm，均较前明显降低；wAMD组的MVD 为120.91±53.50μm，Thick-PCV组为222.33±58.57μm，Thin-PCV组为129.25±39.35μm。wAMD组和Thin-PCV组均较前明显降低，而Thick-PCV组无明显下降。

结论：Thick-PCV患眼的SFCT、MVD较Thin-PCV和wAMD厚，而Thin-PCV和wAMD间脉络膜形态学特征无明显差异。抗VEGF治疗后wAMD组和Thin-PCV组CRT、SFCT、MVD均明显下降，而Thick-PCV治疗后MVD无明显变化，推测Thick-PCV可能是一种独立的疾病，Thin-PCV可能是AMD的一种亚型。

第二部分  息肉状脉络膜血管病变及湿性老年性黄斑变性抗血管内皮生长因子治疗前后房水和血液中细胞因子的测定

目的： 通过测定PCV及wAMD患者抗VEGF治疗前后血液及房水中45种细胞因子浓度的变化，比较PCV和wAMD细胞因子水平的异同，并进一步分析与疗效之间的关系。

方法：前瞻性病例对照研究。本研究纳入从2016年8月至2017年4月在北京协和医院门诊就诊的未经过治疗的患者49例49只眼，其中实验组wAMD患者11只眼，PCV患者24只眼，对照组即欲行白内障手术的老年性白内障患者14只眼。PCV患者和wAMD患者经FFA和ICGA确诊后，每4~6周玻璃体腔注射抗VEGF药物（雷珠单抗）1次，连续3次。实验组每次玻璃体腔注药前和对照组白内障术前，均抽取房水样本100ul及血液2ml。用luminex方法检测45种细胞因子浓度：白细胞介素-1α（interleukin-1α，IL-1α）、白细胞介素-1β（interleukin-1β，IL-1β）、白细胞介素-1RA（interleukin-1RA，IL-1RA）、白细胞介素-2（interleukin-2，IL-2）、白细胞介素-4（interleukin-4，IL-4）、白细胞介素-5（interleukin-5，IL-5）、白细胞介素-6（interleukin-6，IL-6）、白细胞介素-7（interleukin-7，IL-7）、IL-8、白细胞介素-9（interleukin-9，IL-9）、白细胞介素-10（interleukin-10，IL-10）、白细胞介素-13（interleukin-13，IL-13）、白细胞介素-15（interleukin-15，IL-15）、白细胞介素-17A（interleukin-17A，IL-17A）、白细胞介素-18（interleukin-18，IL-18）、白细胞介素-21（interleukin-21，IL-21）、白细胞介素-22（interleukin-22，IL-22）、白细胞介素-23（interleukin-23，IL-23）、白细胞介素-27（interleukin-27，IL-27）、白细胞介素-31（interleukin-31，IL-31）、VEGF-A、VEGF-D、人白血病抑制因子（leukemia inhibitory factor，LIF）、基质细胞衍生因子1-α（stromal-derived factor 1-α，SDF1-α）、脑源性神经营养因子（brain-derived neurotrophic factor，BDNF）、干扰素诱导蛋白10（interferon inducible protein 10，IP-10）、肝细胞生长因子（hepatocyte Growth Factor，HGF）、白细胞介素-12p70（interleukin-12p70，IL-12p70）、PIGF、碱性成纤维细胞生长因子（basic fibroblast growth factor，FGF-basic）、粒细胞-巨噬细胞集落刺激因子（granulocyte macrophage colony stimulating Factor，GMCSF）、表皮生长因子（epidermal growth factor，EGF）、巨噬细胞炎性蛋白1β（macrophage inflammatory protein 1β，MIP-1β）、Eotaxin、正常T细胞表达和分泌的激活调节细胞因子（regulated upon activation normal T cell expressed and secreted，RANTES）、血小板源性生长因子-BB （platelet-derived growth factor-BB，PDGF-BB）、MCP-1、神经生长因子b （nerve growth factor b ，NGFb）、干细胞因子（stem cell factor，SCF）、巨噬细胞炎性蛋白-1α（macrophage inflammatory protein-1α，MIP-1α）、生长相关癌基因产物α（growth-related gene product α，GROα）、干扰素-γ（interferon-γ，IFNγ）、干扰素-α（interferon-α，IFNα）、TNFα和肿瘤坏死因子β（tumor necrosis factor β，TNFβ）。分别比较房水和血清中治疗前wAMD、PCV及正常人之间45种因子浓度的差异，以及wAMD和PCV在抗VEGF治疗前后浓度的变化。

结果：治疗前，房水中，wAMD组和PCV组中IL-8、IL-18、IL-21、IL-31、LIF、SDF1-α、FGF-basic、VEGF-A、VEGF-D浓度均明显升高；BDNF、HGF、IP-10、MCP-1、IL-13均明显降低；IL-17A浓度在wAMD中下降明显，而在PCV组中无明显改变；GMCSF、IL-12p70在PCV中明显下降，而在wAMD中无改变；wAMD组中IL-8和IL-12p70浓度明显高于PCV组。

治疗前，血清中，wAMD组和PCV组中EGF、Eotaxin、GMCSF、MCP-1、MIP-1β、IL-8、IL-21、IL-31、LIF、SDF1-α、VEGF-A、VEGF-D浓度明显升高；PDGF-BB明显降低；FGF-basic在wAMD 中明显升高，但PCV组中无差别；HGF、IL-5在wAMD组中明显降低，而在PCV组中无明显变化；IL-18在PCV组中降低，而在wAMD组中无明显变化； wAMD组中LIF浓度明显高于PCV组。

治疗后，房水中，wAMD组和PCV组中HGF、IL-12p70浓度明显升高；IL-18、IL-21、LIF、SDF1-α、VEGF-A、VEGF-D均明显降低；IL-8、IL-23、PDGF-BB只在wAMD组下降，在PCV组中无明显改变；MCP-1、IL-13只在wAMD组升高，在PCV组无明显改变；GMCSF、IP-10只在PCV组升高，在wAMD组无明显改变。

治疗后，血清中，wAMD组和PCV组HGF浓度均明显升高；IL-21、LIF、SCF、SDF1-α、VEGF-A、VEGF-D均明显降低；IL-8只在wAMD组降低，PCV中无改变；IL-2、IL-6、NGFβ只在PCV组降低，在wAMD组无明显改变。

与对照组相比，wAMD和PCV两种疾病明显相关的细胞因子分别是HGF、IP-10、MCP-1、IL-13、IL-31、LIF、SDF1-α、VEGF-A、VEGF-D。

GROα、IL-1β、IL-1α、IFNγ、IFNα、IL-7、IL-9、IL-10、IL-22、TNFα和TNFβ低于检测下限。

结论：wAMD组的房水IL-8和IL-12p70浓度和血清LIF浓度均明显高于PCV组，提示IL-8、IL-12p70和LIF能用于鉴别wAMD和PCV。房水中VEGF-A、VEGF-D、IL-13、IL-31、LIF、SDF1-α、HGF、IP-10、MCP-1的浓度改变，血清中MCP-1、PDGF-BB、VEGF-A、VEGF-D浓度改变可将wAMD和PCV明显区别于对照组。wAMD和PCV患者房水、血清中VEGF-A、VEGF-D浓度较对照组高，在两种疾病中无明显区别，抗VEGF治疗后浓度的改变可以用于评估疗效。促血管生成因子、抑血管生成因子、促炎因子和抗炎因子共同参与wAMD和PCV的致病过程，应重视免疫失调和慢性炎症在wAMD和PCV发生发展中的重要作用。有些细胞因子的眼部作用不明，变化趋势和既往研究及全身作用机理不相符，仍需进一步研究。

Part One  Research on Choroidal Morphological Changes before and after anti-vascular endothelial growth factor therapy in Patients with Age-Related Macular Degeneration and Polypoidal Choroidal Vasculopathy

 Section I  Choroidal Morphological Changes before and after anti-vascular endothelial growth factor therapy in Patients with Age-Related Macular Degeneration and Polypoidal Choroidal Vasculopathy by Swept-source Optical Coherence Tomography

 Purpose: To investigate the choroidal morphological characteristics and the changes after anti-vascular endothelial growth factor therapy in patients with polypoidal choroidal vasculopathy (PCV) and wet age-related macular degeneration (wAMD) by swept-source optical coherence tomography (SS-OCT).

Design: A prospective, consecutive, case control study

Method: 35 eyes from 35 treatment-naive patients consisting of 11 eyes with wAMD and 24 eyes with PCV were studied from Aug., 2016 to Apr., 2017. 22 eyes from 11 more than 50 years old healthy people were selected as control group. Experimental group was given Ranibizumab (Lucentis) via intraocular vitreous injecton every 4 to 6 weeks and last for 3 mouths after be diagnosed as FFA and ICGA. Experimental and controlled groups were both carried in SS-OCT before treatment and follow-up. We use the calipers in SS-OCT to measure central retina thickness (CRT), subfoveal choroidal thickness(SFCT) and choroidal maximal vessel diameter(MVD), and then analyze the difference and changes of all groups before and after therapy by logMAR VA, CRT, SFCT and MVD.

Results: Before treatment, average logMAR VA in wAMD group and PCV group is 0.94±0.59 and 0.73±0.40 separately. In addition, the range in control group is 0.06±0.10. There is no difference between PCV and wAMD group. The average CRT in wAMD group is 318.73±101.83μm，in PCV group is 421.38±164.19μm and in control group is 185.48±20.30μm. The CRT in PCV group is significantly larger than that in wAMD group. The average SFCT in wAMD group is 155.45±62.22μm, in PCV group is 305.23±98.51μm and in control group is 246.27±62.78μm. The SFCT of PCV group is significantly larger than that of controlled group. The SFCT in wAMD group is thinner than control group. The average MVD in wAMD group is 139.55±48.96μm, in PCV group is 209.09±68.91μm and in control group is 180.82±47.16μm. The MVD in PCV group is significantly larger than that in wAMD group. SFCT and MVD showed a positive correlation in all groups.

After treatment, logMAR VA in PCV group is 0.47±0.28, which is improved significantly compared with before. LogMAR VA in wAMD group is 0.75±0.42, while there is no obvious improvement than that before treatment. CRT in PCV group is 268.06±129.31μm, and in wAMD group is 169.05±90.36μm, both declined significantly than before treatment. SFCT in PCV group is 269.77±93.38μm, while in wAMD group is 120.36±63.33μm, both of them deceased significantly than before treatment. MVD in PCV group is 184.68±63.95μm, while in wAMD group is 120.91±53.50μm, both of them declined significantly than before treatment.

Conclusion: SFCT in PCV group is thicker than control group and wAMD group. SFCT in wAMD group is thinner than control group, and MVD in PCV group are thicker than wAMD gourp, so we can conclude that PCV and wAMD groups show significant differences in retina and choroidal topographic, and SFCT and MVD could be applied to distinguish PCV and wAMD, indicating they are capable to evaluate effection of therapy.

Section II  Choroidal Thickness Changes in Patients with Age-Related Macular Degeneration and Subtype of Polypoidal Choroidal Vasculopathy by Swept-source Optical Coherence Tomography

 Purpose: To investigate the response of choroidal morphological characteristics and the changes of anti-vascular endothelial growth factor treatment in patients with thick type of polypoidal choroidal vasculopathy (Thick-PCV), thin type of polypoidal choroidal vasculopathy (Thin-PCV) and wet age-related macular degeneration (wAMD), in order to futher reveal the PCV is an independent disease or the subtype of PCV belongs to a form of wAMD.

Method: Classify the PCV patients of section 1 into 2 subgroups according to the thickness of choroid, 12 eyes with Thick-PCV (SFCT>=300μm) and 12 eyes with Thin-PCV (SFCT<300μm) were compared with wAMD of section 1 by analyzing the difference and changes logMAR VA, CRT, SFCT and MVD.

Results: Before treatment, average logMAR VA in wAMD group is 0.94±0.59, in Thick-PCV group is 0.73±0.41 and in Thin-PCV group is 0.73±0.41. There is no significant difference among these three groups. The average CRT in wAMD group is 318.73±101.83μm, in Thick-PCV group is 338.96±105.81μm and in Thin-PCV group is 503.79±174.21μm. CRT in Thick-PCV group is significantly larger than that in wAMD and Thin-PCV group. There is no significant difference between Thin-PCV and wAMD. The average SFCT in wAMD group is 155.45±62.22μm, in Thick-PCV group is 369.00±87.73μm and in Thin-PCV group is 212.50±50.25μm. SFCT in Thick-PCV group is significantly larger than that in wAWD and Thin-PCV group. There is no significant difference between Thin-PCV and wAMD group. The average MVD in wAMD group is 139.55±48.96μm, in Thick-PCV group is 247.42±62.61μm and in Thin-PCV group is 153.00±47.32μm. MVD inThick-PCV is larger than that in wAMD group and Thin-PCV group (P<0.0001). There is no difference between Thin-PCV and wAMD groups.

After treatment, logMAR VA in wAMD group is 0.75±0.42, while there is no obvious improvement compared to before treatment. LogMAR VA in Thick-PCV is 0.43±0.31, which improved significantly compared to before treatment. LogMAR VA in Thin-PCV is 0.50±0.26, which improved significantly compared to before treatment. CRT in wAMD group is 169.05±90.36μm, in Thick-PCV group is 203.12±69.73μm and Thin-PCV group is 333.00±144.57μm. All of them had improved significantly than before treatment. SFCT in wAMD group is 120.36±63.33μm, in Thick-PCV group is 337.17±67.61μm, and Thin-PCV group is 176.00±45.81μm. All of them had improved significantly than before treatment. MVD in wAMD group is 120.91±53.50μm, in Thick-PCV group is 222.33±58.57μm and Thin-PCV group is 129.25±39.35μm. wAMD and Thin-PCV had improved significantly than before treatment, but there is no obvious improvement in Thick-PCV compared to before treatment.

Conclusion: SFCT and MVD in Thick-PCV thicker than Thin-PCV group and wAMD group, while there is no obvious difference than before treatment between Thin-PCV and wAMD in choroidal morphology. After anti-VEGF treatment, CRT, SFCT and MVD of the wAMD and Thin-PCV decline. No significant decrease in Thick-PCV MVD, it suggests that Thick-PCV is independent to other diseases. We speculate that Thick-PCV may be an independent disease, Thin-PCV may be a subtype of wAMD.

Part II   Detection of Aqueous Humor and Serum Cytokine Levels Before and After Intravitreal Injection of Anti-VEGF Antibody in Patients with wet Age-Related Macular Degeneration and Polypoidal Choroidal Vasculopathy

 Purpose: To investigate the difference and relationship among 45 cytokines from serum and aqueous humor of patients with polypoidal choroidal vasculopathy (PCV) or wet age-related macular degeneration (wAMD).

Design: A prospective, consecutive, case control study

Method: 49 eyes from 49 treatment-naive patients consisting of 11 eyes with wAMD, 24 eyes with PCV and 14 eyes with senile cataracts were studied from Aug. 2016 to Apr.  2017 in Peking Union Medical College Hospital. wAMD and PCV group were given Ranibizumab (Lucentis) via intraocular vitreous injecton every 4 to 6 weeks and last for 3 mouths. We extracted 100ul aqueous humor and 2ml blood before the treatment. We applied luminex method to test 45 cytokines and growth factors, as follows: interleukin-1α (IL-1α), interleukin-1β (IL-1β), interleukin-1RA (IL-1RA), interleukin-2 (IL-2), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-6 (IL-6), interleukin-7 ( IL-7), interleukin-8 (IL-8), interleukin-9 (IL-9), interleukin-10 (IL-10), interleukin-13 (IL-13), interleukin-15 (IL-15), interleukin-17A (IL-17A), interleukin-18 (IL-18), interleukin-21 (IL-21), interleukin-22 (IL-22), interleukin-23 (IL-23), interleukin-27 (IL-27), interleukin-31 (IL-31), VEGF-A, VEGF-D, leukemia inhibitory factor (LIF), stromal-derived factor 1-α (SDF1-α), brain-derived neurotrophic factor (BDNF), interferon inducible protein 10 (IP-10), hepatocyte Growth Factor (HGF), interleukin-12p70 (IL-12p70), PIGF, basic fibroblast growth factor (FGF-basic), granulocyte macrophage colony stimulating Factor (GMCSF), epidermal growth factor (EGF), macrophage inflammatory protein 1β (MIP-1β), eotaxin, regulated upon activation normal T cell expressed and secreted (RANTES), platelet-derived growth factor-BB (PDGF-BB), MCP-1, nerve growth factor b (NGFb), stem cell factor (SCF), macrophage inflammatory protein-1α (MIP-1α), growth-related gene product α (GROα), interferon-γ (IFNγ), interferon-α (IFNα), tumor necrosis factor α (TNFα) and tumor necrosis factor β (TNFβ). First, we compared concentration among PCV, wAMD and control group, and then compared the changes of concentration among different groups before and after anti-VEGF treatment.

Results: Before treatment, in aqueous humor, the concentration of IL-8, IL-18, IL-21, IL-31, LIF, SDF1-α, FGF-basic, VEGF-A, VEGF-D in wAMD and PCV had increased significantly. And, the concentration of BDNF, HGF, IP-10, MCP-1, IL-13 in wAMD and PCV had decreased significantly. IL-17A has a significant decrease in wAMD group, but there is no significant change in PCV group. GMCSF, IL-12p70 has significant decrease in PCV group, but there is no significant change in wAMD group. The concentrations of IL-8 and IL-12p70 in wAMD group were significantly higher than PCV group.

Before treatment, in serum, the concentration of EGF, Eotaxin, GMCSF, MCP-1, MIP-1β, IL-8, IL-21, IL-31, LIF, SDF1-α, VEGF-A, VEGF-D in wAMD and PCV had increased significantly. PDGF-BB has a significant decrease in wAMD and PCV group. And, FGF-basic has significant increase in wAMD, while there is no obvious change in PCV. HGF, IL-5 have a significant decrease in wAMD group, but there is no significant change in PCV group. IL-18 has obvious decrease in PCV. The concentration of LIF in wAMD group was significantly higher than this in group PCV.

After treatment, in aqueous humor, the concentration of HGF, IL-12p70 in wAMD and PCV had increased significantly. The concentration of IL-18, IL-21, LIF, SDF1-α, VEGF-A, VEGF-D in wAMD and PCV group had decreased significantly. Second, the concentration of IL-8, IL-23, PDGF-BB only had decreased in wAMD group, but there is no significant change in PCV group. MCP-1, IL-13 only had increased in wAMD group, but there is no significant change in PCV group.

After treatment, in serum, HGF concentration of HGF had increased significantly in wAMD and PCV group. And, the concentration of IL-21, LIF, SCF, SDF1-α, VEGF-A, VEGF-D had decreased significantly. IL-8 only had decreased in wAMD group, but there is no significant change in PCV group. IL-2, IL-6, NGFβ only had decreased in PCV group, but there is no significant change in wAMD group.

Compared with the controlled group, HGF, IP-10, MCP-1, IL-13, IL-31, LIF, SDF1-α, VEGF-A, VEGF-D have positive correlation with wAMD and PCV.

GROα, IL-1β, IL-1α, IFNγ, IFNα, IL-7, IL-9, IL-10, IL-22, TNFα and TNFβ below detection limit.

Conclusion: The concentrations of IL-8 and IL-12p70 in aqueous homour and LIF in serum are significantly higher in wAMD group than in PCV. It indicated that concentrations of IL-8, IL-12p70 and LIF may be used to identify wAMD and PCV. The changes in concentrations of VEGF-A, VEGF-D, IL-13, IL-31, LIF, SDF1-α, HGF, IP-10, MCP-1 in aqueous humour and MCP-1, PDGF-BB, VEGF-A, VEGF-D in serum can be used to identify wAMD and PCV with control group. The concentrations of VEGF-A and VEGF-D in aqueous and serum of wAMD and PCV patients were equally higher than control group, and shown no difference between them, suggesting that the changes after anti-VEGF therapy could be used to evaluate the treatment effect. Pro-angiogenesis factor and anti-angiogenesis cytokines, pro- inflammatory cytokines and anti-inflammatory cytokines all participated in the pathogenesis of wAMD and PCV. It is necessary for us to attach importance to the vital role of immunity dysfunction and chronic inflammation in the development and progression of wAMD and PCV. The functions of some cytokines in eyes were not so clear, The change trends is not consistent with past studies and systemic mechanism, further research is still needed.