原发性开角型青光眼患者房水内皮素的检测

目的 探讨内皮素在原发性开角型青光眼发病中的作用。方法 应用放射免疫分析法对３０例原发性开角型青光眼患者和１５例对照组房水中ＥＴ含量进行测定。结果 青光眼患者组房水ＥＴ含量明显高于对照组房水ＥＴ含量（Ｐ〈０．０５）。结论 开角型青光眼患者的眼局部ＥＴ分泌过多。内皮素可能在原发性开角型青光眼的发病机制中起作用。     

原发性开角型青光眼房水内皮素与眼压的相关关系研究

目的 了解ＰＯＡＧ房水内皮素与眼压有无相关关系。方法 通过放射免疫饱和分析法（ＲＩＡ）测定高眼压状态的原发性开角型青光眼（ＰＯＡＧ）及正常眼压的白内障患者房水内皮素（ＥＴ）。结果 ＰＯＡＧ组明显高于白内障组（Ｐ〈０．０１）。两组术前眼压比较,Ｐ〈０．０１ＰＯＡＧ眼压和ＥＴ回归分析,Ｐ〈０．０５,白内障组眼压与ＥＴ回归分析,Ｐ〉０．０５。结论 ＰＯＡＧ眼压与ＥＴ分泌有相关关系,眼部ＥＴ水平的改变是机     

房水流出的影响因素与原发性开角型青光眼

房水流出受阻是导致原发性开角型青光眼（ＰＯＡＧ）发生发展的重要因素之一,回顾了大量文献,从压力敏感性,年龄因素,细胞外基质（ＥＣＭ）的改变及生长因子的作用等４个方面对影响房水流出的因素进行了详尽的综述,以期为ＰＯＡＧ的基础研究提供实验性探讨的方向。     

原发性开角型青光眼

原发性开角型青光眼李美玉青光眼是由于眼压升高引起的视乳头损害和视野缺损的一种眼病。个体眼球对眼压的耐受力不同，有些眼球眼压高于２．８ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ）可产生视乳头和视野损害，形成真正的青光眼；有些眼压虽高出正常值，却不产生视乳头和视野...     

原发性开角型青光眼临床研究进展

自从德国眼科学家Albercht Von Graefe第一个提出青光眼以来,眼科工作者对此病进行了大量的研究,并取得了很大的发展。现就近年来原发性开角型青光眼的临床研究进展综述如下,旨在为临床工作提供借鉴。一、发病机理: 尽管其确切机制尚未明了,但近年来机械学说和血管学说趋于统一,从而更好地解释了青光眼的某些病理变化。机械学说——神经轴浆流传递障碍学说派已肯定了阻滞部位在筛板区,而且承认了贫血会促进轴浆流阻滞。血管学说——眼压所致贫血学说派已证实筛板前区是眼压所致贫血的敏感区,而且承认该区星形胶质细胞的缺血性萎缩,促进神经轴浆流的阻滞。     

原发性开角型青光眼患者焦虑症伴随状况及特征分析

目的:了解原发性开角型青光眼(primary open angle glau-coma,POAG)患者焦虑症伴随状况及其影响因素。方法:用Hamilton焦虑量表(HAMD)对82例POAG患者及82例非青光眼患者进行焦虑测试,对比两组患者焦虑症伴随比率,并对82例POAG患者以不同性别、年龄、文化程度等进行分组比较,分析焦虑症发生的影响因素。结果:POAG组与对照组伴发焦虑者分别为13例(16%)和5例(6%),经χ2检验,差异有统计学意义(P=0.046)。对82例POAG患者内部分组比较显示:性别、年龄、文化水平、病程、视野为POAG伴发焦虑的相关因素。结论:POAG患者心理健康状况应予以关注,尤其对病程长、年龄大、文化程度低、视功能损害严重的女性患者,应同时给予心理评估及干预,以改善POAG患者的生活质量及预后。     

原发性开角型青光眼疾病基因定位

近几年来，有关各型原发性开角型青光眼疾病基因定位的研究取得一定进展。青少年型开角型青光眼疾病基因定位于第１号染色体１ｑ＾２２－ｑ＾２５区域ｆｍ １２６ｙｄ８和ＡＴ３之间。成人型原发性开角型青光眼疾病候基因多个；（１）ＧＬＶＣＩＢ基因，可能来自于不同染色体上的突变；（２）ＧＬＣＩＣ基因，位于第３号染色体３ｑ＾２１－ｑ＾２４区域Ｄ３Ｓ３６３７和Ｄ３Ｓ１７４４之间；（３）第６号染色体６ｐ＾２５区域Ｄ６Ｓ     

房水引流与原发性开角型青光眼的关系

原发性开角型青光眼（ＰＯＡＧ）的发病机制一直是人们致力研究的问题。本文回顾大量文献，对正常房水通路的主要阻力部位以及ＰＯＡＧ房水通路的改变进行了详尽的综述，提示在ＰＯＡＧ的发生发展中所产生的重要影响。     

原发性急性闭角型青光眼患者房水中IL-8和IL-12p70的表达及其临床意义

目的:对原发性急性闭角型青光眼(AACG)和年龄相关性白内障(ARC)患者房水中IL-8及IL-12p70浓度进行检测,并探讨其临床意义.方法:选取2019-10/2020-12于我院治疗的原发性AACG急性发作期患者29例29眼作为研究组,同期于我院行手术治疗的ARC患者17例17眼作为对照组,通过流式液相蛋白定量技...     

Proteome alterations in aqueous humour of primary open angle glaucoma patients

AIM: To unravel the primary open angle glaucoma(POAG) related proteomic changes in aqueous humour(AH).METHODS: Totally 35 patients listed for cataract surgery(controls: n=12, age: 67.4±13.6 y) or trabeculectomy for POAG(n=23, age: 72.5±8.3 y) were included. AH samples of those patients were obtained during cataract surgery or trabeculectomy. AH samples were subsequently pooled into the experimental groups under equal contribution in terms of protein amount of each individual patient. Protein samples were analyzed by a linear trap quadrupol Orbitrap Mass Spectrometry device with an upstream liquid chromatography system. The obtained raw data were analyzed using the Maxquant proteome software and compared. Proteins with a fold-change ratio higher than a cut-off of 2 were considered as noticeably altered.RESULTS: A total number of 175 proteins could be identified out of the AH from POAG and cataract by means of quantitative mass spectrometric analysis. Apolipoprotein D(fold change, 3.16 times), complement C3(2.96), pigment epithelium-derived factor(2.86), dickkopf-related protein 3(2.18) and wingless-related integration(Wnt) inhibitory factor 1(2.35) were significantly upregulated within the AH of glaucoma compared to cataract serving as controls.CONCLUSION: AH provides a tool to analyze changes in glaucoma and shows striking changes in Wnt signaling inhibitory molecules and other proteins.     

A fluorophotometric study on the aqueous humor dynamics in primary open angle glaucoma

One hundred and ten eyes in 40 normal persons with no ocular pathology, 20 with ocular hypertension and 50 with primary open angle glaucoma were studied. The value of the aqueous humor flow was obtained and then compared with the different samples and with general (age, sex) and ocular factors (intraocular pressure, tonographic outflow facility, campimeter and disk/cup ratio, among others.     

原发性闭角型青光眼房水中促炎症因子升高机制的研究进展

青光眼是一组以特征性视神经萎缩和视野缺损为共同特征的疾病,是世界上第二位致盲性眼病.原发性闭角型青光眼是我国原发性青光眼中最常见的类型,关于其发病机制目前有很多学说,如机械学说和血管学说.而近几年研究发现,炎症反应可能也参与了青光眼的发病过程,原发性闭角型青光眼患者房水中多种促炎症因子显著升高.本文总结了两种常用的房水因子的检测方法,并分析原发性闭角型青光眼患者房水中促炎症因子升高的机制.     

正常眼压青光眼与原发性开角型青光眼的比较

正常眼压青光眼（ＮＴＧ）的发病率逐渐增加,日益受到眼科工作者的重视。ＮＴＧ发病隐蔽,早期诊断较其它青光眼显得更为困难和复杂,其发病机制、诊断标准及其与原发性开角型青光眼（ＰＯＡＧ）的异同等一系列问题仍无统一意见。就ＮＴＧ与ＰＯＡＧ的诊断标准,发病机制,临床表现,治疗原则以及相互关系等问题的研究进展等进行综述。     

Inflammatory model in patients with primary open angle glaucoma and diabetes

AIM: To assess the inflammatory cytokines expression in aqueous humor in diabetic primary open angle glaucoma (POAG) patients. METHODS: A cross-sectional study on 87 eyes, distributed as following: 26 eyes from diabetic patients, 16 eyes with POAG and 21 eyes from diabetic POAG patients; healthy controls (24 eyes) were recruited from patients undergoing conventional cataract surgery. A volume of 100 μL of aqueous humor (AH) was collected during phacoemulsification and 21 inflammatory markers were quantified using a Luminex® cytometric bead assay: IL-1Ra, IL-1α, IL-1β, IL-5, IL-6, IL-10, IL-17, GM-CSF, IFNγ, CCL2, CCL3, CCL4, CXCL5, CXCL8, bFGF, VEGF, TNFα. Main changes in cytokine profile were analyzed and compared between groups. Data on demographics, duration of glaucoma, intraocular pressure (IOP), number of anti-glaucoma substances were recorded for correlation analysis and prediction models. RESULTS: Significant differences in cytokine expression between groups were detected for CXCL5 (P<0.001), CXCL8 (P=0.004), IL-1α (P<0.001), IL-2 (P<0.001), CCL4 (P=0.003), CCL5 (P<0.001) and TNFα (P=0.05). Post-hoc analysis identified IL-2 (P=0.009) and CXCL5 (P<0.001) as “separation markers” between POAG and diabetic POAG eyes. In POAG patients, the “separation markers” could highly predict the TNFα levels F(1, 16)=14.639, P<0.001, whereas in diabetic patients F(1, 24)=4.844, P=0.006 and diabetic POAG patients F(1, 19)=2.358, P=0.05 the level of prediction was inferior. CONCLUSION: Our results reveal an inflammatory model based on increased TNFα levels in POAG eyes. Simultaneous co-stimulatory molecules and additional inflammatory pathways need to be further explored in diabetic POAG cases, since the prediction model could only partially explain the increased TNFα level in this category of patients.     

原发性开角型青光眼的早期诊断

青光眼是全世界成人致盲的主要眼病。原发性开角型青光眼做为青光眼的一种类型,其特点是病程进展较为缓慢,多数没有明显症状,不易早期发现。许多患者就诊时已经出现了较严重的视功能障碍,且近年来该病患病率在临床上所占的比例有所上升。而对原发性开角型青光眼的早期诊断,是延缓或停止视功能进行性损害的关键。因此,综合国内外近年来相关文献,对原发性开角型青光眼的早期诊断做以下综述。     

尼日利亚Gwagwalada原发性开角型青光眼患者的社会人口学和临床特征

目的：探讨比较尼日利亚Gwagwalada原发性开角型青光眼(POAG)与非青光眼患者的临床社会人口学特征。

方法：横断面对比研究。共调查235例成年患者,其中96例POAG及139例非青光眼。记录患者年龄、性别、教育程度、职业、种族、青光眼家族史、眼痒、糖尿病和高血压情况。眼部检查包括视力、中央视野、杯盘比、前房角评估和眼压。

结果：平均年龄为49.88±13.75岁,其中男114例(48.5%)。POAG患者包括42个种族,其中伊博人(24/96,25.0%)和约鲁巴人(20/96,20.8%)最为常见。大多数POAG(74/96,77.1%)年龄在40-69岁之间。POAG(73/96,76.0%)有不同程度的视力障碍。POAG组与非青光眼组的对比如下：青光眼阳性家族史(34/96,35.4%)vs(25/139,18.0%; P=0.012); 糖尿病史(8/96,8.3%)vs(6/139,4.3%); 高血压病史(24/96,25.0%)vs(28/139,20.1%); 糖尿病合并高血压病史(1/96,1.0%)vs(4/139,2.9%; P=0.268); 使用抗糖尿病药物者(5/96,5.2%)vs(7/139,5.0%); 使用降压药者(24/96,25.0%)vs(23/139,16.5%); 联合使用抗糖尿病和抗高血压药物者(4/96,4.2%)vs(5/139,3.6%; P=0.328); 有眼痒症状者(18/96,18.7%)vs(37/139,26.6%; P=0.328); 视力障碍\〖右眼(RE)：51/96,53.1%; 左眼(LE)：60/96,62.5%\〗vs(RE：40/139,28.7%; LE：37/139,26.6%; P=0.000); 垂直杯盘比>0.4(RE：96/96,100%; LE：96/96,100%)vs(RE：131/139,94.2%; LE：124/139,89.2%)(RE：P=0.307; LE：P=0.006); 眼压>22 mmHg(RE：17/96,17.7%; LE：22/96,22.9%)vs(RE：2/139,1.4%; LE：2/139,1.4%; P=0.006)。大多数POAG患者(60/96,62.5%)正在服用抗青光眼药物,(23/96,24.0%)尚未开始用药,P=0.000。许多POAG(32/96,33.3%)正在服用β受体阻滞剂、前列腺素抑制剂和碳酸酐酶抑制剂的联合抗青光眼药物。

结论：青光眼具有与其他眼部疾病不同的临床社会人口学特征。许多参与者肯定了青光眼的家族史,大多数青光眼参与者正在接受抗青光眼治疗。包括失明在内的视力障碍与青光眼显著相关。该研究证实,开角型青光眼与高杯盘比和高眼内压有关。     

青光眼患者房水中细胞因子的研究进展

房水由睫状突上皮细胞产生,是前房的重要组成部分,为角膜、晶状体、小梁网等无血管组织提供营养.相较于血液,房水能更好地反映眼内的环境,因此近几年房水中细胞因子检测成为眼科研究的热点之一.研究者已经在多种眼部疾病中发现了房水细胞因子的改变,包括青光眼.一些研究认为,房水中细胞因子的改变可能与青光眼的发病机制有关,甚至可能影响青光眼滤过术的预后.本文总结了几类细胞因子在青光眼房水中的变化,并分析它们与青光眼的关系.