增生细胞核抗原在视网膜色素上皮细胞表达及其反义寡核苷酸的抑制作用

目的 研究视网膜色素上皮(retinal pigment epithelium,RPE)细胞中增生细胞核抗原(proliferating cell nuclear antigen,PCNA)表达及其反义寡核苷酸(antisense oligodeoxynucleotides,AS ODN)对其表达和细胞增生的抑制作用，为增生性玻璃体视网膜病变(proliferative vitreoretinopathy,PVR)治疗探索基因治疗新途径。 方法 (1)体外培养兔眼RPE细胞，在不同时间采用链霉亲合素-生物素化过氧化物酶复合物(streptoavidin-biotin enzyme complex,SABC)免疫组织化学法检测PCNA的表达;(2)脂质体介导下不同浓度的PCNA AS-ODN和正义寡核苷酸(sense oligodeoxynucleotides,S-ODN)分别作用于体外培养的RPE细胞，采用免疫组织化学方法检测PCNA的表达;(3)四唑盐比色法(methyl thiazolyl tetrazolium,MTT)检测在不同浓度的PCNA AS-ODN和S-ODN作用下RPE细胞生长活性及其生长抑制率。 结果 (1)体外培养兔眼RPE细胞表达PCNA，表达高峰为培养后48 h ;(2)在0.28、1.12 μmol/L AS-ODN 作用下，PCNA的表达明显受抑制;(3)0.28、1.12 μmol/L的PCNA AS-ODN 能明显抑制RPE细胞增生活性，并呈剂量依赖性，其生长抑制率分别达53%、81%。 结论 一定浓度PCNA AS-ODN能序列特异性地抑制RPE细胞PCNA表达和增生活性，有望进一步用于PVR的治疗实验研究。 (中华眼底病杂志, 2002, 18: 231-233)     

乙酰肝素酶抑制剂对体外培养视网膜色素上皮细胞增殖的影响

目的：探讨乙酰肝素酶（heparanase-1, HPA-1）抑制剂应用对体外培养的视网膜色素上皮(retinal pigment epithelial, RPE)细胞增殖的影响。方法：采用DMEM培养基(Dulbecco's modified eagles medium, DMEM)体外培养人RPE细胞,选择第5代细胞用于实验。倒置显微镜下直接观察不同质量浓度硫代磷酸甘露醇戊糖（phosphomannopentaose sulfate, PI-88）对人RPE细胞体外生长的干预效果,应用四甲基偶氮唑盐[3-(4,5-dimethylthiazol-2-yl)-2,5-dipheny1 tetrazolium bromide, MTT]比色法检测RPE细胞A₅₇₀值;免疫组织化学方法检测人RPE细胞角蛋白和HPA-1表达。 结果：体外增生的RPE细胞胞浆和细胞核HPA-1呈强阳性表达,以细胞浆内表达为主,PI-88干预后细胞浆表达减弱。PI-88对体外RPE细胞的增生有明显的时效和量效抑制关系,药物干预72h细胞A₅₇₀值随质量浓度不同表现明显下降趋势（P<0.05）;而同一质量浓度,药物质量浓度达到100mg/L及以上时,48~72h才表现A₅₇₀值减小的趋势。结论: HPA-1抑制剂可抑制体外培养RPE细胞的增生,并呈现剂量和时间依赖关系。     

端粒酶相关因素对培养的视网膜色素上皮细胞增生的影响

目的探讨端粒酶相关因素对培养的视网膜色素上皮（retinal pigment epithelium，RPE）细胞增生的影响。方法用常规培养法培养人RPE细胞后，分别用端粒酶抑制剂二甲基亚砜、热休克蛋白90抑制剂、无血清培养、端粒酶反义寡核苷酸、P16反义寡核苷酸处理，然后提取细胞mRNA，PCR扩增后电泳检测端粒酶mRNA表达。然后用MTT法检测无血清培养组、端粒酶反义寡核苷酸处理组、P16反义寡核苷酸处理组与常规培养组细胞增生状况。结果二甲基亚砜组、热休克蛋白90抑制剂组、无血清培养组、端粒酶反叉寡核苷酸处理组，端粒酶mRNA表达受到抑制，凝胶分析系统软件分析结果电泳H值分别为80、116、90、81，而P16反义寡核苷酸处理组端粒酶mRNA表达增强，电泳H值为255。常规培养组H值为162，阴性对照组为0，阳性对照组（胃癌细胞）为255。MTT法显示：无血清培养组，端粒酶反义寡核苷酸处理组细胞活性下降，细胞生长抑制率上升。而P16反义寡核苷酸处理组细胞活性上升，细胞生长抑制率下降。结论端粒酶抑制剂二甲基亚砜、热休克蛋白90抑制剂、无血清培养、端粒酶反义寡核苷酸可抑制RPE细胞端粒酶mRNA表达，从而抑制RPE细胞增生；P16反义寡核苷酸可促进RPE细胞端粒酶mRNA表达，从而促进RPE细胞增生。     

曲安奈德对培养人视网膜色素上皮细胞表达survivin的影响

目的 观察曲安奈德(TA)对体外培养的人视网膜色素上皮(RPE)细胞表达survivin基因的影响,探讨TA治疗增生性玻璃体视网膜病变(PVR)的机制.方法 四甲基偶氮唑盐比色(MTT)法和流式细胞术检测不同质量浓度(0.01、0.1、1.0 g/L)TA对人RPE细胞增生及凋亡的作用,免疫组织化学法、RT-PCR检测药物在蛋白和基因水平对survivin表达的影响. 结果 在不同质量浓度的TA作用下,人RPE细胞的增生受到抑制,凋亡率增加,在蛋白水平和基因水平,药物均对RPE细胞survivin的表达有明显的抑制作用,且均与药物的作用时间和剂量呈正相关.各组与对照组比较差异均有统计学意义(P＜0.05).结论 TA能抑制人RPE细胞的增生及survivin蛋白和mRNA在人RPE细胞的表达,诱导RPE细胞的凋亡.     

TGF-β对体外培养人胚视网膜色素上皮细胞的影响

目的 研究转化生长因子-β（TGF-β）对体外培养人胚视网膜色素上皮（RPE）细胞的影响，从细胞生物学水平和分子生物学水平探讨近视眼的发病机制。方法 外源性TGF-β刺激人RPE细胞后，通过绘制生长曲线、MTT法检测细胞活性及观察透射电镜研究其细胞自身的生长情况；采用酶联免疫吸附实验（ELISA）测定其分泌HGF、bFGF和TGF-β的量；采用RT-PCR法检测其细胞表达HGF的情况，从而分析外源性TGF-β对体外培养的RPE细胞的影响。结果不同质量浓度的TGF-β均可抑制人胚RPE细胞的生长，随时间的延长作用更加明显；TGF-β可使RPE细胞超微结构发生变化；ELISA结果显示TGF-β对其他两种因子的分泌均有抑制作用，但对自身有促进作用，为正反馈调节；同时可明显抑制RPE细胞内HGF的表达。结论 TGF-β可影响RPE细胞增生、改变超微结构及抑制HGF的表达。     

维甲酸对人RPE细胞胞间通讯功能和Cx43表达的影响

目的观察培养的人视网膜色素上皮（RPE）细胞中连接蛋白Cx43的表达特点，以及维甲酸（RA）对人RPE细胞生长和细胞间缝隙连接功能、细胞间通道蛋白Cx43表达的影响及其相互关系。方法免疫组织化学方法观察缝隙连接蛋白（Cx43）在培养的人RPE细胞中的表达特点；不同浓度的RA作用于培养的第4代人的色素上皮细胞，用MTT方法观察RA对体外培养人RPE细胞生长的抑制；用LY染料传输方法测定细胞间隙连接功能，观察这三组不同浓度的RA对人RPE细胞缝隙连接功能的影响；免疫组织化学方法鉴别不同浓度RA影响后的缝隙连接蛋白Cx43的表达，用计算机灰度测量的方法评估表达的强度并作统计学分析。结果免疫组织化学染色显示体外培养的人RPE细胞表达缝隙连接蛋白Cx43，表达的部位主要在细胞浆和细胞膜上；RA对人RPE细胞的生长有明显的抑制作用，其抑制作用呈剂量依赖性；LY染料传输试验表明在RA的作用下RPE细胞间通讯功能明显增强；经计算机图像分析表明RA使连接蛋白Cx43表达增强，增强的程度与RA的浓度呈正相关。结论体外培养的人RPE细胞可以表达Cx43蛋白，RA抑制培养的色素上皮细胞的生长，提高细胞间隙连接通讯功能，上调Cx43蛋白在人RPE细胞中的表达。     

反义寡核苷酸对人视网膜色素上皮细胞迁移的影响

目的探讨脂质体介导表皮生长因子(epidermal growthfactor receptor,EGFR)反义寡核苷酸对人视网膜色素上皮(retinal pigment epithelium,RPE)细胞迁移的影响。方法采用Murphy细胞计数方法评价反义寡核苷酸对人RPE细胞体外迁移的影响;分别应用ELISA法和半定量PCR检测反义寡核苷酸对RPE细胞EGFR蛋白和mRNA的抑制作用。结果脂质体介导EGFR反义寡核苷酸组与对照组比较,细胞迁移活性受到明显抑制(P<0.05),24h后抑制率75.27%.转染24h后EGFR蛋白和mRNA表达的抑制率分别为67.60%和35.20%.结论脂质体介导EGFR反义寡核苷酸可抑制EGFR蛋白表达和mRNA的表达,并可抑制人RPE细胞体外迁移,脂质体介导的反义寡核苷酸可能是针对RPE的一种有希望的基因治疗方法。     

Bcl-2反义寡核苷酸抑制视网膜色素上皮细胞增生的实验研究

目的 探讨不同浓度的Bcl-2反义寡核苷酸(bcl-2AS-ODN)对人视网膜色素上皮(RPE)细胞增生活性的影响。方法 使用不同浓度(0、15、30、45、60μmol／L)的bcl-2AS-ODN和bcl-2 S-ODN处理人RPE细胞24h后，使用MTT、氚-标记脱氧胸苷掺人试验(^3H-TdR)测定RPE细胞增生的抑制率及DNA合成抑制率；使用流式细胞仪检测其对RPE细胞周期的影响；使用免疫组织化学染色法检测不同浓度bcl-2 AS-ODN作用下的RPE细胞bcl-2的表达。结果 不同浓度bcl-2 AS-ODN处理过的RPE细胞的抑制率和DNA合成抑制率随bcl-2 AS-ODN浓度的增高而升高，bcl-2 AS-ODN将RPE细胞阻滞在G0／G1期，免疫组化结果显示：bcl-2 AS-ODN可抑制RPE细胞bcl-2的表达。结论 bcl-2 AS-ODN对RPE细胞的增生有抑制作用且呈浓度依赖性，这一结果有可能成为增生性玻璃体视网膜病变(PVR)基因治疗的一个新靶点。     

小干扰RNA对人视网膜色素上皮细胞缝隙连接蛋白43表达水平的调节

目的 观察体外化学合成的小干扰RNA(small interfering RNA,siRNA)对原代培养的人视网膜色素上皮(retinal pigment epithelium,RPE)细胞缝隙连接蛋白43(connexin43,cx43)基因和蛋白表达的影响.方法 设计合成针对人ex43基因的小干扰片段(siR-NA1、siRNA2、siRNA3)和1条阴性对照siRNA0,在脂质体的介导下转染培养的人RPE细胞,采用RT-PCR确定最有效的抑制片段;针对siRNA的有效片段,分为不同浓度(50～30nmolO·L-1)转染培养细胞,培养72 h后进行MTT增生试验,观察其对人RPE细胞增生能力的影响,确定最有效的浓度;siRNA转染细胞后,分别培养12 h、24 h、48 h、72 h后进行Weston blot试验.观察不同时间点其对cx43蛋白表达的影响.结果 体外合成的3条siRNA均在一定程度上抑制cx43基因的合成,其中 siRNA1是最有效的抑制片段,根据条带灰度比其抑制率达到72%;siRNA1可以显著促进人RPE细胞的增生,增生率达到146%;明显抑制其cx43蛋白的表达(P<0.01),抑制率达到61%;从浓度组间结果可以看出,siRNA的最佳作用浓度是250 nmol·L-1,在此浓度之前效率与浓度呈正比,超过此浓度后各浓度组间差异无统计学意义;比较不同时间点,siRNA转染人RPE细胞24 h后开始抑制cx43表达,48 h后对cx43蛋白合成抑制率最明显.结论 化学合成的siRNA可以有效抑制培养的人RPE细胞cx43基因的表达,促进细胞的增生.这种基因沉默作用可能对于视网膜色素上皮组织的再生有一定作用.     

替德肝素抑制冷冻后视网膜色素上皮细胞分泌肝细胞生长因子的研究

目的探讨替德肝素(tedelparin)在抑制冷冻后的人视网膜色素上皮(humanretinapigmentepithelium,hRPE)细胞分泌肝细胞生长因子(humanhepatocytegrowthfactor,HGF)和生长中的作用。方法体外培养的RPE细胞在-80℃下进行冷冻,冷冻时间分为0、15和60s,随后继续体外培养(体外实验组)和注入正常兔眼玻璃体(体内实验组)并在第6天时取出一些兔眼的玻璃体液加入到正常RPE细胞培养液中孵育48h;每实验组再分为两个亚组替德肝素治疗(终浓度25μl/ml)组和未治疗组,在3d、6d时收集细胞培养上清和玻璃体样本,ELISA法测定HGF含量,MTT法测定48h后RPE细胞的增殖状态。结果在体外实验组,比较未冷冻组,冷冻后的RPE细胞随着冷冻时间延长HGF分泌水平增加(F=2736,P<001),替德肝素干预组HGF分泌水平下降(F=17950,P<001)。在体内实验组(兔玻璃体)随着冷冻时间延长HGF浓度较对照组明显增高(F=624,P<001),当玻璃体液(冷冻15s和60s,第6天)加入到正常RPE细胞培养液48h后刺激细胞增殖(P<001),在替德肝素干预组,细胞增殖明显减弱(F=4490,P<005)。结论冷冻可刺激RPE细胞在体外和体内玻璃体环境中HGF的高分泌,且随着冷冻时间增加更为显著。替德肝素可降低冷冻后RPE细胞分泌HGF水平和抑制促生长环境中的RPE细胞生长,具有预防PVR的作用。     

Distribution,markers, and functions of retinal microglia

Retinal microglia originate from hemopoietic cells and invade the retina from the retinal margin and the optic disc, most likely via the blood vessels of the ciliary body and iris, and the retinal vasculature, respectively. The microglial precursors that appear in the retina prior to vascularization are major histocompatibility complex (MHC) class I- and II-positive and express the CD 45 marker, but lack specific macrophage markers. They differentiate into ramified parenchymal microglia in the adult retina. A second category of microglial precursors, which do express specific macrophage markers, migrate into the retina along with vascular precursors. They appear around blood vessels in the adult retina and are similar to macrophages or cells of the mononuclear phagocyte series (MPS). Microglia are distributed in the outer plexiform layer (OPL), outer nuclear layer (ONL), inner plexiform layer (IPL), ganglion cell layer (GCL), and nerve fiber layer (NFL) of the primate retina. The pattern of microglial distribution in the avascular retina of the quail indicates that blood vessels are not responsible for the final location of microglia in the retina. In the human retina, microglia express MHC class I, MHC class II, CD 45 , CD68, and S22 markers. In the rat and mouse retina, OX 41 , OX 42 , OX 3 , OX6, OX18, ED1, Mac-1, F 4 /80, 5 D 4 anti-keratan sulfate, and lectins are used to recognize microglia. Microglial cells play an important role in host defense against invading microorganisms, immunoregulation, and tissue repair. During neurodegeneration, activated microglial cells participate in the phagocytosis of debris and facilitate regenerative processes. In autoimmune disease, microglia have dual functions: initiating uveoretinitis, but also limiting subsequent inflammation. Retinal microglia may be associated with vitreoretinopathy, diabetic retinopathy, glaucoma, and age-related macular degeneration. The goal of this article was to review the present knowledge about retinal microglia and the function of retinal microglia in pathological conditions.     

Comparative antiproliferative and cytotoxic profile of bevacizumab (Avastin), pegaptanib (Macugen) and ranibizumab (Lucentis) on different ocular cells

Aim To compare the antiproliferative and cytotoxic properties of bevacizumab (Avastin), pegaptanib (Macugen) and ranibizumab (Lucentis) on human retinal pigment epithelium (ARPE19) cells, rat retinal ganglion cells (RGC5) and pig choroidal endothelial cells (CEC). Methods Monolayer cultures of ARPE19, RGC5 and CEC were used. Bevacizumab (0.1–0.3 mg/ml), pegaptanib (0.025–0.08 mg/ml) or ranibizumab (0.04–0.125 mg/ml) diluted in culture medium were added to the cells. Expression of VEGF-receptors (VEGFR1 and VEGFR2) and von Willebrand factor (a marker for endothelial cells) were analysed by immunohistochemistry. CEC cells were stimulated with VEGF. Cellular proliferative activity was monitored by BrdU-incorporation into cellular DNA. For cytotoxicity assays cells were grown to confluence and then cultured in a serum-depleted medium to ensure a static milieu. MTT-test was performed after one day. Results CEC and ARPE19 cells stained positively for VEGFR1 and VEGFR2. More than 95% of the CEC cells were positive for von Willebrand factor. Ranibizumab reduced CEC cell proliferation by 44.1%, bevacizumab by 38.2% and pegaptanib by 35.1% when the drugs were used at their established clinical doses. The differences, however, between the three drugs in respect to cell growth inhibition were not statistically significant. Only a mild antiproliferative effect of bevacizumab or pegaptanib on ARPE19 cells could be observed. Ranibizumab did not alter ARPE19 cell proliferation. No cytotoxicity on RGC5, CEC and ARPE19 cells could be seen. Conclusions Bevacizumab, pegaptanib and ranibizumab significantly suppress choroidal endothelial cell proliferation. However, when used at the currently established doses none of the drugs was superior over the others in respect to endothelial cell growth inhibition. The biocompatibility of all three drugs — including the off-label bevacizumab — seems to be excellent when used at the currently recommended intravitreal dose. This work is presented on behalf of the Tuebingen Bevacizumab Study Group.     

视网膜血管瘤增殖一年龄相关性黄斑变性的特殊类型

本文总结了年龄相关性黄斑变性的特殊类型—视网膜血管瘤增殖(RAP)的临床和造影表现及分期。RAP是起源于黄斑旁视网膜深层毛细血管的、以伴发多灶小片视网膜内出血及盘变前期即有视网膜-脉络膜血管吻合(RCA)形成为特征的新生血管性AMD。     

Intravitreal use of bevacizumab (Avastin) for choroidal neovascularization due to ARMD: a preliminary multifocal-ERG and OCT study

Purpose To evaluate by MFERG and OCT the macular function before and after intravitreal use of bevacizumab (Avastin) in eyes suffering from CNV due to ARMD. Methods Eighteen eyes with subfoveal CNV due to ARMD were studied before and after intravitreal use of bevacizumab with MFERG and OCT. The post treatment follow up was three months. Results Before treatment, OCT shows an increase of the retinal thickening of the fovea and the electrical response densities in the fovea and parafovea were decreased in all patients. Three months after treatment, OCT showed a real resolution of the subretinal fluid. The electrical responses in the fovea and parafovea remained the same or slightly improved in some cases. The intraocular pressure remained normal and no inflammation was observed. Conclusion The intravitreal use of bevacizumab may provide anatomical correlates that support the concept of disease amelioration but the functional improvement of the macula three months after treatment is not obvious. However the method is promising and needs further evaluation.     

视网膜色素上皮挫伤的眼底自发荧光改变

目的 观察视网膜色素上皮挫伤时的眼底自发荧光(AF)形态改变,探讨AF检查对眼外伤造成的视网膜色素上皮挫伤的诊断意义.方法 对31例(36只眼)视网膜色素上皮挫伤的的患者,进行眼底自发荧光检查.采用海德堡激光眼底扫描系统获取自发荧光图像.与同病例的眼底检查及FFA做对比分析,得出其自发荧光特征.结果 所有病例在视网膜色素上皮挫伤区域的自发荧光普遍弥漫性增强,有色素上皮增生处大多表现为更强的自发荧光点,色素脱失处大多表现为低荧光,在总体增强区域表现为地图状的自发荧光.结论 眼球钝挫伤早期导致的视网膜色素上皮的损害会引起相应的自发荧光的改变,主要以自发荧光增强为主,反映该区域色素上皮高代谢状态或增殖活动为主,弱的AF较少,表明挫伤后短期局部的色素上皮萎缩.这些改变与一些以萎缩性病变为主的眼底病的AF有明显区别,因而AF应用于视网膜色素上皮挫伤的诊断有明显的意义.     

糖尿病患者的视网膜电图分析

目的分析糖尿病(DR)患者视网膜电图(F-ERG)的振幅、峰潜时、OPS总和振幅及其与病程的相关性.方法将53例102眼糖尿病患者分为三组(NDR、BDR、PDR),并采用美国UATA-2000型视觉电生理仪对53DR例进行F-ERG检查,主要分析其a、b波峰潜时、振幅、OPS总和振幅.结果随着DR病情的加重,ERG及OPS无波的情况所占比例增大.a波峰潜时BDR组和正常组比较差异有极显著性(P<0.01),BDR组和DM无DR组比较差异有显著性(P[WTBZ〗<0.05);a波振幅正常对照组与其他各组比较差异均有极显著性(P<0.01).b波振幅正常对照组与BDR、PDR间以及DM无DR组与BDR、PDR组间均有极显著性差异(P<0.01).OPS总和振幅除了BDR与PDR间外,其他各组比较差异均有极显著性(P<0.01).结论OPS、ERG之a、b波振幅,尤其是b波振幅,可以作为早期诊断DR患者以及估计预后的敏感指标;良好的血糖控制,可以延缓DM的病情发展.     

30天连续配戴硬性透氧性角膜接触镜的安全性研究

目的为了评价Menicon Z硬性接触镜30 d连续配戴的安全性与有效性,进行了两个为期一年的临床比较试验.方法分别选用了可以7 d连续配戴的Hydrogel材料的Acuvue(1)及可以30 d连续配戴的Si H材料的Focus Night & Day(2)软性接触镜作为对照镜片.结果临床试验(Ⅰ)中,317人参加了Menicon Z组群,313人参加了Acuvue组群.Menicon Z组群有258人(占81.4%)完成了为期一年的试验,而Acuvue组群仅有210人(占67.1%).Acuvue组群中比较常见的副作用为浸润性角膜炎与细菌性结膜炎.相比之下,Menicon Z组群常见的不适症状是由异物飞入角膜造成角膜上皮擦伤所致的.各有50人参加了临床试验(Ⅱ)的Menicon Z组群与Night & Day组群.Menicon Z组群有35人(占70.0%)完成了为期一年的试验,Night & Day组群有33人(占66.0%).Menicon Z组群中常见的副作用表现为3～9点角膜染色,Night & Day组群为接触镜相关性充血、接触镜性角膜周边溃疡、乳头性结膜炎、角膜上方弓状损伤与细菌性角膜炎.结论Menicon Z 30 d连续配戴具有安全性.     

The Analysis of Electroretinography of Diabetes Mellitus

Purpose: In order to get deeper understanding of Diabetic Retinopathy (DR), we analyzed and evauated the results of the amplitude and latency of F-ERG a-wave, b-wave and the total amplitudes of oscillatory potentials(OPs).Methods: F-ERG of 105 eyes from 55 cases of DM were diagnosed by the medical department from July 1997 to July 1998. The 105 eyes were examined by ophthalmoscope and fluorescing in angiography and divided into there groups: 22 eyes with DM without DR(NDR), 56 eyes with background DR(BDR)and 27 eyes with proliferate DR(PDR). In addition, 30 eyes were regard as normal control group(NCG) . We used VATA-2000 type vision electrophysiological instrument and inter-national standard for clinical ERG to do measure meat and recording automatically by computer.Results: 1. The proportion of eyes number of invisible wave of a-wave, b-wave of F-ERG and Ops increased with the development of DR. 2. There were significant differences ( P< 0. 01) in the latency of a-wave between NCG and BDR and statistic     

近视及散光眼LASIK后非接触眼压计测量值的影响因素及其预测

目的 比较近视和(或)散光患者在LASIK手术前后非接触眼压计测量结果的差异及其影响因素,并得到预计眼压的计算公式.方法 对2005年12月至2006年11月在北京协和医院准分子激光手术中心行初次准分子激光原位角膜磨镶术(LASIK)矫正近视和(或)散光的患者进行回顾性研究,共93例(183只眼),采用非接触眼压计(NCT)测量术前和术后2周、1个月、3个月的眼压值,计算眼压变化值并分析其与各种变量之间的相关性,应用多元线性回归从相关变量得到术后预计的测量眼压值及眼压变化值.结果 患者术后3个月眼压较术前平均下降(5.74±2.03)mmHg,其变化与性别、年龄均不相关,但与术前屈光度有明显的关系.多元线性回归分析得到术后实际测量的眼压与术前眼压呈正性相关,而与手术切削量呈负相关(R2=0.442,P<0.001),术后预计测量眼压=5.175+0.411×术前眼压-0.0205×切削量,手术后眼压测量下降值0.589×术前眼压+0.0205×切削量-5.175.结论 通过术后实际测量眼压值与预测值比较,可以及时发现高眼压的患者,避免低估眼压以致漏诊青光眼而造成患者视功能损失.虽然可以通过预测公式来判断实际测量眼压值是否在正常范围.但更有效的方法是使用不受角膜变化影响的眼压计测定眼压.     

CT features of exophthalmos in Chinese subjects with thyroid-associated ophthalmopathy

AIM:To investigate computed tomography (CT) features of exophthalmos in Chinese subjects with thyroid-associated ophthalmopathy (TAO).METHODS:A total of605 eyes of 325 patients with exophthalmos due to TAO were classified as grade I (mild exophthalmos) or II (severe exophthalmos) based on orbital CT imaging. The increased orbital volume features, such as changes from extraocular muscles, orbital fat, or both, were analyzed.RESULTS: A total of 605 eyes were analyzed, among them 62.98% presented grade I exophthalmos, while 36.02% showed grade II exophthalmos.#$TAB In grade I, 56.69% showed orbital fat change, and in grade II, 89.29% exhibited extraocular muscle enlargement.CONCLUSION: Orbital fat and extraocular muscle enlargement are likely to be observed on CTs of subjects with mild and severe exophthalmos, respectively. Our results suggest that CT findings may guide TAO clinical therapy recommendations and prognosis.