青光眼视网膜血氧饱和度与结构功能损害程度的相关分析

目的比较青光眼与正常人视网膜血氧饱和度的差异,分析青光眼患者中视网膜血氧饱和度与结构功能损害程度的相关性。方法病例对照研究。选取原发性开角型青光眼患者28例（35眼）为青光眼组,记录患者年龄、性别、眼压、血压、杯盘比,并进行中心30°阈值视野检测和光学相干断层扫描（OCT）检测视乳头旁视网膜神经纤维层（RNFL）厚度,并纳入27例（41眼）正常人作为对照组,采用视网膜血氧饱和度分析仪测量青光眼患者和正常人视网膜血管血氧饱和度。2组动静脉血氧饱和度差异比较采用独立样本t检验。采用Pearson或Spearman秩相关分析对青光眼组视网膜血氧饱和度与年龄、眼压、血压、杯盘比、视野平均缺损（MD）、视野指数（VFI）、视乳头旁RNFL厚度进行相关分析。结果青光眼组与正常对照组的视网膜动脉血氧饱和度差异无统计学意义,青光眼组静脉血氧饱和度较对照组高（t=4.017,P＜0.001）,动静脉血氧饱和度差值较小（t=-4.431,P＜0.001）。青光眼组视网膜动脉血氧饱和度、静脉血氧饱和度、动静脉血氧饱和度差值与年龄、眼压、血压均无线性相关性。视网膜动脉血氧饱和度与杯盘比、视野MD、VFI、视乳头旁RNFL厚度等均无线性相关。视网膜静脉血氧饱和度与杯盘比、视野MD值呈正相关（杯盘比：r=0.418,P=0.012;视野MD：r=0.504,P=0.002）,与RNFL厚度、VFI呈负相关（RNFL：r=-0.514,P=0.002;VFI：r=-0.470,P=0.004）。视网膜动静脉血氧饱和度差值与杯盘比、视野MD均呈负相关（杯盘比：r=-0.390,P=0.021;视野MD：r=-0.478,P=0.004）,与VFI、视乳头旁RNFL厚度呈正相关（VFI：r=0.449,P=0.007;RNFL：r=0.385,P=0.022）。结论随着青光眼加重,静脉血氧饱和度增加,动静脉血氧饱和度差值降低。青光眼患者视网膜耗氧量降低可能与视网膜神经组织萎缩有关。     

可疑青光眼患者视野检测的表现特征及相关分析

目的 探讨可疑青光眼患者中心30°阈值视野检测的表现特征及其影响因素.方法 采用横断面研究设计,对就诊的可疑青光眼患者应用Octopus- 101型视野计进行中心30.阈值视野检测.统计分析平均视网膜光敏感度(MS)、平均视野缺损度(MD)及丢失方差(LV)视野指数,并进行视野指数影响因素相关分析.结果 可疑青光眼者不同眼别、不同性别间的视网膜光敏感度比较差异无统计学意义(P＞0.05);高眼压者与仅有可疑症状者视野指数比较差异有统计学意义(P＜0.05);杯盘比大者与可疑症状者视野指数比较差异有统计学意义(P＜0.05).Pearson相关统计分析显示:＞21 mm Hg的可疑青光眼者眼压与平均视网膜光敏感度存在负相关(r =-0.654,P＜0.05);＞21 mm Hg的可疑青光眼者眼压与平均视野缺损值存在正相关(r =0.792,P＜0.05).结论 可疑青光眼者的视网膜光敏感度不受眼别和性别的影响,可疑青光眼视野指数主要受可疑指标影响,存在杯盘比大或者眼压高者应慎重筛查并积极复查随诊.     

原发性开角型青光眼和可疑开角型青光眼HRT视盘参数与视野缺损的相关性研究

目的探讨原发性开角型青光眼和可疑性开角型青光眼的视盘参数与视野平均缺损（Mean defect，MD）之间的相关性。方法用海德堡激光眼底扫描仪（HRT—Ⅱ）和自动视野计测定128只原发性开角型青光眼和78只可疑性开角型青光眼患者的视盘参数和静态视网膜光阈值。从视盘参数中选择盘沿面积（rim area，RA）、杯盘面积比（cup／disk area ratio，C/D AR）、视杯面积（cup area，CA）和平均视网膜神经纤维层厚度（mean retinal nerve fibre layer thickness，mRNFLT）与MD作相关分析和多元线性回归分析。结果两组间的视盘参数存在显著性差异（P〈0．001）。在原发性开角型青光眼组，RA、C/D AR和CA与MD之间均显著相关（P〈0．001）。其中盘沿面积每减少1mm^2，MD的绝对值将增加7．291dB；在可疑性开角型青光眼组，RA与MD之间显著相关（P〈0．001）。两组中mRNFLT与MD无明显相关性。结论在HRT-Ⅱ的各项视盘参数中，RA最能反映青光眼的视野平均缺损程度。     

糖尿病视网膜病变患者的血小板平均体积、红细胞平均体积临床分析

目的：探讨单纯型糖尿病视网膜病变（BDR）与血小板平均体积（MPV）、红细胞平均体积（MCV）、血小板计数（PLT）、细胞计数（RBC）的关系。方法：采用美国CD－1600型血液分析仪对BDR、Ⅱ型糖尿病（DM）、对照组共60例的MPV、MCV、PLT、RBC测定。统计学统计，方差分析。结果：对PLT分析（F＝4．76，F0．05＝3．50），DM组显著多于BDR组和对照组（P＜0．05）。对于MCV分析（F＝3．60，F0．05＝3．50），BDR组显著大于DM组（P＜0．05）。对BRC、MPV分析，各组无显著差异。结论：BDR患者MCV大可能是促进其发生的原因之一。     

糖尿病患者视网膜血管血氧饱和度变化研究

目的 观察糖尿病患者与健康人群视网膜血管血氧饱和度的差异.方法 临床确诊为糖尿病的71例(71眼)患者和91名(91眼)健康者分别纳入糖尿病组和正常组.采用视网膜血管血氧饱和度测量仪检测两组受检者,并应用仪器配套软件分析距离视盘中心1.5-3.0个视盘直径的视网膜动脉、静脉血氧饱和度值.结果 71例糖尿病患者中,男性与女性、各个年龄段、不同糖尿病病程间比较,视网膜动脉、静脉及其各象限分支动脉、静脉的血氧饱和度差异均无统计学意义(均为P ＞0.05).糖尿病组视网膜动脉血氧饱和度较正常组显著升高(P=0.00);糖尿病组视网膜动脉各象限的血氧饱和度均较正常组高,其中颞上分支、颞下分支与正常组相比差异均有统计学意义(均为P ＜0.05).糖尿病组视网膜静脉血氧饱和度较正常组有升高的趋势,但差异无统计学意义(P＞0.05);糖尿病组视网膜静脉血氧饱和度颞上分支、颞下分支较正常组高,鼻下分支较正常组低,差异均有统计学意义(均为P ＜0.05).糖尿病组视网膜动静脉血氧饱和度差值较正常组显著升高(P=0.00).结论 糖尿病患者视网膜血管血氧饱和度与健康人群存在显著差异;糖尿病患者不同象限的血管血氧饱和度存在不同程度的改变,提示视网膜氧代谢异常程度在各象限的分布并不均匀.     

准分子激光原位角膜磨镶术后视野分析

目的探讨准分子激光原位角膜磨镶术（LASIK）对患者视野的影响。方法对实施LASIK的近视患者46例（92只眼）术前、术后1d、1个月、3个月、6个月用Humphrey视野计30-2SITA快速阈值检测程序行视野检查。统计学分析采用配伍组设计的两因素方差分析,分析各时间点视野指数。结果视野检查中术后各时间点平均缺损（MD）与术前相比,差异均有统计学意义（P〈0．05）,但术后各时间点MD之间差异无统计学意义（P〉0．05）,术前视力与MD无显著相关性（P〉0．05）,但MD与术后各次检测视力均呈显著负相关（P〈0．05）。而模式标准差（PSD）在手术前后差异无统计学意义（P〉0．05）,PSD与术前视力呈显著相关性（P〈0．05）,但术后各次检测视力与PSD均无显著相关性（P〉0．05）。手术前后MD和PSD平均差值与术前屈光度、切削厚度、激光脉冲数、激光切削时间、负压吸引时间做Person相关分析均无相关性（P〉0．05）。结论LASIK前后视野连续观测无显著变化,说明LASIK对视网膜结构和功能的影响还不足以导致临床上显著的形态和视功能改变,对视网膜正常生理功能无明显影响。     

青光眼中倍频视野检查与Octopus视野检查的相关性

目的 评价青光眼中倍频视野计（Frequency Doubling Technique FDT）与传统自动视野计Octopus检查结果的相关性。方法 35例正常对照，27例可疑青光眼患者，37例原发性开角型青光眼和50例正常眼压性青光眼患者进行FDT和Octopus检查。记录FDT视野检查的平均缺损（MeanDefect，MD）、图形标准偏差（Pattem Standard Deviation，PSI）），Octopus视野检查中的平均缺损、丢失方差（Loss Variance，LV）。应用线性回归分析计算回归方程及相关系数。结果 原发性开角型青光眼中，FDT-MD与Octopus-MD，FDT-PSD与Octopus-LV均显著相关（r=0．828，r=0．758，P均＜0．001）。正常眼压性青光眼中，FDT-MD与Octopus-MD，PDT-PSI）与Octopus-LV均显著相关（r=0．827，r=0．783，P均＜0．001）。结论 FDT检查的各指标无论在POAG还是NTG中均与传统自动视野计Octopus有很好的相关性。     

mfERG分析雷珠单抗眼内注射对RVO合并黄斑水肿的疗效

目的：利用多焦视网膜电流图（ multifocal ERG,mfERG）对雷珠单抗（ranibizumab）治疗视网膜静脉阻塞合并黄斑水肿的患者黄斑区视网膜功能变化进行检测,分析雷珠单抗治疗黄斑水肿后视网膜功能的变化,评价雷珠单抗治疗黄斑水肿的效果。
　　方法：采用回顾性,自身对照研究方法,将临床确诊为视网膜静脉阻塞合并黄斑水肿的15例患者15眼纳入研究。所有患者均常规行矫正视力,裂隙灯显微镜,眼压,彩色眼底照相,FFA及OCT,中心10°视野,mfERG检查,矫正视力检查采用ETDRS视力表进行。所有患者玻璃腔注射雷珠单抗注射液0．05mL／0．5mg,治疗后随访3～12mo,每月复查一次。观察最佳矫正视力,眼压,眼底,中央黄斑厚度,中心10°视野,mfERG的变化。根据复诊情况,确定有无重复注射治疗的需要。以末次随访为疗效判定时间点,记录并分析治疗前及治疗后患者视野和mfERG的变化。结果：末次随访时,治疗前后中心视野平均缺损显著减少（t＝4．01,P＜0．01）,1环和2环N1波潜伏期、P1波潜伏期较治疗前显著降低（t＝13．65,16．31,P＜0．01）,1环P1波反应密度值与治疗前相比提高,差异有统计学意义（t＝7．78,P＜0．01）。
　　结论：玻璃体腔注射雷珠单抗治疗静脉阻塞继发黄斑水肿预后较好,有利于改善患者黄斑区视网膜的敏感度。mfERG方法能准确客观的反应黄斑水肿患者视网膜功能变化,具有较高的临床应用价值。     

应用SD-OCT纵向比较正常人群和青光眼进展及非进展人群的RNFL厚度

目的：应用频域光学相干断层扫描（ spectral－domain optical coherence tomography ,SD－OCT）纵向比较正常人群、青光眼进展及非进展人群的视网膜神经纤维层（ retinal nerve fiber layer ,RNFL）厚度。方法：应用SD－OCT对36例POAG患者和24例正常人监测RNFL厚度。受试者行视盘OCT、眼底照相及视野检查,每6mo一次,随访2a,至少有4次可信的OCT检查结果。根据视野及眼底照相结果将POAG患者划分为进展组和非进展组。分析各组RNFL厚度变化差异,同视野参数变化值做相关性分析。结果：平均随访2．1±0．3 a。17例被确定为POAG进展组。POAG进展组平均RNFL厚度损失速率明显高于POAG非进展组（2．46μm／a vs 1．21μm／a,P＜0．001）。下方RNFL厚度变化同视野平均偏差（ mean deviation ,MD）变化相关性最佳（r＝0．423,P＝0．03）。结论：应用SD－OCT纵向监测RNFL厚度, POAG进展者RNFL厚度丢失速率明显增高,下方RNFL厚度参数变化可能在监测中意义较大。     

银杏叶提取物对糖尿病视网膜病变的临床疗效评价

目的：探讨银杏叶提取物对轻中度非增生期糖尿病视网膜病变的临床疗效。方法：采用随机对照试验,将轻中度非增生期糖尿病视网膜病变患者80例150眼随机分为对照组和治疗组,治疗组41例78眼,对照组39例72眼。对照组给予拜阿司匹林肠溶片100mg,口服,1次／d。在上述治疗的基础上,治疗组患者加用银杏叶酊2 mL,口服,3次／d 进行干预。6 mo后,观察并分析两组患者视神经病变的总体疗效、视力、视野平均缺损、眼底荧光血管造影结果、血脂水平、血小板聚集率及血小板粘附率的改善情况。结果：治疗后,治疗组患者视网膜病变的总有效率为75．6％,显著高于对照组58．7％（ Z ＝2．6002, P ＝0．0047）;治疗组患者的视力显著提高,和视野平均缺损显著减少,差异均有统计学意义（t＝－2．01,P＝0．0477;t＝4．06,P＝0．0001）;治疗组患者的视网膜微血管瘤数、出血面积均显著减少,差异均有统计学意义（ t＝7．86,P ＜0．01;t＝3．13,P＝0．0024）;治疗组患者的血清总胆固醇、甘油三脂、低密度脂蛋白胆固醇水平均下降,高密度脂蛋白胆固醇升高,差异有统计学意义（t＝2．25,P＝0．0270;t＝3．41,P＝0．0010;t＝3．34, P＝0．0013;t＝3．76, P＝0．0003;t＝－3．30,P＝0．0014）;治疗组患者的血小板聚集率和血小板粘附率均下降,差异均有统计学意义（t＝4．31,P ＜0．01;t＝4．93,P ＜0．01）。结论：银杏叶提取物对轻中度非增生期糖尿病视网膜病变具有确切疗效。     

频域OCT检测RNFL厚度在原发性青光眼早期诊断中的意义

目的 应用频域光学相干断层成像技术(optical coherence tomography,OCT)检测CACG和POAG患者的视网膜神经纤维层(retinal nerve fiber layer,RNFL)厚度,探讨其与视野平均缺损(mean defect,MD)的相关性,并揭示早期原发性青光眼RNFL厚度的特征性改变,从而客观评价频域OCT在原发性青光眼早期诊断中的临床应用价值.方法 分别采用Zeiss Cirrus HD-OCT 4000型和Zeiss Humphrey 750型全自动视野计对正常组20例(40只眼)和分成早期、中期、晚期的原发性青光眼组30例(52只眼)进行检测,将各个青光眼组中心30°视野内的MD和OCT检测的RNFL厚度进行比较,并做相关性分析.结果 青光眼组RNFL厚度及视野MD程度与正常对照组差异均有统计学意义,其中正常人RNFL厚度为(112.91±9.36)μm,早期青光眼组为(94.43±7.67) μm,中期青光眼组为(80.82±10.36) μm,晚期青光眼组为(67.86±8.01)μm;正常人视野MD为(-0.88±1.53)dB,早期青光眼组为(-4.26±1.83)dB,中期青光眼组为(-7.43±2.64)dB,晚期青光眼组为(-17.06±5.85) dB.青光眼组RNFL与视野MD具有负相关,其中早期青光眼组相关系数为-0.537;中期青光眼组为-0.615;晚期青光眼组为-0.804.早期青光眼组各象限RNFL厚度为:上方(116.32±11.65) μm;下方(105.58±9.73)μm;鼻侧(75.40±10.91)μm;颞侧(70.28±13.08) μm.B组各象限RNFL厚度分别为:上方(140.15±8.79)μm;下方(137.29±10.07) μm;鼻侧(90.20±14.19) μm;颞侧(88.43±10.85)μm.经独立样本t检验A1组与B组上方及下方RNFL厚度差异有统计学意义(P＜0.05),而鼻侧及颞侧差异无统计学意义(P＞0.05).结论 (1)频域OCT检测各期原发性青光眼患者的RNFL平均厚度随病程进展逐渐变薄.(2).频域OCT检测原发性青光眼患者的RNFL平均厚度与视野MD具有负相关性,能够客观地反应出青光眼视神经损害程度.(3)早期原发性青光眼患者中上方、下方RNFL厚度均已明显变薄,通过频域OCT对上述两个RNFL厚度参数的检测,有助于更早地发现原发性青光眼的视神经损害,为青光眼的早期诊断带来一定的临床应用价值.     

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.     

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.     

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.     

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。     

Long Noncoding RNA 3632454L22Rik Contributes to Corneal Epithelial Wound Healing by Sponging miR-181a-5p in Diabetic Mice

PurposeThis work explores the abnormal expression of long noncoding RNAs (lncRNAs), microRNAs (miRNAs) and messenger RNAs (mRNAs) in diabetic corneal epithelial cells (CECs) and constructs an associated competitive endogenous RNA (ceRNA) network. Moreover, we revealed that Rik may exert advantageous effects on diabetic corneal epithelial wound closure by sponging miR-181a-5p.MethodsWe obtained the profiles of differentially expressed lncRNAs (DELs) of CECs of type 1 diabetic versus control corneas by microarray and summarized the differentially expressed miRNAs (DEmiRs) and differentially expressed genes (DEGs) data by published literature. Subsequently, the ceRNA network was constructed using bioinformatics analyses. The levels of lncRNA ENSMUST00000153610/3632454L22Rik (Rik) and miR-181a-5p were verified. The localization of Rik was identified with fluorescence in situ hybridization (FISH), and dual-luciferase assays proved the targeted relationship between Rik and miR-181a-5p. Furthermore, we validated the functional impact of Rik in vitro.ResultsOverall, 111 upregulated and 117 downregulated DELs were detected in diabetic versus control CECs. The level of Rik located in both the cytoplasm and the nucleus was clearly downregulated, whereas miR-181a-5p was upregulated in vitro and in vivo in the diabetic group versus the control group. Rik can act as a ceRNA to bind to miR-181a-5p, thus promoting diabetic corneal epithelial wound healing in vitro.ConclusionsThis work investigated the expression profile of DELs and constructed ceRNA networks of diabetic CECs for the first time. Furthermore, we revealed that Rik may positively impact diabetic corneal epithelial wound healing by sponging miR-181a-5p, providing a novel potential therapeutic target of diabetic keratopathy (DK).     

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.     

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.