363例原发性慢性闭角型青光眼的小梁组织学改变及临床病理分析

目的:观察慢性闭角型青光眼的小梁组织学改变,结合临床资料探讨周边虹膜前粘连程度与小梁病变的关系.方法:对慢性闭角型青光眼手术切除的小梁标本用10%福尔马林溶液固定，火棉胶包埋，苏木素-伊红染色，光镜下观察。结果：经组织学检查确定为小梁组织的共363例（412眼），小梁均显示不同程度的纤维化，小梁网及内皮细胞中有程度不等色素沉积，内皮细胞数减少或消失。Schlemm管压缩或闭塞，虹膜萎缩变性，周边部虹膜与小梁粘连者病变明显。凡有反复发作性眼压升高史，视力，视盘，视野有损害，周边前房深度≤1/3CT～1/4CT，前房角为窄Ⅲ～Ⅳ的病均显示出不同程度的周边虹膜前粘连，小梁纤维化，色素沉积，Schlemm管压缩或闭塞；且眼压控制不良，病程越长，则周边虹膜前粘连越广泛，小梁损害越显著。     

原发性闭角型青光眼虹膜基质中Ⅰ,Ⅲ,Ⅳ型胶原纤维的表达

目的:研究原发性闭角型青光眼虹膜基质胶原纤维含量的变化,为虹膜生物力学及闭角型青光眼发病机制的研究提供依据。方法:取排除内眼、外眼疾患的人眼根部虹膜11例,闭角型青光眼虹膜根部切除标本29例,置于40g/L甲醛溶液中固定48h,常规石蜡包埋,进行免疫组织化学染色。结果:Ⅰ,Ⅲ,Ⅳ型胶原在人眼虹膜中均有表达,其中I型胶原纤维在患者组表达减少,与正常组比较差异有显著性(P<0.05),Ⅲ,Ⅳ型胶原纤维的表达在两组无明显差异(P>0.05)。结论:原发性闭角型青光眼虹膜基质中Ⅰ型胶原纤维的表达减少提示其虹膜根部与正常眼相比具有较低的抗张能力,易导致周边虹膜向前膨隆而促发房角关闭。     

虹膜周边切除术后眼压不降原因分析

虹膜周边切除对解除原发性急性闭角型青光眼临床前期,先兆期、缓解期以及慢性闭角型青光眼早期的瞳孔阻滞,防止青光跟发作的疗效,已得到充分肯定。近5年来,我们曾遇到20例被诊断为原发性急性闭角型青光眼缓解期和慢性闭角型青光眼早期,并行虹膜周边切除术后眼压不降的患者。为了提高对原发性闭角型青光眼的诊断水平,更好地掌握虹膜周边切除术的适应征。现对20     

激光周边虹膜成形术治疗虹膜切除术后暗室俯卧试验阳性的原发性闭角型青光眼

目的　评价激光周边虹膜成形术治疗虹膜切除术后暗室俯卧试验阳性的原发性闭角型青光眼的临床效果。方法　对激光周边虹膜切除术后暗室俯卧试验阳性的 34例 (5 6只眼 )原发性闭角型青光眼 (非眼外引流手术指征 ,前房角粘连 <1/2周前房角范围 )患者行激光周边虹膜成形术。其中急性闭角型青光眼 2 7例 (49只眼 ) ,慢性闭角型青光眼 7例 (7只眼 )。对患者治疗前后的周边前房深度、前房角、眼压、视野及周边虹膜形态进行详细的对比观察 ,并行暗室俯卧试验及散瞳试验检查。患者术后随访 1～ 4年。结果　所有患者治疗后周边前房深度均明显加深 ,静态前房角镜检查小梁网可见范围增宽。随访期间患者未发生高眼压、前房角进行性粘连及视野损害 ,暗室俯卧试验及散瞳试验均阴性。结论　虹膜切除术后暗室俯卧试验阳性的原发性闭角型青光眼的发病机制是当瞳孔散大时 ,异常的周边虹膜组织堵塞小梁网而引起高眼压 ,瞳孔阻滞因素不起主导作用。激光周边虹膜成形术可以明显改变此类青光眼患者 (前房角粘连 <1/2周前房角范围 )的周边虹膜形态 ,从而控制病情进展。     

组织型谷氨酰胺转移酶在开角型青光眼患者房角组织的表达

目的探讨组织型谷氨酰胺转移酶(tissue transglu-taminase,tTG)在原发性开角型青光眼患者房角组织中的表达情况及其与闭角型青光眼患者和正常人眼房角组织中表达情况的比较。方法术中取青光眼患者房角组织,采用免疫组织化学染色方法观察开角型、闭角型青光眼患者及正常人房角组织内tTG的表达情况,用RT-PCR方法分析组织内tTG的表达水平。结果免疫组织化学及RT-PCR结果均显示,正常组与闭角型青光眼组房角tTG的表达差异并无显著性(分别为0.180±0.032,0.212±0.019,P>0.05),而正常组与开角型青光眼组、闭角型青光眼组与开角型青光眼组房角组织tTG的表达差异有极显著性(分别为0.180±0.032,0.325±0.052;0.212±0.019,0.325±0.052,P<0.01)。结论开角型青光眼房角组织tTG的表达增加,tTG的增加可能与开角型青光眼的发病有关。     

国内原发性闭角型青光眼治疗方案及手术指征的问卷调查

目的 了解眼科医生对原发性闭角型青光眼的主要治疗方法的选择及其依据.方法 在第十届全国眼科会议期间(2005年9月11日)于青光眼会场参会的眼科医生.采用问卷调查的形式,调查表内容包括:被调查者基本信息、对原发性闭角犁青光眼治疗方法的选择及选择依据.主要分析调查眼科医生中针对不同类型闭角型青光眼进行不同治疗方法选择的比例和不同手术指征的比例.结果 共发出问卷表330份,收回293份.接受本次问卷调查的与会代表涵盖了29个省市.经过逻辑检查和完整型检查,有效问卷262份,有效应答率为79.4%.在被调查的医生中53.1%(139/262)的医生认为,氩激光周边虹膜成形术可以用于急性闭角型青光眼的治疗,31.3%的医生使用过氩激光周边虹膜成形术治疗急性闭角型青光眼.对于早期原发性闭角型青光眼,39.3%(103/262)的医生选择药物作为首选治疗方案,而58.8%的医牛选择激光周边虹膜切除术作为首选.急性闭角型青光眼中进行小梁切除术的比例为66.5%,而对慢性闭角型青光眼,73.3%的医生选择小梁切除术作为首选的治疗方式.43.1%的医生在闭角型青光眼的小梁切除术中常规使用了可拆除缝线技术,而18.3%的医生从不使用.结论 国内闭角型青光眼进行滤过手术的比例较高,原因可能在于眼科将小梁切除术作为了闭角型青光眼治疗的一线治疗方案;采用激光方式进行周边虹膜切除术,由于设备原因在国内还远未普及;可拆除缝线技术在闭角型青光眼的应用率较低.     

周边虹膜切除术后疗效分析

目的探讨周边虹膜切除术的适应证及疗效。方法对闭角型青光眼患者，房角开放超过2／3，行周边虹膜切除术，术后随诊4～10年，统计眼压升高及进行性视野损害情况。结果在本组病例2986例2996眼中，均行周边虹膜切除术，随诊4～10年，眼压控制在21mmHg以下者2086眼，其中，急性闭角型青光眼1234眼，慢性闭角型青光眼852眼；眼压高于30．39mmHg，有进行性视神经损害者610眼，其中急性闭角型青光眼54眼，慢性闭角型青光眼556眼。结论以往对闭角型青光眼的发病机制及类型认识不足，不能很好地掌握周边虹膜切除术的适应证，今后应对闭角型青光眼要多做检查，特别是超声生物显微镜，以确定类型和发病机制，正确选择手术方式。     

应用Nd—YAG激光周边虹膜切除术治疗闭角型青光眼

原发性闭角型青光眼发病机理的瞳孔阻滞学说,已为人们所公认。因此,在疾病的早期,若能施行周边虹膜切除术,则可中断疾病的病理进程,从而达到预防和治疗闭角型青光眼的目的。特别是慢性闭角型青光眼,其病情进展较为隐蔽,早期常常是虹膜与小梁网功能性相贴。若治疗及时可使房角重新开放。因之,对慢性闭角型青光眼的早期诊     

小梁切开联合虹膜根切术治疗原发性闭角型青光眼

目的 观察外路小梁切开术联合虹膜周边切除治疗原发性闭角型青光眼的疗效.方法 对31例(31眼)原发性闭角型青光眼行外路小梁切开及虹膜周边切除术.其中急性闭角型青光眼22例,慢性闭角型青光眼9例.术后1周,1、3、6个月观察患者眼压和房角情况.结果 术后1个月和3个月,不用降眼压药眼压≤21 mm Hg(1 mm Hg=0.133 kPa)者分别为29例和27例,完全成功率分别为93.5%和87.1%.19例(19眼)随访6个月,不用降眼压药眼压≤21 mm Hg者16例(84.2%).术后房角检查显示上方120°范围房角开放和小梁组织切开的裂隙.术后并发症:前房出血31眼,均自行吸收,后弹力层损伤6眼、虹膜根部断离2眼、虹膜后粘连4眼.结论 外路小梁切开联合周边虹膜切除术能有效治疗原发性闭角型青光眼.     

激光周边虹膜成形术治疗原发性闭角型青光眼房角相关结构的超声生物显微镜观察

目的应用超声生物显微镜(ultrasoundbiomicroscopy,UBM)观察激光周边虹膜成形术治疗原发性闭角型青光眼房角结构的变化,进一步做疗效评价。方法对原发性闭角型青光眼经虹膜切除术后暗室俯卧试验阳性的31例38眼行激光周边虹膜成形术治疗,治疗前后均行眼前节裂隙灯显微镜、房角镜及UBM检查,对于治疗后无发作性眼压升高且连续两次暗室俯卧试验阴性的病例,应用0.5%托吡卡胺点眼散瞳后再行上述检查。结果36眼(94.7%)成功治愈。表现为:无青光眼发作、连续两次暗室俯卧试验阴性且散瞳试验均阴性。所有病例经治疗后周边前房深度均明显加深,静态房角镜检查小梁网可见范围增宽。UBM检查显示周边虹膜形态较术前明显变薄而平直,500um处小梁虹膜夹角(TIA500)、250um和500um处前房角开放距离(AOD250、AOD500)均较术前显著增加(p<0.01),周边虹膜厚度(IT1)明显变薄(p<0.01)。术后观察(1～2)年,疗效稳定且未见明显并发症。结论激光周边虹膜成形术可有效的改变周边虹膜形态,增加前房角宽度,防止瞳孔散大所造成的周边虹膜堆积,是治疗虹膜切除术后仍有急性发作或激发试验阳性的原发性闭角型青光眼安全、有效的治疗方法。     

Localization of myocilin/trabecular meshwork--inducible glucocorticoid response protein in the human eye

PURPOSE: To study distribution and cellular localization of myocilin/trabecular meshwork-inducible glucocorticoid response protein (TIGR) in the human eye. METHODS: A peptide antibody against a portion of the myosin-like domain of myocilin/TIGR was developed. Different ocular tissues from three human donors were investigated by one- and two-dimensional gel electrophoresis and Western blot analysis. Immunohistochemistry was performed on 25 human eyes enucleated because of posterior choroidal melanoma and on 7 normal human donor eyes. RESULTS: By Western blot analysis, a band at approximately 57 kDa was visualized in cornea, trabecular meshwork, lamina cribrosa, optic nerve, retina, iris, ciliary body, and vitreous humor. By immunohistochemistry, immunoreactivity for myocilin/TIGR was observed in cells of the corneal epi- and endothelium and extracellularly in the corneal stroma and sclera. In the trabecular meshwork, cells of the uveal and corneoscleral meshwork were stained, as was the cribriform area directly adjacent to Schlemm's canal. Positive staining was seen in cells of the ciliary epithelium, ciliary muscle, lens epithelium, and in stromal and smooth muscle cells of the iris. Throughout the entire vitreous body, fine filamentous material was positively labeled. In the retina, staining was seen along the outer surface of rods and cones, in neurons of the inner and outer nuclear layer, and in the axons of optic nerve ganglion cells. Optic nerve axons were stained in the prelaminar, laminar, and postlaminar parts of the nerve. In the region of the lamina cribrosa, astrocytes in the glial columns and cribriform plates were positively labeled. CONCLUSIONS: Myocilin TIGR is expressed in almost every ocular tissue. Depending on the respective tissue, it is observed extra- or intracellularly. The presence of myocilin/TIGR in optic nerve axons and lamina cribrosa astrocytes indicates that the trabecular meshwork might not be the only target of abnormal myocilin/TIGR in GLC1A-linked open-angle glaucoma.     

MMP-1、TIMP-1及TIMP-2在正常人眼前段组织的表达

目的观察正常人眼前段组织中基质金属蛋白酶1(MMP-1)、基质金属蛋白酶抑制剂1(TIMP-1)和TIMP-2的表达,探讨正常生理状态下MMP及TIMP在小梁网房水流出及葡萄膜巩膜房水流出通道中的作用。方法应用酶免疫组织化学技术,检测正常人眼前段组织中MMP-1、TIMP-1和TIMP-2的定位。阳性结果应用图像分析系统进行定量分析。结果免疫组织化学结果显示MMP-1和TIMP-2广泛分布于人眼的虹膜、睫状体(包括睫状突上皮细胞和睫状肌)、小梁网、视网膜色素上皮(RPE)层、脉络膜及巩膜,TIMP-1分布于除小梁网外的其余组织。结论MMP-1、TIMP-2广泛分布于人眼小梁网及葡萄膜巩膜房水流出通道、RPE、脉络膜,TIMP-1广泛分布于人眼葡萄膜巩膜房水流出通道及RPE、脉络膜,对维持人眼正常房水流出及维持RPE、脉络膜功能可能具有一定作用。     

Mucogenic secondary open-angle glaucoma in diffuse epithelial ingrowth treated by block-excision

We treated a 40-year-old man with an acute, unilateral, open-angle glaucoma caused by a gelatinous translucent material in the anterior chamber. A clinical diagnosis of mucogenic secondary open-angle glaucoma caused by diffuse epithelial ingrowth after ocular trauma one year earlier was suspected, but a primary or secondary ciliary body or iris neoplasm could not be ruled out. A curative 9-mm block-excision was performed. Six years later, intraocular pressure was normal, and the visual function was unchanged. Light and electron microscopy disclosed an island of diffuse columnar epithelium with numerous goblet cells on the iris surface and copious mucinous material extending into the trabecular mesh-work.     

Extracellular glycoproteins of the ocular trabecular zone in patients with primary open-angle glaucoma

The content of fibronectin, an extracellular glycoprotein, in the drainage out-flow system of human eyes was measured by the indirect immunoperoxidase staining technique. The degree of fibronectin accumulation in ocular tissues was evaluated by quantitative morphometric analysis. Fibronectin level in the ocular drainage system of humans grows with ageing and rapidly increases at different stages of primary open-angle glaucoma development. Increased deposit of fibronectin in trabecular tissue, mainly in the inner wall of Schlemm's canal and juxtacanalicular or cribriform part of trabecular meshwork, was demonstrated. A hypothesis explaining the development of the glaucomatous process by an adhesive impairment is proposed.     

The histopathology of pigmentary dispersion syndrome with glaucoma.

Iris tissue and trabecular meshwork, obtained at time of trabeculectomy, was studied using the light and electron microscope in a 54-year-old woman with pigmentary dispersion syndrome with glaucoma. The specific defect was a loss of the outer epithelial cells of the iris with marked thinning of the remaining outer layers so that the two-cell architecture of the iris epithelium was maintained. In addition, the radial muscle layer was increased in both number and size of muscle fiber. It would appear that the pigmentary dispersion syndrome may represent a congenital or developmental abnormality of the iris epithelium, or both, and that the glaucoma which occasionally occurs in conjunction with this syndrome is of the usual open-angle type.     

Ultrasound biomicroscopical study of the irido-corneal angle in dominant juvenile open-angle glaucoma, in POAG, and in normal eyes.

PURPOSE: To compare various parameters of the chamber angle in a pedigree with dominant goniodysgenesis and juvenile open-angle glaucoma linked to chromosome 1q, GLC1A, with those in patients with adult-onset primary open-angle glaucoma, and in normal eyes. METHODS: Ultrasound biomicroscopy was performed on 10 eyes with dominant goniodysgenesis and juvenile open-angle glaucoma, on 12 eyes with adult-onset primary open-angle glaucoma, and 24 normal eyes. Eight parameters were measured. RESULTS: The anterior chamber angle, angle opening distance 500 microm from the scleral spur, trabecular meshwork--iris distance, and trabecular meshwork--iris pigment epithelium distance were statistically significantly higher in the group with juvenile glaucoma. CONCLUSION: The wider chamber angle in dominant juvenile open-angle glaucoma could suggest a more complex anomaly with involvement of cornea and iris in addition to goniodysgenesis. The presence of goniodysgenesis in the dominant juvenile open-angle glaucoma patients could not be detected by ultrasound biomicroscopy, however.     

Relevance of the pseudoexfoliation syndrome for the glaucomas

Secondary chronic open-angle glaucoma associated with pseudoexfoliation (PEX) syndrome accounts for approximately 25% of all glaucomas and represents the most common identifiable cause of glaucoma overall. The underlying disorder, PEX syndrome, is a generalized process of the extracellular matrix characterized by production and progressive accumulation of an abnormal extracellular material in many intra- and extraocular tissues. Recent data support the pathogenetic concept of PEX syndrome as a type of elastosis affecting particularly elastic microfibrils. Active involvement of the trabecular meshwork in this characteristic matrix process may lead to glaucoma development in 40-60% of the patients. In addition, PEX syndrome also represents an important risk factor for a broad spectrum of spontaneous or intra- and postoperative ocular complications as well as for systemic cardiovascular diseases. PEX-associated open-angle glaucoma represents a relatively severe and progressive type of glaucoma with a generally poor prognosis due to high intraocular pressure levels and fluctuations in the diurnal pressure curve. The primary cause of chronic pressure elevation appears to be local production of PEX material by trabecular meshwork cells and Schlemm's canal cells with subsequent degenerative changes of Schlemm's canal and juxtacanalicular tissues. Additional pathogenetic factors contributing to pressure increase include pronounced melanin dispersion, increased protein concentrations of the aqueous humor, vascular factors, and connective tissue alterations of the lamina cribrosa. Other types of glaucoma, such as acute open-angle glaucoma, provoked by melanin showers during diagnostic mydriasis, or secondary angle closure glaucoma due to pupillary or ciliary block, are also common in PEX patients. The pathogenetic factors TGF-beta1 and TIMP-1/2 appear to be causally involved in this fibrotic process and thus may represent potential targets for specific, rational therapeutic approaches.     

The similarity of protein expression in trabecular meshwork and lamina cribrosa: implications for glaucoma

The purpose of the present investigation was to compare protein expression in various ocular cells and tissues including the human trabecular meshwork (TM) and the lamina cribrosa (LC). To conduct the comparisons, we primarily utilized autofluorography of one-dimensional (1D) and high resolution, two-dimensional (2D) polyacrylamide gels of proteins from radiolabelled tissues and cultured cells. Results from the investigations indicated that patterns of protein expression from TM and LC were the most similar among the ocular cells and tissues compared.Specifically, these autofluorographic ' fingerprints' indicated that proteins in TM and LC cultured cells and tissue were exceptionally similar (a) in band position and intensity (1D gels) and (b) in spot congruence (2D gels) as compared to other ocular cells and tissues. We conclude that the TM and the LC, two ocular tissues intimately linked to the pathogenesis of primary open-angle glaucoma, display remarkable similarity in protein expression. This finding may have implications for the molecular etiology of glaucoma.     

Immunolocalization of CYP1B1 in normal, human, fetal and adult eyes

CYP1B1 is a cytochrome P450 enzyme implicated in autosomal recessive primary congenital glaucoma (PCG). The mechanism and function of CYP1B1 in the development of the PCG phenotype is unknown. Previously, investigators have reported detection of Cyp1b1 mRNA in the ciliary body and epithelium and neuroepithelium in the developing mouse eye, employing in situ hybridization techniques. Similarly, additional investigators have detected CYP1B1 mRNA in the iris, ciliary body, non-pigmented ciliary epithelial line, cornea, retinal-pigment epithelium, and retina in the human adult eye, using Northern blotting. This study was designed to immunolocalize CYP1B1 protein in the various ocular structures of normal, human fetal and adult eyes. Normal fetal and adult eyes were immunolabeled with a polyclonal antibody against human CYP1B1 using indirect immunofluorescence, and then compared with appropriate controls. The intensity of immunolabeling of the various ocular structures was assessed by qualitative and semi-quantitative techniques. In the anterior segment anti-CYP1B1 immunoreactivity (IR) was detected early in fetal development in the primitive ciliary epithelium. As well, the most intense CYP1B1 IR was in the non-pigmented ciliary epithelium. In addition, CYP1B1 IR was also present in the corneal epithelium and keratocytes, both layers of the iris pigmented epithelium, and retina. However, CYP1B1 IR was absent in the trabecular meshwork in all of the samples. In general, CYP1B1 immunolabeling in the human fetal eyes was more intense when compared to adult eyes. CYP1B1 IR was primarily immunolocalized to the non-pigmented ciliary epithelium and early in fetal development. In addition, CYP1B1 IR was not detected in the trabecular meshwork. These findings suggest that the abnormalities in the development of the trabecular meshwork in PCG may result from diminished or absent metabolism of important endogenous substrates in the ciliary epithelium due to non-functional CYP1B1 enzyme.