晶体囊内摘出后剥脱综合征的发作

作者(1976)对一例剥脱综合征观察结果认为Bertelsen等提出的来自晶体上皮的纤维物质通过囊膜而呈现在晶体表面的理论是不够确切的。而作者认为晶体表面的物质是与有病的虹膜色素上皮接触沉积而来,或间接地来自睫状上皮。而在晶体内形成的物质不能穿过纤维层和带状板层。作者报告一例女性89岁双眼剥脱综合征患者,在顺利地囊内摘除白内障后15年期间,剥脱物质在玻璃体上不断增加以证明其论点。后又见2例在晶体囊内摘除时,未见有剥脱综合征,但1     

晶体囊和囊下上皮的超微结构——胎儿及成人晶体透射电镜和扫描电镜观察

对胎儿、正常成人晶体囊和囊下上皮进行透射电镜和扫描电镜观察。晶体囊由细纤维状结构组成,表层疏松,深层较致密,二者无截然界限,未看到光镜下的两层结构。成人晶体囊的结构型式不随年龄增长而发生变化。18～65岁赤道前部及赤道部的晶体囊内有包涵物形成。在赤道部晶体囊的浅层看到插入的悬韧带纤维。晶体前囊下及赤道前部上皮细胞内见到纤毛。     

基底膜剥脱综合征

最近20年内,许多学者应用电子显微镜检查拟确定有争议的所谓“晶体囊膜假性剥脱”的性质及其起源。“假性剥脱”是1954年Dvorak-Theobald提出,旨在把这种假想的晶体囊膜沉着物区别于晶体囊膜内的真正的分离即“真性”晶体囊膜剥脱。Bertelsen等(1964)和Ashton等(1965)分别发表其电子显微镜检查所见,明确指出产生此种脱落物质的是晶体上皮,这种脱屑能穿过邻近赤道部的晶体前囊。其后许多人对老年人晶体或病眼的检查都同意这种说法。目前有证据(包括临床观察所见)说明虹膜和睫状上皮也能产生脱落物质。此外,不论临床有无病变,     

伴有剥脱综合征的青光眼房水动力学研究

剥脱综合征(exfoliation syndrome)常伴有房水动力学方面的异常。某些伴有青光眼的人,对药物的治疗反应极差。白色的剥脱物出现在睫状突、晶体韧带、晶体表面和虹膜瞳孔缘,偶而可在角膜后及小梁上见到。多见于老年人,但年青人中也有报导,双眼者较多见,但临床上表现为不对称者也不少见。电镜研究证明剥脱物质具有一     

糖尿病患者的老年白内障晶体上皮细胞超微结构及酶组织化学变化的研究

目的 :研究糖尿病患者的老年障晶体上皮细胞超微结构及酶组织化学变化 ,探讨该类型白内障发病的可能机制。方法 :应用眼组织透射及扫描电镜和酶组织化学的制作方法 ,对 17只糖尿病患者的老年障眼的晶体前囊膜上皮细胞进行研究 ,5只同年龄组老年障眼的前囊膜上皮组织为对照组。结果 :发现糖尿病患者的老年障眼的晶体上皮细胞膜出现水泡、细胞核固缩、溶解。胞浆中线粒体减少 ,并发生气球样变和形成髓鞘样结构。细胞变形 ,指状突起增多 ,可见细胞核丢失、死亡细胞及细胞脱落后残存的细胞框架。晶体上皮细胞由琥珀酸脱氢酶 (SDH )、乳酸脱氢酶 (LDH)、葡萄糖 -6-磷酸脱氢酶 (G -6-PD)、ATP酶 (ATPase)活性下降并维持于低水平。结论 :晶体前囊膜上皮细胞的变性可能是糖尿病患者的老年障形成的形态学基础 ,而晶体上皮细胞中参与能量代谢的各种酶活性降低 ,使Na -K 泵功能失调 ,晶体细胞肿胀破坏。     

假性剥脱症眼内的酸性磷酸酶

有关假性囊膜剥脱的来源问题,历来有许多说法。早年,Vogt(1926)认为是晶体周边部囊膜的分离和剥落。Gifford(1957)和Sugar(1976)提出与小带层有关。但是Busacca从组织学上不能证明有囊膜分裂,认为这是一种来源不明的不能确定的物质。为了有别于热性晶体囊膜剥脱有人建议使用假性剥脱(Pseudoexfoliation)一词(以下简称“剥脱”)。近年来,透射电镜和扫描电镜的研究证明,真正的晶体表面囊膜剥脱是     

剥脱综合征的房角所见

剥脱综合征是一种不明原因的灰白色物质沉积于晶体、虹膜、睫状小带和睫状突等部位的疾病,亦可沉积于角膜内皮和前房角。这种脱落物可为多源性,可能是老化细胞合成的异常基底膜所导致的结果。在房角下部Schwalbe线以前的角膜内皮有一波浪形色素线被作为剥落综合征的一个特点。青光眼伴有剥脱综合征已被明确地证实。作者从1982年1月到1983年5月共研究88例剥脱综合征患者,有12例由于外伤、葡萄膜炎、激光小梁成形术和内眼手术等外来因素影响房角所见而被除外。所有患者均作了视盘照相、眼压测量、视野检查和房角检查。并随机选择80例原发性青光眼作对比观察。房角检查内容包括:(1)房角结构,周围虹膜曲度和虹膜附着位     

剥脱综合征

一、历史背景多年来关于剥脱综合征(Exfoliation Syndrome)有许多描述和命名,Vogt(1925)首次提出老年性晶体囊膜剥脱和晶体囊膜性青光眼(Senile exfoliation of the lens capsule and glaucoma capsular),以后又有老年性炎性青光眼(Glaucoma senilis),晶体囊膜假性剥脱(Pseudoexfoliation of the lens capsule)等名称。电子显微镜研究证实除晶体囊膜外,眼的其他结构如房角小梁、睫状体、虹膜、结膜等都存在着剥脱物质。晶体摘出后,剥脱物质仍存在于玻璃体前表面,说明晶体囊膜并不是剥脱物质的唯一来源。鉴于眼的多种结构被累及,所以Sunde(1956)称之为剥脱综合征,这个名称是迄今为止最能为大家所接受的。Eagle等(1979)发现睫状体后短动脉被累及,提示剥脱综合征是一种基底膜疾病,因而命名为基底膜剥脱综合征(Basement Membrane Exfoliation Syndrome)。     

剥脱综合征性青光眼

剥脱综合征（Exfoliation Syndrome XFS）是一种常见的年龄相关的系统性疾病，其特点为一种纤维状的细胞外物质在许多眼部组织中的产生和进行性蓄积，类似的物质在皮肤、内脏器官的结缔组织中也被发现。其临床特征为细小的、白色头皮屑样物质沉积在眼前段组织中，最常见于瞳孔缘及晶体前囊膜。除了剥脱物沉积，另一个重要体征是眼前节色素的脱失与沉积。近来XFS已被认为是导致青光眼的最常见原因，在一些国家它是大多数青光眼的产生原因。     

晶体囊真性剥脱

晶体囊真性剥脱是晶体前囊的剥脱。患者78岁,男性。主诉:左眼视物不清。检查:视力:右0.3,左0.1。眼压:右14mmHg,左12mmHg。双眼均在前房中可见到薄而透明的玻璃纸样膜,晶体核及后囊下有混浊。左眼底可见到黄斑破口,但未见到视网膜脱离。房角双眼均为宽角,色素沉着正常,未见剥脱物质。前房中可见到的膜状物与晶体前囊相连     

Long anterior zonules and pigment dispersion

PURPOSE: To describe pigment dispersion associated with long anterior zonules. DESIGN: Multicenter observational case series. METHODS: Fifteen patients, seven of whom were treated for glaucoma or ocular hypertension, were identified with long anterior zonules and pigment dispersion. Transmission electron microscopy was performed on one anterior capsule specimen. RESULTS: All patients had anterior zonules that inserted centrally on the lens capsule. Signs of pigment dispersion included corneal endothelial pigmentation, loss of the pupillary ruff, and variable trabecular meshwork pigmentation. Ultrasound biomicroscopy verified the lack of posterior iris insertion and concavity. There was no exfoliation material. Transmission electron microscopy showed zonular lamellae with adherent pigment granules, and no exfoliation material. CONCLUSIONS: Long anterior zonules inserted onto the central lens capsule may cause mechanical disruption of the pigment epithelium at the pupillary ruff and central iris leading to pigment dispersion.     

Clinical signs of the pseudoexfoliation syndrome

Pseudoexfoliation syndrome (PXS) is a common cause of glaucoma throughout the world. It is most commonly diagnosed after the observation of pseudoexfoliation material (PXM) on the anterior lens surface. However, there are numerous clinical signs of PXS that should alert the examiner to search carefully for PXM on the anterior lens surface. These include pupillary ruff defects, iris sphincter transillumination, a characteristic whorl-like pattern of particulate pigment deposition on the iris sphincter, particulate pigment deposition on the peripheral iris and trabecular meshwork, and exfoliation material on the zonules and ciliary body. Accuracy of diagnosis is important for purposes of treatment, prognosis, and basic research in he mechanisms of glaucoma, particularly tissue culture.     

The pseudo-exfoliation syndrome. A scanning electron microscopic study. II. The posterior chamber region.

The distribution of pseudo-exfoliation (PE) material as well as the finer details of its surface has been studied by scanning electron microscopy on the surfaces facing the posterior chamber. The specimens were fixed in glutaraldehyde and OSO4 and dried by the critical point method, after careful dissection of the anterior hyaloid surface. Granules and plaques of PE material were found to attach to the iris, to the ridges of the ciliary processes, to the zonules, and along radial stripes on the anterior hyaloid surface, one for each zonule touching this surface. It seems as if the PE material is located mainly on sites on contact between two surfaces. In high mangnification it is found that the surface of the PE material is formed by an irregular meshwork of fibrils, the diameter of which is about 550-700 A. The fibrils are characteristically coiled, partly into regular spirals. The hypothesis is put forward that these fibrils are formed by a condensation of mucopolysaccharides forming the ground substance of the PE material.     

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.     

Alterations in rabbit vitreal fine structure following C3F8 injection

This study examines the morphological and histochemical changes in the cortical vitreous of 36 rabbit eyes following C₃F₈ intravitreal gas injection. Eyes were examined by light microscopy (LM) using a modified cryofixation and cryosectioning technique that prevented the loss of soluble tissue moieties and permitted collagen and proteoglycan histochemistry as well as enzyme digestion with hyaluronidase. LM and scanning electron microscopy (SEM) of cryosectioned normal eyes revealed an elaborate fibrillar matrix extending 100–190 gin from the basal lamina of the retina into the vitreous proper, which seemed to be composed of collagen fibrils intimately associated or wrapped in proteoglycan. Following the full expansion of the C₃F₈ gas bubble in the vitreous, the cortical fibrillar meshwork was absent from the retinal surface and a dense, collagenous material accumulated in the anterior vitreous, especially between the ciliary processes and over the posterior face of the lens. At 41 days postinjection, the fibrillar matrix was reforming and the vitreal cavity was filled with fluid and numerous fibrillar-mucinous islands. These islands did not form sheets or membranes, nor. did they attach to either the posterior or the anterior retinal surface. The cortical fibrillar meshwork had reformed at 61 days' recovery; however, the condensed fibrillar material against the lens and filling the spaces between the ciliary processes had not resorbed. Neither shearing of the cortical gel or fibrillar matrix nor congestion of the anterior vitreous was observed in eyes only partially filled with gas.This research was supported in part by United States Department of Energy contract DE-AC-02-76CH00016 and grants EYO-3422 and EYO-5916-01 from the National Eye Institute     

Iris involvement in granulocytic sarcoma.

A 6-year-old boy with a diagnosis of acute myeoblastic leukemia in remission developed iris infiltration accompanied by uveitis, hypopyon, and vitreous hemorrhage, which was initially unilateral, later becoming bilateral. Pathologically, the eyes showed leukemic infiltrates in the conjunctiva, episclera, sclera, ciliary body, trabecular meshwork, canal of Schlemm, choroid, vitreous, and the iris. Leder stain studies showed positive esterase activity, indicating granulocytic sarcoma. Granulocytic sarcoma may appear intraocularly as iris nodules. These iris nodules may be the initial manifestation of granulocytic leukemia.     

Pigment dispersion with elevated intraocular pressure after AcrySof intraocular lens implantation in the ciliary sulcus

A 45-year-old white woman had phacoemulsification with intraocular lens (IOL) implantation. The surgery was routine except for a linear tear in the posterior capsule; there was no disruption of the anterior vitreous face. After residual soft lens matter was removed, an AcrySof IOL was placed in the ciliary sulcus. One month postoperatively, the patient presented with an intraocular pressure (IOP) of 30 mm Hg and signs of pigment dispersion with 360 degrees of heavy pigmentation of the trabecular meshwork and iris transillumination defects. Intraocular pressure was controlled with a topical beta-blocker. The optic disc appearance and visual field remained normal, but the uniocular hyperpigmentation of the trabecular meshwork was still present. We hypothesize that the sharp square edge of the AcrySof IOL increases the risk of a chafing effect on the posterior iris pigment and advocate that this IOL be placed in the capsular bag and ideally have 360 degrees of protective overlapping of the anterior capsule over the edge of the optic.     

An Unusual Case of Ocular Involvement in Primary Systemic Nonfamilial Amyloldosis

A case of primary amyloidosis with vitreous involvement was diagnosed by study of a specimen obtained by pars plana vitrectomy. Vitreous opacities had been interpreted clinically as a vitreous hemorrhage. Medical evaluation after study of the vitreous specimen failed to demonstrate evidence of amyloidosis, although postmortem examination 19 months later established the systemic diagnosis of nonfamilial systemic primary amyloidosis. Both eyes were obtained postmortem. Amyloid involvement of the vitreous, retina, and choroid was found. There was also amyloid deposition in the trabecular meshwork, although the intraocular pressure was normal. Amyloid was deposited along the anterior, pupillary, and posterior surfaces of the iris. The histochemistry, ultrastructure, and treatment of this condition are discussed.     

CYP1B1基因缺失小鼠眼前房角组织结构的观察

目的 研究细胞色素P450 181(CYP1B1)基因对小鼠眼前房角组织结构的影响.方法 实验研究.采用成年CYP1B1基因缺失小鼠模型,以同龄C57BL/6J小鼠为对照.通过塑料包埋切片技术,用光学显微镜和透射电子显微镜观察两组小鼠眼前房角组织的形态和超微结构.结果 C57BL/6J小鼠眼前房角组织发育正常;CYP1B1因缺失小鼠存在不同程度的房水引流系统发育畸形,表现为小梁网发育不良,网眼狭窄,小梁细胞结构变异,有时可见小梁柱间有异常存在的均质膜,Schlemm管狭窄或缺失,虹膜突从虹膜根直达全部小梁网.这些异常改变在CYP1B1基因缺失小鼠眼前房角内呈局灶性分布.结论 CYP1B1基因在房角的发育过程中有重要作用,其缺失可导致小梁网、Schlemm管、虹膜突等房水滤过道的结构异常,可能影响房水引流系统的代谢和功能.     

Experimental obstruction to aqueous outflow by pigment particles in living monkeys

Pigment particles (1 X 10(6)/microliters) isolated from the iris and ciliary body of enucleated cynomolgus monkey eyes were infused into the anterior chamber of seven living cynomolgus monkeys and aqueous humor outflow facility determined by the two-step constant-pressure perfusion technique. Outflow facility acutely decreased 64% in the experimental pigment perfused eyes compared to a 76% increase in the sham-manipulated fellow eyes (P less than 0.001). However, when next measured 1 wk later, facility in the pigment perfused eyes had returned to baseline levels. Repetitive pigment perfusions similarly failed to produce any long-term abnormality in outflow facility. Gonioscopically, a well-defined band of pigment was observed in the trabecular meshwork, which decreased in density with time. Scanning and transmission electron microscopy documented pigment particle phagocytosis by trabecular endothelial cells and macrophages. Forty-two and 105 days after pigment infusion the trabecular meshwork was normal morphologically, and, despite an observed decrease in trabecular pigmentation, morphometry failed to reveal a decrease in trabecular meshwork cellularity in experimental compared to control eyes. These results suggest that factors other than, or in addition to, pigment particle accumulation in the trabecular meshwork must be involved in the mechanism of human pigmentary glaucoma.