剥脱性青光眼的研究进展

剥脱性青光眼是继发于剥脱综合征的一种青光眼类型,剥脱综合征目前是继发性开角型青光眼最常见的原因之一。近年来,剥脱综合征和剥脱性青光眼受到越来越多的研究者关注,开展了大量的相关性研究,获得了较多的研究资料。因此,有必要就剥脱性青光眼的患病率、遗传特性、剥脱物质的形成机制、基因和治疗研究进展进行综述。     

剥脱性青光眼患者视网膜神经纤维层厚度变化分析

目的：比较维吾尔族假性剥脱综合征(PEX)患者、剥脱性青光眼(PEXG)患者视网膜神经纤维层(RNFL)厚度,为早期诊断剥脱性青光眼提供理论依据。

方法：回顾性病例对照研究。选取2018-04/ 2020-06在我院就诊治疗的维吾尔族假性剥脱综合征患者70例70 眼,剥脱性青光眼患者 80例80 眼,按照视野缺损分期分为早中期剥脱性青光眼患者56眼、晚期剥脱性青光眼患者24眼,选取同期本院收治的维吾尔族年龄相关性白内障病例60例60 眼作为对照组。比较四组患者视盘不同位置RNFL厚度。

结果：对照组、假性剥脱综合征组及剥脱性青光眼组患者视野缺损(MD)逐渐加重且剥脱性青光眼组患者MD显著高于假性剥脱综合征组(P<0.01); 假性剥脱综合征组、早中期剥脱性青光眼组及晚期剥脱性青光眼组视盘不同位置RNFL厚度较对照组均变薄(均P<0.01); 假性剥脱综合征组患者视盘平均RNFL、下方、上方RNFL厚度均低于对照组(均P<0.01)); 晚期剥脱性青光眼组患者视盘各个位置RNFL厚度明显低于早中期剥脱性青光眼患者(均P<0.01)。

结论：维吾尔族假性剥脱综合征患者早期RNFL厚度较未患有剥脱综合征人群开始变薄,早期对于假性剥脱综合征患者RNFL进行检测有助于剥脱性青光眼疾病诊断并进行治疗。     

剥脱综合征性青光眼的发病机制

剥脱综合征是一种常见的年龄相关性眼病,是导致青光眼的常见原因.剥脱综合征性青光眼较慢性单纯性青光眼更严重、预后更差.在此文中对近年来,剥脱综合征性青光眼发病机制的有关论著作一综述.     

剥脱性青光眼的临床和病理

前　　言剥脱综合征 exfoliation syndrome表现为高龄者的晶体前囊和虹膜瞳孔缘部出现灰白色头皮屑样物质 ,多伴发难治性青光眼。剥脱综合征伴发的青光眼称为剥脱性青光眼 exfoliation glaucoma。剥脱性青光眼基本无自觉症状 ,当发现患病时已经出现显著的视野损害 ,已不能恢复视功能。所以对本病的早期发现、早期治疗极为重要。剥脱综合征以前高发于已进入老龄化社会的北欧各国 ,在其他国家比较少见〔1〕。但是 ,最近在九州大学就诊的 5 0岁以上发生开角型青光眼的老龄患者多半归于本病〔2〕,所以对剥脱综合征和剥脱性青光眼的研究十分必要…     

剥脱性青光眼22例临床分析

剥脱性青光眼又称囊性青光眼，国内报道较少。自1983年夏恒需等报告2例以来，迄今公开报道者已搜集到118例。近年来随着对剥脱性青光眼认识的提高。发现率也随之增加。我院青光眼病组于1999年1月～2002年6月问连续收治的剥脱性青光眼22例29眼，现结合临床分析讨论如下。     

剥脱综合征的遗传学

剥脱综合征(exfoliation syndrome XFS)是一种常见的年龄相关性细胞外基质代谢异常性眼病,是导致青光眼的常见原因.对剥脱综合征患者进行的全基因组关联性研究表明剥脱综合征和剥脱性青光眼(exfoliative glaucoma XFG)与赖氨酸氧化酶样基因1(lysyl oxidase-like 1 gene LOXL1)中的3个单核苷酸多态性(single nucleotide polymorphisms SNPs)密切相关.此文对近年来剥脱综合征遗传学方面的研究进展作一综述.     

剥脱综合征的遗传学

剥脱综合征(exfoliation syndrome XFS)是一种常见的年龄相关性细胞外基质代谢异常性眼病,是导致青光眼的常见原因.对剥脱综合征患者进行的全基因组关联性研究表明剥脱综合征和剥脱性青光眼(exfoliative glaucoma XFG)与赖氨酸氧化酶样基因1(lysyl oxidase-like 1 gene LOXL1)中的3个单核苷酸多态性(single nucleotide polymorphisms SNPs)密切相关.此文对近年来剥脱综合征遗传学方面的研究进展作一综述.     

色素性青光眼和囊性青光眼：临床和组织病理学报告

本文报告色素性青光眼7例(13眼),囊性青光眼9例(12眼)。眼前段色素播散和剥脱物质沉着分别是色素性青光眼和囊性青光眼的特征性改变,而囊性青光眼也可见非典型眼前段色素播散。小梁标本的组织病理学研究表明色素性青光眼中色素颗粒,囊性青光眼中剥脱物质和色素颗粒在阻塞房水排出通道中起重要作用。本文还讨论了这二型青光眼的诊断和鉴别诊断。     

剥脱综合征

剥脱综合征的特点是临床上见淡灰色或白色碎片位于瞳孔缘和晶体前囊,也出现于虹膜的两面、小带、睫状体、玻璃体、小梁和角膜内面。常合并青光眼。作者注意到单眼剥脱病人中93%需要在双眼进行抗青光眼治疗。这表明在未发生剥脱症的另一眼多有异常高眼压,并由此推测囊性青光眼可能经常与原发性开角青光眼并存。作者复查了1977年74例患单眼或双眼剥脱综合征的病人及其资料。都曾经过散瞳裂隙灯下检查、房角检查、视盘的描绘或照像和视力、视野的测量。剥脱综合征的诊断是通过对晶体、小带等处典型碎片的观察而做出的。眼压数次测量为     

小梁抽吸术

假性剥脱综合症（ｐｓｅｕｄｏｅｘｆｏｌｉａｔｉｏｎ，ＰＥＸ）的临床特点是伴发青光眼的患病率很高，且通常为开角型青光眼。早在１９３０年，Ｖｏｇｔ就注意到假性剥脱性青光眼（ｐｓｅｕｄｏｅｘｆｏｌｉａｔｉｏｎｇｌａｕｃｏｍａ，ＰＥＧ）或称囊膜性青光眼（ｇｌ...     

Strabisme Alternant - Etude clinique - traitement

The author defines motor and sensory alternation: the term alternation should not be used in isolation, it should always be accompanied by the name of the parameter concerned. Sensory alternation is always found together with motor alternation but the reverse is not true.The examining criteria for a diagnosis of sensory alternation are given, sensory alternation must not be confused with alternating inhibition. Working from clinical observations of cases of motor alternating strabismus, the author selects 2 types of binocular sensory relations which allow one to differentiate between:- cases of primary alternating strabismus- cases of secondary alternating strabismusThese forms will develop in different ways; in both cases a cure is possible providing that the right treatment is prescribed and once prescribed carefully followed, etc. It is always a case of serious forms of strabismus whose developmental period is spread over several years.According to the authors, the frequency of cases of true primary strabismus is from 1–3%, the frequency of cases of secondary alternating strabismus varies according to the type of therapy practised on cases of monocular strabismus with amblyopia. These latter will become cases of alternating strabismus under the influence of certain types of therapy carried out over several years (penalization, rocking, alternated occlusion, etc...).Experimental data on kittens confirm clinical data; kittens placed in abnormal environments during the sensitive period will show modification in the distribution of cortical cells and the absence of binocular cells (either because the excitation of the two eyes was not simultaneous, or not identical: artificial strabismus, occlusion, opaque glasses). This disturbances become irreversible after a certain period of exposure (a function of age, length of exposure, etc...).It is thus necessary to bear in mind: 1) the iatrogenic risks of certain orthoptic treatments, 2) the necessity for a binocular form of treatment as soon as possible, as once a certain stage is passed, cortical plasticity diminishes and the elaboration of normal binocular relations becomes impossible.

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Effects of Adenosine Agonists on Intraocular Pressure and Aqueous Humor Dynamics in Cynomolgus Monkeys

The effects of single or multiple topical doses of the relatively selective A₁adenosine receptor agonists (R)-phenylisopropyladenosine (R-PIA) and N⁶-cyclohexyladenosine (CHA) on intraocular pressure (IOP), aqueous humor flow (AHF) and outflow facility were investigated in ocular normotensive cynomolgus monkeys. IOP and AHF were determined, under ketamine anesthesia, by Goldmann applanation tonometry and fluorophotometry, respectively. Total outflow facility was determined by anterior chamber perfusion under pentobarbital anesthesia. A single unilateral topical application of R-PIA (20–250 μg) or CHA (20–500 μg) produced ocular hypertension (maximum rise=4.9 or 3.5 mmHg) within 30 min, followed by ocular hypotension (maximum fall=2.1 or 3.6 mmHg) from 2–6 hr. The relatively selective adenosine A₂antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 320 μg) inhibited the early hypertension, without influencing the hypotension. Neither 100 μg R-PIA nor 500 μg CHA clearly altered AHF. Total outflow facility was increased by 71% 3 hr after 100 μg R-PIA. In conclusion, the early ocular hypertension produced by topical adenosine agonists in cynomolgus monkeys is associated with the activation of adenosine A₂receptors, while the subsequent hypotension appears to be mediated by adenosine A₁receptors and results primarily from increased outflow facility.