原发性闭角型青光眼患者血浆心钠素水平的研究

本文采用放射免疫分析法检测60例原发性闭角青光眼患者的血浆心钠素水平,并与10例健康人血浆心钠素水平进行对照。结果:试验组血浆心钠素水平明显高于对照组。试验组血浆心钠素水平与眼压呈正相关。提示血浆心钠素水平的改变是机体对眼压升高产生的一种保护性应激反应,即眼压的自身体液性调节。心钠素可能与青光眼发病有关。     

原发性闭角型青光眼患者血浆心钠素水平的研究

本文采用放射免疫分析法检测６０例原发性闭角青光眼患者的血浆心钠素水平，并与１０例健康人血浆心钠素水平进行对照。结果：试验组血浆心钠素水平明显高于对照组。试验组血钠素水平与眼压呈正相关，提示血浆心钠素水平的改变是机体对眼压升高产生的一种保护性应激反应，即眼压的自身体液性调节，心钠素可能与青光眼发病有关。     

心纳素与青光眼

心钠素作为一种循环激素已深入医学各个领域。在眼科已证实，睫状体内存在高密度的心钠素受体，在眼组织中，前葡萄膜、脉络膜、视网膜及房水中均检测有心钠素存在。家兔青光眼动物模型及临床青光眼患者的血浆及房水中心钠素显著增高，对其全身及局部应用合成的心钠素均可见眼压不同程度的下降及房水分泌减少。心钠素与青光眼关系密切，它在调节眼压中可能起重要作用。本文介绍了有关心钠素的研究现状。     

青光眼房水心钠素含量及与眼压关系探讨

为探讨青光眼患者房水心钠素含量与眼压的关系，用放射免疫分析方法测定房水心钠素含量。结果：房水心钠素平均含量，青光眼组３４例４５．０３±１７．３２ｐｇ／ｍｌ，青光眼术前高眼压组２３例５１．９８±１５．７５ｐｇ／ｍｌ，青光眼术前正常眼压组１１例３０．４８±１０．０２ｐｇ／ｍｌ，对照组２０例１３．５１±３．９８ｐｇ／ｍｌ。青光眼患者房水心钠素水平与眼压之间呈正相关。结论：①青光眼组房水心钠素明显高于对照组。②心钠素水平与眼压呈正相关。③青光眼暂时正常眼压组心钠素明显低于青光眼高眼压组，仍明显高于对照组。④不同类型青光眼之间房水心钠素水平无显著性差异     

心钠素与青光眼

心钠素作为一种循环激素已深入医学各个领域。在眼科已证实，睫状体内存在高密度的心钠素受体，在眼组织中，前葡萄膜、脉络膜、视网膜及房水中均检测有心钠素存在。家兔青光眼动物模型及临床青光眼患的血浆及房水中心钠素显增高，对其全身及局部应用合成的心钠素均可见眼压不同程度的下降及房水分泌减少。心钠素与青餐眼关系密切，它在调节眼压中可能起重要作用。本介绍了有关心钠素的研究现状。     

青光眼患者房水与血浆心钠素水平的临床研究

心纳素 (atrial natriuretie peptide,AN P)是近年来新发现的一种循环激素 ,具有强大的利尿排钠、扩张血管的作用 [1]。为探讨心钠素水平与眼压的直接关系 ,进一步探讨心钠素对眼局部的体液调节作用。我们于 1996～ 1997年对 16例青光眼患者进行房水与血浆心钠素含量的测定。现报告如下。1　对象与方法1.1　对象　选择无全身疾患、需住院手术的急性闭角型青光眼患者 16例。其中 8例 (3男 5女 )为缓解期 ,另 8例 (4男 4女 )为急性发作期 ,眼压均大于6.0 0 k Pa。另一眼均为临床前期 ,年龄 56～ 68岁 ,平均 62岁。1.2　方法1.2 .1　血浆采集…     

心钠素与青光眼

心钠素与青光眼心钠素是以心房为主的多种器官产生的一组血管活性蛋白，它能降低血管阻力，参与调节全身或局部的水、电解质平衡，与许多疾病的病理生理及治疗有联系．近十年来眼科领域的研究表明，心钠素主要和青光眼有关，现将研究现状综述如下。一、心钻素简介（一）简...     

心钠素对兔眼压的影响

目的探讨心钠素对青光眼的治疗价值。方法对白色家兔结膜下注射不同剂量的心钠素，动态观察心钠素对兔眼压的影响。结果结膜下注射２０、３０、４０μｇ的心钠素，均可见有意义的眼压下降。４０μｇ的心钠素眼压下降幅度最大，维持时间最长，眼压下降高峰时间均在用药后１小时。同时可见随给药浓度增加，眼压下降幅度加大，呈量效关系。结论心钠素可作为一种新的抗青光眼药物应用于临床。     

慢性闭角青光眼患者血浆心钠素水平与眼压关系的研究

由于放射免疫检测技术的不断发展,对于近年来逐渐认识的一种循环激素——心房利钠因子(Atrial Natriuretic Factor心钠素,简称ANF)的研究已经达到了特异准确、迅速的定量分析,并且能够化学合成和应用基因工程合成.医学领域对ANF的研究巳深入到各有关科室,在眼科方面,目前学者认为ANF与眼压调节有关,并在临床和实验中发现急性闭角青光眼患者的血浆和实验性兔眼青光眼的房水中ANF水平明显升高。最近有报导对青光眼患者静脉注射ANF有降低眼内压的作用。为了探讨ANF与青光眼发病之间的     

甲亢患者治疗前后血浆心钠素水平的变化

作者检测了３９例甲亢患者治疗前后蝗血浆心钠素水平，结果显示：单纯甲亢组及合并甲亢性心脏病组治疗前血浆心钠素较正常人增，治疗后降低，甲亢性心脏病治疗前后分别高于单纯甲亢组治疗后，甲亢时血浆心钠素增高可能与继发的血流动力学改变，内分泌能改变和交感神经兴奋等有关。     

减少青光眼导致的盲和视力损伤是防盲的重要内容

由于国际眼科学界和世界卫生组织(WHO)已经注意到青光眼问题的严重性和加强青光眼防治的重要性,因此WHO采取了一些可行措施,以加强全球因青光眼致盲和视力损伤的防治工作.之所以采取这些措施是由于青光眼已经对全球的公共卫生造成了沉重负担,而且采用目前循证的临床干预措施治疗青光眼是有效的.将防治青光眼纳入防盲的重点就意味着不仅采用临床的途径,还要采用公共卫生的途径,整合各种眼保健力量做好青光眼的防治工作,这是青光眼防治策略的重要改变.筛查和早期诊断青光眼是防治青光眼的一项非常重要的工作,目前主要通过加强机会性筛查青光眼的工作,以发现更多的未诊断和未治疗的青光眼患者.所采用的防治青光眼的策略应当与当地的社会经济状况相适应,这样才能有利于推进防盲工作的顺利开展.     

The impact of exfoliation syndrome on therapeutic efficacy in open-angle glaucoma

Exfoliation syndrome is the most common identifiable cause leading to chronic open-angle glaucoma. It affects the treatment of glaucoma in various ways. The prognosis of capsular glaucoma (exfoliative glaucoma) is worse than that of open-angle glaucoma. Medical therapy and the long-term effect of laser treatment seem to be unsatisfactory in capsular glaucoma. Surgical intervention may be needed early, although eyes with exfoliation syndrome are prone to surgical complications. Finally, absolute glaucoma and blindness are more common in capsular glaucoma than in primary open-angle glaucoma. This article deals with the impact of exfoliation syndrome on therapeutic efficacy in open-angle glaucoma. It reviews the literature between October 1993 and September 1994; only a few studies concerning this important subject have been published during the given period.     

Autoimmunity and glaucoma

Elevated intraocular pressure does not explain glaucoma in all patients, but there is information that autoimmune mechanisms may be involved in this disorder. This review attempts to reveal the findings about specific changes in autoantibody profiles in glaucoma patients and their possible role in glaucoma. Considering that these changes in natural autoimmunity can be found consistently among different study populations, it might be a promising new tool for glaucoma detection.     

Cataract surgery and trabeculectomy at the same time (author's transl)]

It is not unusual to observe in the same eye a chronic glaucoma and a cataract. Surgery may be indicated for one of these diseases separately or for both of them. For simultaneous operation on glaucoma and cataract several attitudes could be discussed: a) cataract surgery and medical treatment of glaucoma, b) glaucoma surgery at first and then cataract surgery, c) cataract and glaucoma surgery at the same time. Since trabeculectomy is used for glaucoma surgery, the author performs the combined method, i.e. the simultaneous lens extraction and the operation of glaucoma through trabeculectomy. The advantages of trabec-lectomy over the other techniques for glaucoma surgery indicated that trabeculectomy over the other techniques for glaucoma surgery indicated that trabeculectomy is the best technique to be used in association with intracapsular cataract extraction. Our material consists of 65 patients, amongst which there are 11 patients with diabetes. 91 eyes have been operated upon during the last 2 years. Most of the postoperative complications, i.e. hyphaema, vitreous haemorrhage and prolapse, pupillary block, postoperatve rise of i.o. pressure are not severe and have no influence in the desired fall of i.o. pressure. It may be pointed out that a permanent regulation of i.o. pressure often occurs only 3 months postoperatively. Finally it can be said that the trabeculectomy associated with intracapsular cataract extraction appeared to be the best operation in case of glaucoma and cataract, provided that on the one hand the vascular status of these patients is controlled and on the other hand the operation microscope is exclusively used in surgery of the trabeculum.     

青光眼的定义及其研究发展方向

回顾性分析了视神经损害性理论的形成与青光眼定义的被改变过程,揭示了目前青光眼的定义及其研究发展方向是不正确的,指出青光眼的定义不是视神经损害性疾病,而是眼压增高病,用两路房水循环的观点,重新认识青光眼、研究青光眼是青光眼研究发展的正确方向。     

挫伤性青光眼临床分型和治疗方法（附74例临床分析）

目的探讨眼挫伤早期发生的外伤性青光眼的分类及治疗方法。方法对74例眼挫伤后早期发生的青光眼其治疗方法及其结果进行分析探讨。结果试将挫伤性青光眼分为眼内积血型、房角挫伤型、品状体相关型、眼内炎型、粘连增生型、外伤性睫状环阻塞型、外伤性瞳孔散大型等7个类型。治疗后随访时间4～62个月,未用降跟压药物、眼压正常者（眼压6～21mmHg）59眼,治愈率为79．7％;出院视力较入院时增加者56眼（75．6％）。结论眼挫伤早期外伤性青光眼临床表现复杂,可分做7个类型,对每一病例应采取具体有针对性的治疗方法。     

Primary open-angle glaucoma genes

A substantial fraction of glaucoma has a genetic basis. About 5% of primary open angle glaucoma (POAG) is currently attributed to single-gene or Mendelian forms of glaucoma (ie glaucoma caused by mutations in myocilin or optineurin). Mutations in these genes have a high likelihood of leading to glaucoma and are rarely seen in normal subjects. Other cases of POAG have a more complex genetic basis and are caused by the combined effects of many genetic and environmental risk factors, each of which do not act alone to cause glaucoma. These factors are more frequently detected in patients with POAG, but are also commonly observed in normal subjects. Additional genes that may be important in glaucoma pathogenesis have been investigated using quantitative traits approaches. Such studies have begun to identify genes that control the magnitude of important quantitative features of glaucoma that may also be important risk factors for POAG, such as central corneal thickness. Each of these different approaches to study glaucoma genetics is providing new insights into the pathogenesis of POAG.     

Age-dependent prevalence of mutations at the GLC1A locus in primary open-angle glaucoma

PURPOSE: To screen a population with primary open-angle glaucoma for mutations in the gene that encodes the trabecular meshwork inducible glucocorticoid response protein (TIGR), also known as myocilin (MYOC). METHODS: Ophthalmologic information was collected for study subjects with primary open-angle glaucoma and their relatives. Mutation screening of 74 primary open-angle glaucoma probands was conducted by sequencing TIGR/MYOC coding sequence and splice sites. RESULTS: In 23 families we detected 13 nonsynonymous sequence changes, nine of which appear to be mutations likely to cause or contribute to primary open-angle glaucoma. Two mutations, Arg272Gly and Ile499Ser, and one nonsynonymous sequence variant, Asn57Asp, are novel. We found mutations in nine of 25 juvenile glaucoma probands (36%) and two of 49 adult-onset glaucoma probands (4%). Age classification of families rather than individual probands revealed mutations in three of nine families with strictly juvenile primary open-angle glaucoma (33%), and no mutations in 39 families with strictly adult-onset primary open-angle glaucoma (0%). In families with mixed-onset primary open-angle glaucoma containing both juvenile primary open-angle glaucoma and adult-onset primary open-angle glaucoma cases, we found mutations in eight of 26 families (31%). CONCLUSIONS: Our data suggest that Gly252Arg, Arg272Gly, Glu323Lys, Gln368STOP, Pro370Leu, Thr377Met, Val426Phe, Ile477Asn, and Ile499Ser are likely to play roles that cause or contribute to the etiology of autosomal dominant primary open-angle glaucoma. Our finding of more TIGR/MYOC mutations in families with mixed-onset primary open-angle glaucoma than in the families with strictly adult-onset primary open-angle glaucoma implies that the presence of relatives with juvenile primary open-angle glaucoma in a family could be used as a basis for identifying a subset of the population with adult-onset primary open-angle glaucoma with higher prevalence of TIGR/MYOC mutations. To address this issue, and to refine estimations of mutation prevalence in these age-defined subpopulations, prospective study of a larger population ascertained entirely through adult-onset primary open-angle glaucoma probands will be needed.     

The genetic basis for adult onset glaucoma: Recent advances and future directions

Glaucoma, a diverse group of eye disorders that results in the degeneration of retinal ganglion cells, is the world's leading cause of irreversible blindness. Apart from age and ancestry, the major risk factor for glaucoma is increased intraocular pressure (IOP). In primary open-angle glaucoma (POAG), the anterior chamber angle is open but there is resistance to aqueous outflow. In primary angle-closure glaucoma (PACG), crowding of the anterior chamber angle due to anatomical alterations impede aqueous drainage through the angle. In exfoliation syndrome and exfoliation glaucoma, deposition of white flaky material throughout the anterior chamber directly interfere with aqueous outflow.Observational studies have established that there is a strong hereditable component for glaucoma onset and progression. Indeed, a succession of genome wide association studies (GWAS) that were centered upon single nucleotide polymorphisms (SNP) have yielded more than a hundred genetic markers associated with glaucoma risk. However, a shortcoming of GWAS studies is the difficulty in identifying the actual effector genes responsible for disease pathogenesis. Building on the foundation laid by GWAS studies, research groups have recently begun to perform whole exome-sequencing to evaluate the contribution of protein-changing, coding sequence genetic variants to glaucoma risk. The adoption of this technology in both large population-based studies as well as family studies are revealing the presence of novel, protein-changing genetic variants that could enrich our understanding of the pathogenesis of glaucoma.This review will cover recent advances in the genetics of primary open-angle glaucoma, primary angle-closure glaucoma and exfoliation glaucoma, which collectively make up the vast majority of all glaucoma cases in the world today. We will discuss how recent advances in research methodology have uncovered new risk genes, and how follow up biological investigations could be undertaken in order to define how the risk encoded by a genetic sequence variant comes into play in patients. We will also hypothesise how data arising from characterising these genetic variants could be utilized to predict glaucoma risk and the manner in which new therapeutic strategies might be informed.