黄斑色素光学密度相关的临床应用

人类视网膜黄斑区富含黄斑色素（macular pigment,MP）,MP对视网膜具有重要的保护意义,且与人类视功能密切相关。MP水平可通过黄斑色素光学密度（macular pigment optical density,MPOD）来评估。研究表明,MP的减少或缺失对多种眼科疾病（包括年龄相关性黄斑病变、糖尿病性视网膜病变、青光眼等）的发生发展及预后的判断具有重要意义,MPOD的测量在相关全身疾病（如Sjogren-Larsson综合征）的诊断、管理和治疗中同样发挥作用。     

眼外伤所致继发性青光眼临床分析

目的探讨眼外伤所致继发性青光眼的发病原因和防治方法。方法对48例（48眼）眼外伤所致继发性青光眼的临床表现和治疗进行回顾性分析。结果眼外伤所致继发性青光眼可由多种原因引起,根据不同的原因采取药物或手术治疗,42眼（87.5%）眼压控制在正常范围。结论眼外伤所致继发性青光眼应针对不同原因进行治疗,预防继发性青光眼的发生是挽救视功能和减少并发症的发生有重要临床意义。     

原发性开角型青光眼进展的危险因素研究概况

原发性开角型青光眼(POAG)进展的危险因素包括全身性及眼部因素,眼部因素包括眼压及非眼压因素.在以往的多中心研究中,眼压对于由高眼压症发展为POAG及其在POAG进展中的作用已经明确,而目前降低眼压也是临床惟一有效地延缓、控制青光眼视神经损害进展的主要因素.制定目标眼压,进行降眼压治疗尤其是控制昼夜眼压波动对于阻止青光眼进展非常重要.非眼压危险因素包括高龄、中央角膜厚度增厚、视乳头出血、晶状体囊膜剥脱征、初始的青光眼严重程度及双眼罹患青光眼等.其他因素包括近视、青光眼家族史、眼部低灌注压、低血压、心血管疾病、高血压、高血脂等血管或血液性因素.POAG进展的危险因素研究在一定程度上揭示了POAG的发病机制及临床发病规律,对于指导临床医师决定随诊频率、选择治疗方案及提高治疗效率意义重大.     

线粒体功能异常与青光眼的关系

线粒体既是细胞内能量转换器,又是决定细胞存活的重要因素。线粒体损伤、功能失调与多种神经元退行性变疾病发生发展均密切相关。青光眼为视神经病变的一种,近年来研究发现线粒体功能异常在其视神经损害过程,如氧化应激、谷氨酸兴奋性毒性、钙超载、机械压力、神经营养因子的剥夺、胶质细胞的激活等的病理机制中起着尤为重要的作用。本文对线粒体功能异常与青光眼关系的最新研究进展作以综述。（国际眼科纵览,2012,36：302-306）     

利用OCT观察非脉络膜疾病中黄斑中心凹脉络膜厚度变化

利用光学相干断层扫描（OCT）检测黄斑中心凹脉络膜厚度（SFCT）变化已经成为研究眼部疾病和全身性疾病的重要指标之一。不仅在一些眼科疾病中，SFCT的改变呈多样性，表现出脉络膜在疾病的发病机制中极其复杂的改变，而且在血管性相关性疾病，或因缺血、缺氧等因素导致的全身性疾病中，SFCT的变化也为这些疾病的早期诊断提供依据。笔者现对非脉络膜疾病中SFCT的变化进行综述。     

2006-2013年河北省眼科医院住院继发性青光眼患者的类型及治疗方法

 目的  回顾2006-2013年河北省眼科医院住院继发性青光眼患病人群的类型及治疗方法。设计 回顾性病例系列。研究对象 2006年6月-2013年3月河北省眼科医院青光眼科住院的继发性青光眼1178例1361眼。方法 回顾患者病历资料,分析患病年龄、病因、治疗方法等。病因构成比按例数计算。主要指标  继发性青光眼的病因及构成比。结果 1178例继发性青光眼患者中新生血管性青光眼436例522眼（37.0%）,外伤性青光眼166例166眼（12.2%）,晶状体源性青光眼185例201眼（15.7%）,
葡萄膜炎继发青光眼160例176眼（13.6%）,角膜炎所致青光眼63例71眼（5.4%）,其他病因者168例225眼（14.3%）。新生血管性青光眼中以糖尿病视网膜病变（46.2%）和视网膜静脉阻塞（32.8%）为多。外伤性青光眼以眼球钝挫伤晶状体脱位（27.7%）、前房玻璃体出血（25.9%）比例较大。晶状体源性青光眼以晶状体膨胀因素（36.8%）居多。手术治疗1204眼（88.5%）,其中小梁切除术351眼（29.2%）,Ahmed阀植入术257眼（21.3%）,睫状体冷冻术131眼（10.9%）,白内障摘除联合滤过性手术127例（10.5%）,睫状体光凝术122眼（10.1%）,晶状体摘除术84眼（7.0%）,其他手术132眼（11.0%）。结论 2006-2013年河北省眼科医院住院继发性青光眼以新生血管性青光眼为首位病因。其次为外伤性青光眼、晶状体源性青光眼和葡萄膜炎继发青光眼。依据继发性青光眼的病因不同,采用多种不同的治疗方式。（眼科,2015,24： 40-43）     

再论晶状体悬韧带异常与闭角型青光眼的关系

晶状体位置异常是原发性闭角型青光眼的重要发病机制之一,往往与晶状体悬韧带异常相关。晶状体悬韧带异常主要影响晶状体的厚度、屈光力与位置,进而影响眼前节解剖结构和屈光状态,导致前房深度变化或不稳定。衰老、遗传、外伤、炎症等因素均可影响悬韧带结构与功能。深入研究悬韧带的病理生理有助于理解一些常见的临床现象如合并近视（甚至是高度近视）的闭角型青光眼、闭角型青光眼中的隐匿性晶状体不全脱位、一些闭角型青光眼对缩瞳及虹膜周切治疗的反常反应、年轻的闭角型青光眼往往是全身遗传性疾病的眼部表现等。目前亟需研究与开发简便、精准的术前和术中悬韧带的评估手段和标准。（眼科,2022, 31： 169-174）     

视网膜中央静脉阻塞发病因素的病例对照观察

目的 观察视网膜中央静脉阻塞(CRVO)患者与主要的全身性疾病、眼局部疾病以及相关危险因素的关系。 方法 病例对照研究。患者组：76例病程在3个月内、经荧光素眼底血管造影(FFA)检查确诊、未进行过药物治疗的CRVO患者；对照组：76例非CRVO患者，既往无眼底血管性疾病史，以年龄和性别与患者组一对一相匹配。患者组按年龄分为≤45岁（25例，占32.9%）和＞45岁（51例，占67.1%）两个亚组；按FFA检查结果分为非缺血型（40例，占52.6%）和缺血型（36例，占47.4%）两个亚组。检测血脂、血压和空腹血糖等。各组之间分别进行全身性和眼局部性疾病以及相关危险因素的统计学比较。 结果 患者组高血压和高脂血症患病率明显高于对照组（P＜0.001，P=0.001），而心、脑血管疾病、开角型青光眼的发病率、以及吸烟和饮酒生活习性上差异无统计学意义（P＞0.05）。年龄≤45岁组中，患者组各项指标与对照组差异无统计学意义（P＞0.05）。缺血型CRVO组，除高血压和高脂血症外, 糖尿病发病率明显高于对照组（P＜0.001，P=0.031，P=0.024）。 结论 高血压和高脂血症为CRVO发病的全身性因素。此外，糖尿病与缺血型CRVO发病也相关。及时诊断和治疗全身性疾患对于CRVO的防治具有重要指导意义。 (中华眼底病杂志，2007，23：159-162)     

正常眼压性青光眼的危险因素

正常眼压性青光眼（normal tension glaucoma,NTG）在临床特征上除了眼压在正常范围外,其余均与开角型青光眼有许多相同之处,故以往一直被认为是开角型青光眼的一个亚型.但随着对此疾病的认识逐渐加深,发现其危险因素与高眼压性开角型青光眼有所不同,全身情况及眼局部因素都对NTG的发生发展产生影响,主要包括性别、年龄、脑供血不足、眼压波动、眼轴长度、屈光度等方面.     

重视局部抗青光眼药物对眼表的影响

 原发性青光眼多为慢性病,不能被根治,只能通过降眼压的方法来控制视野的恶化,其中滴眼药是最常用和最安全的方法,往往伴随患者一生,长期滴眼药必然会引起一些副作用,对眼表健康的影响尤为突出,甚至影响治疗效果。因此,关注青光眼患者的眼表健康状况是青光眼治疗所面临的重要问题。本文对长期用药的青光眼患者发生眼表疾病的危害及其发病机制,以及临床上如何维护青光眼患者的眼表健康等问题进行讨论。     

原发性开角型青光眼的系统性危险因素

眼压异常升高是原发性开角型青光眼最主要的危险因素。临床目前一直沿用以眼压为靶点的青光眼诊疗模式。近年来发现，循环血流、体质指数、颅内压、营养代谢、中医偏颇体质类型、某些系统性疾病等多种系统性危险因素可能与青光眼发生、发展和转归相关。纠正系统性危险因素能否延缓青光眼进展被日益关注，成为潜在的青光眼辅助诊疗靶点。本文对各类青光眼系统性危险因素进行介绍，倡导重视系统性危险因素，提出以系统危险因素评估和个性化眼体同治相结合的青光眼诊疗体系。（眼科， 2022， 31： 325-329）     

Glaucoma and obstructive sleep apnoea syndrome

Glaucoma is increasingly recognized as a manifestation of both ocular and systemic risk factors. A number of disorders associated with reduced blood flow and ischaemia, collectively termed vascular risk factors, such as migraine, Raynaud's phenomenon, atrial fibrillation and reduced nocturnal blood pressure, lead to decreased ocular perfusion pressure. During sleep, alterations occur in cardiovascular physiology that are balanced by autoregulation to maintain homeostasis. However, in obstructive sleep apnoea (OSA), the normal physiological balance is upset. A potentially modifiable risk factor, OSA has been increasingly associated with glaucoma independent of intraocular pressure. OSA may alter blood flow to the optic nerve head and, in combination with other predisposing factors, lead to decreased ocular perfusion pressure. This in turn may directly affect the optic nerve or it may indirectly increase its susceptibility to other insults. The purpose of this review is to shed light on the association between OSA and glaucoma.     

亚在地区青光眼的流行病学

Primary open angle glaucoma is the second most important cause of permanent blindness in the Asia-Pacific region. Thus it is very important to identify epidemiological and other risk factors which are associated with open angle glaucoma. The risk for glaucoma optic nerve damage increases with the age and with the level of the intraocular pressure. In this paper, I will highlight our study of several risk factors for development of the open angle glaucoma like (1) elevated intraocular pressure, (2) myopia, (3) suspicious large optic disc cup, (4) cupping with disc haemorrhages and (5) nerve fibre defect. The general and systemic conditions which are implicated as risk factors are (1) family history of glaucoma. (2) increase in age, (3) diabetes mellitus, (4) cardiovascular conditions like central retinal vein occlusion etc. (5) the endocrine disorders with increased thyroid and increased corticosteroids responsiveness in patients with glaucoma will be discussed.     

Obstructive sleep apnea–hypopnea syndrome (OSAHS) and glaucomatous optic neuropathy

Obstructive sleep apnea–hypopnea syndrome (OSAHS) is becoming widely accepted as a risk factor for glaucoma. We discuss the proposed mechanism involved in the pathogenesis of glaucoma in OSAHS, and review the published data on the association between these two conditions, as well as papers regarding functional and structural tests related with glaucomatous damage. There is increasing evidence that the prevalence of glaucoma is higher in OSAHS patients, especially in those with severe disease with apnea-hypopnea index (AHI) >30, and also that sleep disorders may be more frequent in patients with glaucoma, especially in those with normal tension glaucoma (NTG). Several ophthalmic signs and symptoms have been associated with this condition. Raised intraocular pressure (IOP), possibly related to increased body mass index, thinning of retinal nerve fiber layer (RNFL), and alteration of visual field (VF) indices has been demonstrated in many studies, in patients with no history of glaucoma or evidence of glaucomatous changes in the ophthalmic examination. A correlation of AHI with RNFL and VF indices has been described in some studies. Finally, corneal thinning, suspicious glaucomatous disc changes and anomalies in electrophysiological tests such as multifocal visual evoked potential have been described in patients with OSAHS, even in patients with normal findings in the optic nerve and VF, suggesting subclinical optic nerve involvement not detectable in conventional ophthalmic examinations. The pathogenesis of optic nerve involvement has been related to vascular and mechanical factors. Vascular factors include recurrent hypoxia with increased vascular resistance, autonomic deregulation, oxidative stress and inflammation linked to hypoxia and subsequent reperfusion, decreased cerebral perfusion pressure and direct hypoxic damage to the optic nerve. Proposed mechanical factors include increased IOP at night related to supine position and obesity, raised intracranial pressure and elastic fiber depletion in the lamina cribosa and/or trabeculum. In conclusion, ophthalmic evaluation should be recommended in patients with severe OSAHS, and the presence of sleep disorders should be investigated in patients with glaucoma, especially in NTG patients and in those with progressive damage despite controlled IOP, as treatment with continuous positive airway pressure may contribute to stabilizing the progression of glaucomatous damage.     

青光眼视神经损伤机制的研究进展

青光眼是目前全球范围内致盲性最高的疾病之一,是以进行性视网膜神经节细胞丧失、不可逆的视野损害等病理性改变为特征,最终导致视神经萎缩及视功能丧失的疾病。目前青光眼的发病机制并不完全清楚,其中视神经损伤的机制有多种学说,包括眼压因素及非眼压因素,非眼压因素包括血管因素、免疫作用、远端轴突病变、氧化应激作用、细胞因子的变化及自噬等机制。本文综述了有关青光眼视神经损伤机制的研究进展,为进一步研究青光眼视神经病变提供依据。     

青光眼与Th1、Th2相关细胞因子研究进展

青光眼是导致不可逆盲的首要原因,包括视野缺损和视神经的慢性退行性病变,如视网膜神经节细胞(RGCs)的凋亡和视神经轴突的逐步缺失.目前普遍认为高眼压是青光艰的主要危险因素,降低眼压是减缓青光眼发生和发展的首选治疗方法.近年来发现免疫因素是青光眼视神经损害的非压力依赖性危险因素之一.大部分免疫,甚至非免疫性生物效应都通过细胞因子来调控,而CD4+辅助性T细胞是细胞因子产生和调节的主要来源,其中Th1和Th2相关细胞因子在青光眼的发病机制中起着不可或缺的作用,并关系着RGCs的存活和凋亡.本文就近年Th1和Th2主要的相关细胞因子及Th1/Th2平衡与青光眼潜在关系的研究进展进行综述.     

The vascular pattern of the optic nerve and its potential relevance in glaucoma

Evidence that vascular factors contribute to the pathogenesis and development of glaucomatous optic neuropathy continues to accumulate. A higher than expected prevalence of systemic vascular disorders in individuals with glaucoma has been documented. New sophisticated in vivo analysis techniques, such as ultrasound color Doppler imaging, suggest that decreased blood flow velocity and increased vascular resistance are present in the vessels serving the optic nerve of human subjects with glaucoma, implying the presence of either organic or functional vascular disorders in these individuals. Recognizing that different analysis techniques have led to conflicting observations, experimental models have been developed to provide an additional tool with which to interpret the effects of compromised optic nerve perfusion.     

Abnormalities of microcirculation in glaucoma: facts and hints

Many risk factors associated with glaucoma have been identified recently. The best known of these is increased intraocular pressure (IOP). Among the others, however, vascular risk factors play a major role. Although such vascular factors were already postulated more than 100 years ago, only recent technical developments have afforded systematic investigations of associated microcirculatory disturbances and basic principles of blood flow regulation. In glaucoma, besides IOP, vascular dysregulation (such as local vasospasm and systemic hypotension, resulting in impaired autoregulation of blood flow in the optic nerve head, the choroid, and other ocular tissues) seems to be a major risk factor. However, multiple coacting factors, which are not limited to the eye but are, rather, symptoms of a systemic disease, seem to be involved in the damaging process.     

Endothelial dysfunction in glaucoma

Glaucoma is a group of ocular diseases characterized by optic neuropathy associated with loss of the retinal nerve fibre layer and re‐modelling of the optic nerve head, and a subsequent particular pattern of visual field loss. Increased intraocular pressure is the most important risk factor for the disease, but the pathogenesis of glaucoma is not monofactorial. Among other factors, ischaemia and vascular dysregulation have been implicated in the mechanisms underlying glaucoma. The vascular endothelium plays an important role in the regulation of ocular blood flow and pathological alterations of vascular endothelial cells may induce ischaemia and dysregulation. The present review summarizes our current evidence of endothelial dysfunction in glaucoma. This is of interest because endothelial dysfunction is a good prognostic factor for progression in several diseases. Although such data are lacking for glaucoma, endothelial dysfunction may provide an attractive target for therapeutic intervention in open‐angle glaucoma and other vascular disorders of the eye.     

Argumente f��r eine prophylaktische Therapie der okul?ren Hypertension

Increased intraocular pressure is currently the only manipulable risk factor for glaucoma. In ocular hypertension the intraocular pressure is increased but the optic nerve head and visual field are thought to show no damage. Classification into glaucoma by means of the optic nerve head is often possible only over a period of time because there is a large overlap between the already pathological and still normal findings. In the Ocular Hypertension Treatment Study (OHTS) the effectiveness of prophylactic treatment was demonstrated. In the OHTS and the European Glaucoma Prevention Study (EGPS) risk factors have been identified, such as increased intraocular pressure, size of the excavation of the optic nerve head, decreased central corneal thickness, increased pattern standard deviation in the visual field and age. Before treatment of ocular hypertension is initiated these risk factors and the patient's personal situation should be considered. The higher the intraocular pressure, the smaller the central corneal thickness and the larger the excavation of the optic nerve and the younger the patient, the earlier treatment should be started.