高度近视合并原发性开角型青光眼的临床特点研究进展

许多研究显示高度近视与青光眼密切相关,高度近视因患者眼轴长、前房深、房角宽的特点,并发青光眼的类型常为原发性开角型青光眼.然而,由于高度近视可导致一系列的眼底病变,使青光眼的早期眼底改变易被高度近视造成的眼底病变所掩盖,所以,认识高度近视合并原发性开角型青光眼的临床特点及诊断要点,有利于疾病的早期诊断和减少漏诊、误诊.本文对高度近视合并原发性开角型青光眼的临床特点进行总结归纳,提高对疾病的认识,为疾病的早期诊断提供依据.     

高度近视合并原发性开角型青光眼的临床诊断研究进展

临床和试验研究均发现,高度近视患者并发原发性开角型青光眼的概率高于非高度近视患者,特别是当高度近视与原发性开角型青光眼并存时,病情变得尤其复杂。对于个体而言,近视和青光眼之间的关系在很多情况下仍然很不明确,高度近视是造成青光眼的风险因素之一,多数情况下从青光眼的眼底变化中也很难分辨出是近视导致还是功能异常,因此高度近视合并原发性开角型青光眼的早期诊断非常困难但意义重大。本文从流行病学特征、视盘结构、视野改变、眼压测量等方面对高度近视与原发性开角型青光眼的关系及诊断进行综述。     

高度近视合并原发性开角型青光眼的眼底改变

高度近视是原发性开角型青光眼(POAG)的高危因素.受高度近视因素的干扰,早期轻度的青光眼症状,常被误认为视疲劳或近视加重而被忽略.由于原发性开角型青光眼症状不明显,就诊时通常已是晚期.本文对高度近视合并POAG的眼底改变,从视神经纤维层厚度、视盘改变、视盘周围脉络膜损伤及早期检查方法进展四方面作一综述,为提高高度近视中POAG的早期诊断提供依据.     

高度近视合并原发性开角型青光眼眼底结构改变的研究进展

高度近视是原发性开角型青光眼(POAG)发生发展的重要危险因素，如何在高度近视人群中发现POAG患者一直是国内外学者研究的热点和难点。高度近视患者并发POAG的概率明显高于非高度近视患者。高度近视本身就可能发生眼部一系列结构和功能的改变，当高度近视合并POAG时，复杂的眼底改变造成近视与早期开角型青光眼相互混淆，使早期青光眼的诊断具有一定的难度。本文将回顾高度近视合并POAG的相关文献，从流行病学、视盘、视神经节细胞层、视网膜神经纤维层、血管密度等眼底结构特点做一综述。     

高度近视合并原发性开角型青光眼的早期诊断与研究

高度近视(high myopia,HM)是原发性开角型青光眼(primary open angle glaucoma,POAG)的高危人群。临床上我们发现原发性开角型青光眼与高度近视有着密切关联,所以认识高度近视合并原发性开角型青光眼时的临床特点,重视高度近视合并原发性开角型青光眼的早期诊断,避免漏诊或降低误诊率,有利于提高临床医师对该病的警惕性和早期诊断的水平。本文就高度近视合并原发性开角型的临床特征、早期诊断注意要点的研究进展等进行综述。     

高度近视视神经改变与原发性开角型青光眼的相关性研究进展

高度近视(high myopia,HM)作为一种特殊类型的屈光型眼病,不仅会导致进行性、退行性眼底改变,其视神经损伤的患病率也很高。青光眼是全球范围内最常见的一种不可逆致盲性眼病,原发性开角型青光眼(primary open-angle glaucoma,POAG)是最常见的青光眼类型。近年来的研究发现HM与POAG的病理改变存在相似之处。由于HM眼底改变与早期POAG眼底改变容易混淆,HM患者早期发现POAG对延缓或阻止疾病进展很重要。HM患者长期随访不仅要观察黄斑病变,视神经形态与结构改变的观察也不容忽视。     

高度近视与原发性开角型青光眼

临床上发现高度近视与原发性开角型青光眼密切相关 ,其可能的机制有 :( 1 )升压基因学说 ;( 2 )胶原基因学说。高度近视眼与原发性开角型青光眼对糖皮质激素反应增高表明 ,二者的基因在糖皮质激素诱导下最易表达特异性蛋白 ,这可能与高度近视、原发性开角型青光眼的TIGR基因突变有关。本文从流行病学、临床特征及诊断、遗传学说及机制等方面对高度近视与原发性开角型青光眼的关系及研究进展进行综述。     

高度近视与原发性开角型青光眼

目的:从流行病学、临床特征及诊断、遗传学说及机制等方面对高度近视与原发性开角型青光眼的关系及研究进展进行综述。方法:仔细分析了28篇原文,总结出高度近视与原发性开角型青光眼的可能机理。结果:高度近视与原发性开角型青光眼密切相关,其可能的机制有:①升压基因学说。②胶原基因学说。结论:高度近视与原发性开角型青光眼密切相关,根据TIGR基因理论和胶原基因理论,高度近视与原发性开角型青光眼都与TIGR基因突变和胶原疾病有关。     

高度近视与原发性开角型青光眼

临床上发现高度近视与原发性开角型青光眼密切相关，其可能的机制有：（1）升压基因学说；（2）胶原基因学说。高度近视眼与原发性开角型青光眼对糖皮质激素反应增高表明，二的基因在糖皮质激素诱导下最易表达特异性蛋白，这可能与高度近视，原发性开角型青光眼的TIGR基因突变有关。本从流行病学、临床特征及诊断，遗传学说及机制等方面对高度近视与原发性开角型青光眼的关系及研究进展进行综述。     

高度近视与原发性开角型青光眼关系的研究进展

临床和实验研究均发现,青光眼患者近视发生率高于非青光眼人群。反之,近视,尤其高度近视（high myopia,HM）人群较其它人群更常伴有青光眼。当HM与原发性开角型青光眼（primary open—angle glaucoma,POAG）并存时,病情变得尤其复杂。两者发病机制之间的关系,目前在分子和基因水平的研究重点是：胶原基因学说和升压基因学说。从病理学角度讲,高度近视与青光眼都是胶原病变;此外,二者的小梁网细胞在糖皮质激素诱导下易表达特异性蛋白,这可能与高度近视、原发性开角型青光眼的TIGR（trabecular meshwork induced glucocorticoid response protein）基因突变有关。本文从流行病学、发病机制、临床特征及诊断注意要点等方面对高度近视与原发性开角型青光眼的关系及研究进展进行综述。     

高度近视合并POAG的临床特征研究进展

高度近视常常同时合并POAG,由于其眼底视盘和视网膜脉络膜等改变使其很难在早期发现POAG的合并存在。早期诊断和及时治疗高度近视合并POAG对提高患者的视觉和生存质量具有重要意义。现就高度近视与POAG的联系,高度近视合并POAG时相关的视功能改变做一综述,期望为临床诊断提供有益线索。     

高度近视合并原发性开角型青光眼延误诊的临床因素分析

目的探讨高度近视合并开角型青光眼发生延误诊的临床因素。方法对42例81眼病因回顾性分析,包括眼压、视野、矫正视力、眼底视盘、视杯、RNFL以及就诊时最早测量眼压和视野的时间情况。结果发现从就诊到确诊的时间为2m～7y,眼压、视野以及眼底情况有其特异性。结论高度近视合并原发性开角型青光发生延误因素,包括患者、医生以及疾病本身的特异性,提醒我们对高度近视的患者就诊时要重视。     

高度近视准分子激光角膜原位磨镶术后并发开角型青光眼的早期诊断

目的探讨高度近视行准分子激光角膜原位磨镶术（LASIK）后开角型青光眼患者的临床特征。方法回顾性分析2008年7月-2009年6月以屈光回退或眩光为主诉复诊的高度近视行LASIK术后患者13例25眼的临床资料;所有患者屈光回退现象均发生存术后2a,其中男8例,女5例;平均年龄30．1岁,均进行视力、屈光度、角膜地形图、Goldman眼压、眼轴、视野及OCT检查,原发性开角型青光眼的诊断依据全国青光眼学组建议的诊断标准,所有患者术前均签署知情同意书。结果12例23眼中,术后平均回退屈光度为（-1．57±0．36）D,裸眼视力0．42±0．14;1例患者双眼眩光加重,瞳孔散大,直径为4．5～5．0mm,夜间瞳孔直径为5．8～6．1mm;6例12眼术后校正眼压为21—26mmHg,合并有视网膜神经纤维层（RNFL）变薄及相应的青光眼典型视野改变;7例13眼屈光回退者中OCT检查RNFL变薄者3例5眼,用眼过度致视疲劳者4例8眼。结论高度近视患者行LASIK 2a后出现视力下降及眩光现象,且单纯以屈光回退及光学区过小无法解释者,要考虑到并发开角型青光眼的可能。     

近视眼视盘形态学变化与开角型青光眼的相关性研究进展

近年来研究发现,近视尤其是高度近视的眼部形态改变与开角型青光眼的关系密切,这些形态改变 不仅是近视患者易患青光眼的危险因素,同时也对此类患者病程进展有着一定影响。开角型青光眼 是进行性、不可逆性的致盲性眼病,因此近视患者早期发现、确诊、病情进展时及时干预显得十分 重要。现笔者回顾近年文献,在形态学变化上就近视与开角型青光眼的相关性做一综述。     

Is myopia a risk factor for glaucoma?

Controversy exists in the literature concerning the role of axial myopia as a risk factor for primary open-angle glaucoma. Epidemiologic evidence suggests that moderate and especially high myopia with a refractive error exceeding -6D is a risk factor for the development and the progression of glaucomatous optic neuropathy, with a twofold to threefold increased risk of glaucoma compared with that of nonmyopic subjects. This risk has been proven to be independent of other glaucoma risk factors and intraocular pressure (IOP). Myopic eyes have slightly although probably not clinically relevant, higher IOPs than emmetropic or hyperopic eyes. Selection bias could account for some of the reported association between glaucoma and myopia given that myopic subjects are likely to consult their ophthalmologist more frequently and glaucoma is underdiagnosed in myopic patients due to the great variability of their optic disc morphology, especially in high myopia, and the difficulty to interpret their visual field. The weakness of the fibroglial matrix of the nerve fibers at the optic disc together with the structural alterations in the lamina cribrosa and choroid, could contribute to the high susceptibility of the optic disc to IOP fluctuations and to increasing the risk of glaucomatous neuropathy, especially in high myopic eyes. Special attention will be given to patients with mild myopia who present with both elevated IOP levels and a positive family history. On the other hand, high myopic subjects should be screened for glaucoma at closer intervals. Moreover, after appropriate adjustments for deviations in central corneal thickness have been made, IOP greater than 17 mmHg must already be regarded as critical and initiation of medical treatment considered.     

Optic nerve blood flow is diminished in eyes of primary open-angle glaucoma suspects.

PURPOSE: The purpose of this study was to evaluate optic nerve blood flow in primary open-angle glaucoma suspect eyes with normal automated visual fields, in an attempt to elucidate how early in the glaucomatous disease process changes in optic nerve blood flow become apparent. METHODS: Twenty-one eyes (21 patients) suspected of having primary open-angle glaucoma were studied prospectively and compared with a previously reported cohort of 22 eyes (22 patients) with primary open-angle glaucoma and 15 eyes (15 subjects) of age-matched controls. Primary open-angle glaucoma suspect eyes had untreated intraocular pressure greater than 21 mm Hg and normal visual fields using Humphrey program 24-2 or 30-2 with a full threshold strategy. Laser Doppler flowmetry was used to measure optic nerve head blood velocity, volume, and flow at four quadrants in the optic nerve, in the cup, and in the foveola of one eye of each patient. The mean flow from the superotemporal rim, inferotemporal rim, and cup was calculated (Flow(3)) and identified as the main outcome measure. Measurements from primary open-angle glaucoma suspect eyes were compared with corresponding measurements from controls and eyes with primary open-angle glaucoma; a Student t test was employed with a Bonferroni corrected P value of.025 to account for comparisons of primary open-angle glaucoma suspects both to controls and to eyes with primary open-angle glaucoma. RESULTS: Compared with controls, Flow(3) was 24% lower in primary open-angle glaucoma suspect eyes (P <.0003). In primary open-angle glaucoma suspect eyes, flow was 16% lower in the superotemporal rim (P <.007), 35% lower in the cup (P <.007), and 22% lower in the inferotemporal neuroretinal rim (P <.029) compared with controls. No significant difference between primary open-angle glaucoma suspect and control eyes was seen in the inferonasal rim, superonasal rim, or foveola. No significant difference was detected at any location between primary open-angle glaucoma suspect eyes and eyes with primary open-angle glaucoma. CONCLUSIONS: Laser Doppler flowmetry detected circulatory abnormalities in primary open-angle glaucoma suspects who did not have any manifest visual field defect. Decreases in flow in glaucoma suspects were similar in magnitude to those of subjects with primary open-angle glaucoma. These data suggest that impaired optic nerve blood flow develops early in the glaucomatous process and does not develop solely as a result of glaucoma damage.     

Medical treatment for correction of hemodynamic, rheological and metabolic changes in young patients with glaucoma associated with myopia

The goal is to estimate the use and efficacy of differentiated approach to complex treatment of glaucomatous optic neuropathy in patients with primary open-angle glaucoma (POAG) associated with myopia. 71 patients aged 18-32 years old with POAG and high myopia and surgically or drug-induced normalized intraocular pressure were examined. The 1st group included 39 patients with ischemic form of POAG, 2nd group--32 patients with discirculatory form of POAG and the 3rd control group--10 patients of similar age with stable high myopia. Patients of the 1st group took glycine, ceraxon, actovegin and lymphotropic 1.0% nicotinic acid solution. Vasobral and cortexin were administered in the 2nd group. Medication provides correction of hemodynamic, theological and metabolic changes, that influence the clinical course of glaucoma associated with myopia.