原发性开角型青光眼的免疫机制

非眼压因素造成的视网膜神经节细胞(RGC)及其轴突发生原发性损害的机制,以及原发性开角型青光眼(POAG)进展过程中RGC/轴突不依赖于眼压的继发性损害机制均是POAG发病机制中亟待回答的问题.视网膜是中枢神经系统(CNS)的一部分,POAG与CNS神经元退行性疾病的发病机制在一定程度上具有相似性,其中神经免疫-炎症与...     

原发性开角型青光眼血管学说的研究进展

青光眼是临床上常见的眼病之一,致残致盲率极高,特别是开角型青光眼(POAG)疗效较差,其病因及发病机理较复杂。既往研究表明眼内压增高改变了视神经乳头筛板的结构,造成神经纤维的机械性损伤,即机械学说。但眼压正常的POAG也有同样的视盘改变及视野缺损,而且有些青光眼患者即使用药物或者手术控制眼压后,视盘及视野损害仍然继续,提示还有其他因素影响着POAG的发生,其中血管学说一血流动力学的改变是其研究热点之一,本文就近年来有关开角型青光眼血流动力学发病机理研究及进展作一综述。     

原发性开角型青光眼视神经损害进展的相关危险因素研究:207例患者的随诊观察结果

目的 探讨原发性开角型青光眼(POAG)病情进展的相关危险因素.方法 回顾性分析北京同仁医院POAG患者中,随诊达3年以上,有5次以上眼压记录者的病情进展情况.将符合入选标准的207例(338眼)患者的基线立体眼底照片与随诊眼底照片,在计算机图像配准软件处理下进行闪烁对比,以发现盘沿及神经纤维层缺损进展情况.青光眼视神...     

原发性开角型青光眼对皮质激素、肾上腺素敏感反应及其与HLA抗原间的关系

Becket及Kass等近年来发表了一系列有关原发性开角型青光眼(Primary open-angle glautcoma,简称POAG)对皮质激素和肾上腺素的高敏反应及与HLA-B_7、B_(12)等抗原相互关系的文献,认为POAG的这些特征与临床上青光眼视野进展有关的各项危险指标如阳性家族史、高眼压,较大的C/D比率(C/D>0.3)等有不同程度的联系。Becker等人对POAG发病机理在细胞和分子水平的研究和遗传方式的探讨上已自成一个学派。在近代有关POAG发病的基础研究中已成为一个争论的焦点。本文着重介绍近十年来该     

原发性开角型青光眼全身危险因素及眼体同治的系统回顾和Meta分析

目的系统回顾原发性开角型青光眼(POAG)存在的全身危险因素,分析眼体同治对POAG的治疗效果。 方法对Embase、Medline、Pubmed、Google Scholarship、ISI Web of Knowledge及the Cochrane Central Register of Controlled Trials等英文文献数据库和维普、万方、中国知网及生物医学文献数据库等中文文献数据库进行检索。在检索结果中,选取以POAG患者作为研究对象,以身体质量指数(BMI)、雌激素相关情况、甲皱襞微循环情况、传统降眼压治疗联合口服硝苯地平以及中西医结合治疗效果为主要分析因素的研究。用Meta分析评估POAG患者BMI情况;并对雌激素及微循环异常在POAG发病中的作用、传统降眼压联合口服硝苯地平及中西医结合对POAG的治疗效果进行系统回顾。 结果BMI相关文献中共6篇文章符合纳入标准进行Meta分析。总样本量26 835例,包括POAG患者3058例,正常对照23 777例。POAG患者BMI (MD＝-0.64,95% CI：-1.06,-0.21)较正常人明显降低,差异有统计学意义( I²＝99%,P<0.05)。共分析雌激素相关文献7篇,其中2项研究结果表明女性停经时间相对较迟可以降低POAG的发病风险,3项研究结果表明停经后雌激素替代治疗降低POAG发病的风险。分析微循环相关文献5篇,研究结果表明POAG患者存在甲皱襞毛细血管出血、扩张、无血管区、血管形态异常、血流流速减慢、流量降低情况。分析传统降眼压治疗联合口服硝苯地平治疗青光眼相关文献10篇,其中4项研究结果表明口服硝苯地平后视野无明显进展或较传统治疗方法视野进展缓慢,5项研究针对口服硝苯地平后青光眼患者眼部血流情况进行研究,其中2项证明眼部血流有改善并且差异有统计学意义(P<0.05),3项无统计学意义( P>0.05)。分析5篇中西医结合治疗POAG相关研究,其中4项研究结果表明中西医结合治疗效果更好,1项研究结果表明组间差异无统计学意义(t＝-0.510,0.140; P>0.05)。 结论POAG患者BMI较正常人低,低雌激素、微循环异常可能增加POAG发病风险。联合硝苯地平及中西医结合的眼体同治方法对POAG治疗效果较传统降眼压治疗效果好。     

原发性开角型青光眼降眼压药物治疗进展

原发性开角型青光眼（POAG）的治疗目的主要是停止视力能受损的过程，阻止其因视神经纤维丧失而导致的视功能明显损害。药物治疗是临床治疗原发性开角型青光眼的主要措施，随着人们对青光眼发病机制的不断研究，抗青光眼药物也有了很大进展。本文就近年来有关局部应用治疗原发性开角型青光眼的降眼压药物研究及其进展作一综述。     

压力对小梁网途径房水外流通路的影响

病理性高眼压是原发性开角型青光眼(primary open-angle glaucoma,POAG)发病的重要危险因素之一,主要是由小梁网途径房水外流阻力增加所致.高眼压本身通过机械压力导致小梁网细胞老化、细胞骨架成分改变、细胞外基质异常沉积、氧化应激损伤、基因表达异常等影响小梁网途径房水外流阻力,这为探讨POAG的发病机制及治疗方向奠定了一定的基础.     

原发性开角型和闭角型青光眼眼压降低前后视盘改变和筛板顺应性的对比研究

目的比较降跟压前后原发性慢性闭角型青光眼（PACG）与原发性开角型青光眼（POAG）的视盘结构改变,了解两者间筛板顺应性是否存在差异。设计前瞻性对比研究。研究对象PACG36例49眼和POAG35例49眼。方法眼压降低前全部患者进行海德堡视网膜断层扫描（HRT—II）及Humphrey静态视野检查。根据病情选择手术、激光或药物治疗,使眼压降至正常范围。眼压降低后1个月重复HRT检查和视野检查。比较POAG和PACG眼压降低前后HRT视盘参数的变化,采用多元线性逐步回归法校正治疗前眼压、眼压降低幅度、年龄、杯盘比等因素影响。主要指标眼压降低前后HRT视杯面积、盘沿面积、视杯容积、平均视杯深度的差值。结果PACG及POAG组的视杯面积、视杯容积、平均视杯深度等指标在眼压降低后均明显降低（P〈0．05）,盘沿面积在眼压降低后均明显增加（P〈0．05）。视杯面积、盘沿面积、视杯容积、平均视杯深度在跟压降低前后的差值两组间无显著性差异（P〉0．05）。眼压降低前后这4个参数的差值与眼压降低幅度及杯盘比有关（P〈0．05）;与年龄及治疗前眼压无关（P〉0．05）。结论眼压降低后青光眼视盘形态结构有一定回复;但在PACG和POAG间,视盘形态结构回复的程度无明显差异,PACG和POAG的筛板顺应性可能无差异。（眼科,2009,18：264—269）     

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。     

CYP1B1基因突变与原发性开角型青光眼发病关系的研究进展

原发性青光眼包括原发性开角型青光眼（POAG）、原发性闭角型青光眼（PACG）及原发性婴幼儿青光眼（PCG）.目前认为原发性青光眼的发病是遗传因素、环境因素、生活习惯等多种因素综合作用的结果,其中遗传因素,尤其是基因突变,在青光眼的发病过程中起着重要作用.自1997年发现CYP1B1基因为PCG的致病基因以来,关于CYP1B1基因突变与青光眼发病关系的研究成为青光眼遗传和基因研究的热点.随着研究的逐渐深入,许多学者认为CYP1B1基因也是POAG致病基因的候选基因.本研究对近十余年来对CYP1 B1基因的结构和功能以及CYP1B1基因突变与POAG发病及进展关系的研究进展进行总结.     

The role of blood pressure in glaucoma

Although intraocular pressure (IOP) remains an important risk factor for glaucoma, it is clear that other factors can also influence disease development and progression. More recently, the role that blood pressure (BP) has in the genesis of glaucoma has attracted attention, as it represents a clinically modifiable risk factor and thus provides the potential for new treatment strategies beyond IOP reduction. The interplay between blood pressure and IOP determines the ocular perfusion pressure (OPP), which regulates blood flow to the optic nerve. If OPP is a more important determinant of ganglion cell injury than IOP, then hypotension should exacerbate the detrimental effects of IOP elevation, whereas hypertension should provide protection against IOP elevation. Epidemiological evidence provides some conflicting outcomes of the role of systemic hypertension in the development and progression of glaucoma. The most recent study showed that patients at both extremes of the blood pressure spectrum show an increased prevalence of glaucoma. Those with low blood pressure would have low OPP and thus reduced blood flow; however, that people with hypertension also show increased risk is more difficult to reconcile. This finding may reflect an inherent blood flow dysregulation secondary to chronic hypertension that would render retinal blood flow less able to resist changes in ocular perfusion pressure. Here we review both clinical and experimental studies that have attempted to clarify the relationships among blood pressure, OPP and blood flow autoregulation in the pathogenesis of glaucoma.     

Glaucoma update: epidemiology and new approaches to medical management

Glaucoma describes a group of ocular conditions which involve progressive optic nerve damage associated with loss of visual function and, frequently, with elevated intraocular pressure. Recent estimates of worldwide prevalence predict that 67 million people will suffer from glaucoma by the year 2000. Although the clinical features of glaucoma are reasonably well described, the pathogenesis of optic nerve damage remains unclear. Intraocular pressure (IOP) is accepted as an important risk factor; however, it is clear that other factors play a role in the pathogenesis of the disease, and such factors may interact with IOP to greatly enhance its harmful effects. Many of the new therapeutic approaches to the stabilisation and potential cure of glaucoma attempt to address these non-IOP factors. The aim of the following paper is to consider the implications of new estimates of disease prevalence, discuss theories related to optic nerve damage and outline new and future approaches to the medical management of the disease.     

颅内压与青光眼及其无创测量技术的研究进展

青光眼是世界上第二位致盲性眼病,第一位不可复性致盲性眼病。尽管眼压增高被认为是青光眼性视神经损害的主要危险因素,但是50%的原发性开角型青光眼患者的日常眼压正常,还有一些患者尽管眼压控制良好,但青光眼性视神经损害仍继续发展。这些现象无法用高眼压理论来解释,青光眼患者视神经损害的发病机制仍待探讨。目前国内外的一些研究表明：（1）视神经周围的生物力学的解剖结构包括眼内压,筛板和球后的脑脊液压力在原发性开角型青光眼的发病机制中发挥重要的作用;（2）正常眼压性青光眼患者的脑脊液压力比正常人低,而跨筛板压力差比正常人高;（3）高眼压症患者的脑脊液压力比正常人群高,而跨筛板压力差和正常人之间没有统计学意义。基于以上研究,本文就颅内压与青光眼性视神经损害之间关系的相关研究进展及临床上可行的无创颅内压测量方法作一综述。     

原发性开角型青光眼与24h眼压及眼灌注压的研究进展

原发性开角型青光眼是一类早期无明显临床症状,但随病情进展将导致不可逆的视神经损害及视野缺损的致盲性眼病。眼压是原发性开角型青光眼诊断及评定治疗效果的简单而又重要的指标。临床上,一些治疗中的原发性开角型青光眼患者白天就诊时间所测眼压已达靶眼压,但视神经损害却仍在进展,研究表明可能与夜间眼压的升高、24 h较大的眼压波动及夜间眼灌注压的降低有关。因此,我们对原发性开角型青光眼与眼压及眼灌注压波动的相关文献予以综述,以更好的理解三者之间的关系。     

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）     

Absolute filling defects of the optic disc in fluorescein angiograms in glaucoma--a retrospective clinical study

BACKGROUND: Analysis of clinical importance of the size of filling defects in fluorescein angiograms in primary open-angle glaucoma (POAG), normal-tension glaucoma (NTG), ocular hypertension and subjects with physiological excavations in comparison to visual field loss, optic nerve head morphology and hemodynamics. PATIENTS AND METHODS: 75 patients (POAG, NTG, ocular hypertension) and 10 healthy subjects with physiological excavations were included in this study. In digitized video fluorescein angiograms (Scanning Laser Ophthalmoscope) the size of absolute filling defects of the optic disc was quantified in the early venous phase and expressed by percentage of the optic disc. Visual fields were obtained by conventional static perimetry (Humphrey 24-2) and graded in stages of glaucoma visual field defects (Aulhorn I-V). Optic disc excavations were evaluated as cup-to-disc-area-ratios. RESULTS: The filling defects correlated with the visual-field loss stages of Aulhorn and the visual field indices MD (mean deviation), PSD (pattern standard deviation) and CPSD (corrected pattern standard deviation). There was no correlation with the index SF (short-term fluctuation) and with systemic hemodynamics (blood pressure, perfusion pressure) or the IOP. Absolute filling defects correlated with the cup-to-disc-area-ratio in NTG. The absolute filling defects were larger in patients with glaucoma (POAG, NTG) in comparison to patients without glaucomatous visual field loss (ocular hypertension, glaucoma-like discs). No difference of filling defects was found in the glaucoma group (POAG, NTG). Patients with NTG had larger excavations and lower systolic blood pressures than patients with POAG. CONCLUSION: The size of fluorescein filling defects may be useful as a parameter for the evaluation of an ischemic lesion of the optic nerve head. Absolute filling defects may differentiate POAG from ocular hypertension and NTG from glaucoma-like discs without field defects. The results support the hypothesis that in POAG and NTG disturbances of the circulation result in similar filling defects of the optic disc and visual field loss.     

Quantifying the effect of intraocular pressure reduction on the occurrence of glaucoma

Purpose: To estimate the effect of reducing intraocular pressure (IOP) on: (i) the incidence of primary open‐angle glaucoma (POAG) in patients with ocular hypertension (OH), and (ii) the progression of glaucoma. Methods: A meta‐analysis of relevant randomized controlled trials was conducted. A literature search was performed to identify trials with: a randomized comparison of IOP‐lowering intervention versus placebo or no treatment; visual field loss or optic disc changes as outcome; and follow‐up >6 months. A pooled relative risk (RR) was calculated by a random effects model. Risk reduction of glaucoma conversion per mmHg of IOP reduction was quantified in a meta‐regression model. Results: We identified nine OH and one POAG trials. A meta‐analysis of OH trials gives a pooled RR of 0.61 [95% confidence interval (CI) 0.45–0.83]. A meta‐regression shows a decrease of the RR of glaucoma conversion by 14% with each mmHg extra IOP reduction (P = 0.045). No meta‐analysis of POAG trials was performed because only one study has been identified. Conclusion: There is sufficient evidence that OH therapy reduces the risk of conversion to glaucoma. This risk reduction increases with greater IOP reduction.     

Vascular risk factors for primary open angle glaucoma: the Egna-Neumarkt Study

OBJECTIVE: To assess the impact of vascular risk factors on the prevalence of primary open angle glaucoma. DESIGN: Population-based cross-sectional study. PARTICIPANTS: Four thousand two hundred ninety-seven patients more than 40 years of age underwent a complete ocular examination in the context of the Egna-Neumarkt Glaucoma Study. INTERVENTION: Ocular examinations were performed by trained, quality-controlled ophthalmologists according to a predefined standardized protocol including medical interview, blood pressure reading, applanation tonometry, computerized perimetry, and optic nerve head examination. MAIN OUTCOME MEASURES: Prevalences of ocular hypertension, primary open-angle glaucoma, normal-tension glaucoma, and other types of glaucoma were determined. Correlation coefficients were calculated for the association between systemic blood pressure and age-adjusted intraocular pressure (IOP) and between age and both intraocular and systemic blood pressures. Odds ratios were computed to assess the risk of primary open-angle glaucoma and normal-tension glaucoma in relation to systemic hypertension or antihypertensive medication, blood pressure levels, diastolic perfusion pressure, and a number of other cardiovascular risk factors. RESULTS: A positive correlation was found between systemic blood pressure and IOP, and an association was found between diagnosis of primary open-angle glaucoma and systemic hypertension. Lower diastolic perfusion pressure is associated with a marked, progressive increase in the frequency of hypertensive glaucoma. No relationship was found between systemic diseases of vascular origin and glaucoma. CONCLUSIONS: Our data are in line with those reported in other recent epidemiologic studies and show that reduced diastolic perfusion pressure is an important risk factor for primary open-angle glaucoma.     

The relationship between central corneal thickness-adjusted intraocular pressure and glaucomatous visual-field loss.

BACKGROUND: Although measurement of central corneal thickness (CCT) is increasingly becoming an important component of glaucoma risk analysis, significant controversy exists regarding the benefit of calculating a corrected intraocular pressure (IOP) value from measured IOP and CCT data. METHODS: Three hundred forty-four male subjects were identified from a VA eye clinic with one of the following clinical diagnoses: ocular hypertension (OHT), primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and normal tension glaucoma suspect (NTGS). Using one eye per subject, multivariate logistic regression and correlational analyses were performed to determine relationships between glaucomatous visual-field loss and several glaucoma risk factors, including adjusted IOP values. RESULTS: Multivariate logistic regression analysis did not identify CCT-adjusted IOP values as independent risk factors for development of either NTG or POAG-related glaucomatous visual-field loss. CCT, however, was found to be strongly associated with both NTG and POAG-related visual-field loss. Correlational analysis revealed a weak correlation between Ehlers-adjusted pre-treatment IOP and severity of POAG-related visual-field loss, but no other adjusted IOP values significantly correlated with severity of visual-field loss in either POAG or NTG. CONCLUSIONS: Our results suggest that adjusted IOP, as calculated using current algorithms, is not useful within glaucoma risk analysis, since adjusted IOP was unable to predict either presence or severity of glaucomatous visual-field loss in this study. CCT, conversely, was found to be a robust and independent predictor of glaucomatous visual-field loss. These findings, while supporting routine CCT measurements for all glaucoma suspects, do not support routine clinical computation of adjusted IOP values using current algorithms.     

New directions in the treatment of normal tension glaucoma

Glaucoma is a progressive optic neuropathy that causes characteristic changes of the optic nerve and visual field in relation to intraocular pressure (IOP). It is now known that glaucoma can occur at statistically normal IOPs and prevalence studies have shown that normal tension glaucoma (NTG) is more common than previously thought. While IOP is believed to be the predominant risk factor in primary open angle glaucoma (POAG), IOP-independent risk factors, such as vascular dysregulation, are believed to play an important part in the pathogenesis of NTG. Though certain distinguishing phenotypic features of NTG have been reported, such as an increased frequency of disc hemorrhages, acquired pits of the optic nerve and characteristic patterns of disc cupping and visual field loss, there is much overlap of the clinical findings in NTG with POAG, suggesting that NTG is likely part of a continuum of open angle glaucomas. However, IOP modification is still the mainstay of treatment in NTG. As in traditional POAG, reduction of IOP can be achieved with the use of medications, laser trabeculoplasty or surgery. Studies now show that the choice of medication may also be important in determining the outcomes of these patients. Though it is likely that future treatment of NTG will involve modification of both IOP and IOP-independent risk factors, current efforts to develop IOP-independent neuroprotective treatments have not yet proven to be effective in humans.