OBJECTIVES: To assess whether open angle glaucoma (OAG) screening meets the UK National Screening Committee criteria, to compare screening strategies with case finding, to estimate test parameters, to model estimates of cost and cost-effectiveness, and to identify areas for future research. DATA SOURCES: Major electronic databases were searched up to December 2005. REVIEW METHODS: Screening strategies were developed by wide consultation. Markov submodels were developed to represent screening strategies. Parameter estimates were determined by systematic reviews of epidemiology, economic evaluations of screening, and effectiveness (test accuracy, screening and treatment). Tailored highly sensitive electronic searches were undertaken. RESULTS: Most potential screening tests reviewed had an estimated specificity of 85% or higher. No test was clearly most accurate, with only a few, heterogeneous studies for each test. No randomised controlled trials (RCTs) of screening were identified. Based on two treatment RCTs, early treatment reduces the risk of progression. Extrapolating from this, and assuming accelerated progression with advancing disease severity, without treatment the mean time to blindness in at least one eye was approximately 23 years, compared to 35 years with treatment. Prevalence would have to be about 3-4% in 40 year olds with a screening interval of 10 years to approach cost-effectiveness. It is predicted that screening might be cost-effective in a 50-year-old cohort at a prevalence of 4% with a 10-year screening interval. General population screening at any age, thus, appears not to be cost-effective. Selective screening of groups with higher prevalence (family history, black ethnicity) might be worthwhile, although this would only cover 6% of the population. Extension to include other at-risk cohorts (e.g. myopia and diabetes) would include 37% of the general population, but the prevalence is then too low for screening to be considered cost-effective. Screening using a test with initial automated classification followed by assessment by a specialised optometrist, for test positives, was more cost-effective than initial specialised optometric assessment. The cost-effectiveness of the screening programme was highly sensitive to the perspective on costs (NHS or societal). In the base-case model, the NHS costs of visual impairment were estimated as 669 pounds. If annual societal costs were 8800 pounds, then screening might be considered cost-effective for a 40-year-old cohort with 1% OAG prevalence assuming a willingness to pay of 30,000 pounds per quality-adjusted life-year. Of lesser importance were changes to estimates of attendance for sight tests, incidence of OAG, rate of progression and utility values for each stage of OAG severity. Cost-effectiveness was not particularly sensitive to the accuracy of screening tests within the ranges observed. However, a highly specific test is required to reduce large numbers of false-positive referrals. The findings that population screening is unlikely to be cost-effective are based on an economic model whose parameter estimates have considerable uncertainty. In particular, if rate of progression and/or costs of visual impairment are higher than estimated then screening could be cost-effective. CONCLUSIONS: While population screening is not cost-effective, the targeted screening of high-risk groups may be. Procedures for identifying those at risk, for quality assuring the programme, as well as adequate service provision for those screened positive would all be needed. Glaucoma detection can be improved by increasing attendance for eye examination, and improving the performance of current testing by either refining practice or adding in a technology-based first assessment, the latter being the more cost-effective option. This has implications for any future organisational changes in community eye-care services. Further research should aim to develop and provide quality data to populate the economic model, by conducting a feasibility study of interventions to improve detection, by obtaining further data on costs of blindness, risk of progression and health outcomes, and by conducting an RCT of interventions to improve the uptake of glaucoma testing.

The clinical effectiveness and cost-effectiveness of screening for open angle glaucoma: a systematic review and economic evaluation.

The role of matricellular proteins in glaucoma.

Background Primary open-angle glaucoma (POAG) is a multifactorial pathology involving a variety of pathogenic mechanisms, including oxidative/nitrosative stress. This latter is the consequence of the imbalance between excessive formation and insufficient protection against reactive oxygen/nitrogen species. Objective Our main goal is to gather molecular information to better managing pathologic variants that may determine the individual susceptibility to oxidative/nitrosative stress (OS/NS) and POAG. Method An extensive search of the scientific literature was conducted using PUBMED, the Web of Science, the Cochrane Library, and other references on the topic of POAG and OS/NS from human and animal model studies published between 2010 and 2017. Finally, 152 works containing relevant information that may help understanding the role of antioxidants, essential fatty acids, natural compounds and other similar strategies for counteracting OS/NS in POAG were considered. Results A wide variety of studies have proven that antioxidants, among them vitamins B3, C and E, Coenzyme Q10 or melatonin, ω-3/ω-6 fatty acids and other natural compounds (such as coffee, green tea, bear bile, gingko biloba, coleus, tropical fruits, etc.,) may help regulating the intraocular pressure as well as protecting the retinal neurons against OS/NS in POAG. Conclusion Based on the impact of antioxidants and ω-3/ω-6 fatty acids at the molecular level in the glaucomatous anterior and posterior eye segments, further studies are needed by integrating all issues involved in glaucoma pathogenesis, endogenous and exogenous risk factors and their interactions that will allow us to reach newer effective biotherapies for preventing glaucomatous irreversible blindness.

Strategies to Reduce Oxidative Stress in Glaucoma Patients.

Relationship between Severity of Visual Field Loss at Presentation and Rate of Visual Field Progression in Glaucoma

PURPOSE. We have previously demonstrated elevated levels of connective tissue growth factor (CTGF/CCN2) in the aqueous humor (AqH) of pseudoexfoliation glaucoma (PXFG) patients when compared with cataract controls. Furthermore, there is a significant trabecular meshwork (TM) and lamina cribrosa (LC) fibrotic phenotype associated with glaucoma, possibly driven by CTGF. The purpose of this study was to investigate the potential of antiCTGF immunotherapy in glaucoma. METHODS. Primary TM and LC cells were cultured from human donors with (GTM/GLC) and without (NTM/NLC) primary open angle glaucoma (POAG). Aqueous humor samples from PXFG, POAG, and control cataract patients were applied to N/GTM and N/GLC cells in the presence or absence of a therapeutic, humanized monoclonal anti-CTGF antibody FG-3019 (10 lg/mL). Hydrogen peroxide (H2O2) was also used as a stimulus. Expression of fibrotic genes (fibronectin-1, fibrillin-1, CTGF, collagen type I a1, and a-smooth muscle actin) was assessed by q-PCR. Protein expression of collagen 1A1 and a-smooth muscle actin was examined in N/G TM cells by SDS-PAGE. The modulatory effect of FG-3019 (10 lg/mL) and IgG (10 lg/mL) were also assessed. RESULTS. Treatment of cells with AqH from PXFG and POAG patients and H2O2 induced a significant (P < 0.05) increase in expression of profibrotic genes, which was significantly reduced by pretreatment with FG-3019 (P < 0.05). FG-3019 also reduced expression of asmooth muscle actin and collagen 1A1 protein expression in N/GTM cells. CONCLUSIONS. FG-3019 is effective in blocking extracellular matrix production in TM and LC cells, thus supporting a role for the use of anti-CTGF immunotherapy in the treatment of glaucoma.

Anti-connective tissue growth factor antibody treatment reduces extracellular matrix production in trabecular meshwork and lamina cribrosa cells.

Risk Factors for Progressive Visual Field Loss in Primary Open Angle Glaucoma

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Risk Factors for Progressive Visual Field Loss in Primary Open Angle Glaucoma