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- W2020158637 abstract "Glaucoma, or the sea-colored blindness, is a disease we still have much to learn about. It was described by Hippocrates in ancient Greece and differentiated from cataract, the white blindness (in cataract the pupil became white like broken whitewater; in glaucoma the blind pupil had the blue-green haze from a clear lens). The importance of increased intraocular pressure was recognized and accepted only in the early 1800s. The invention of the ophthalmoscope by Helmholtz in 1850 led to the recognition of disc cupping and a greater understanding of glaucoma. This new instrument was one of the main topics at the first International Congress of Ophthalmology in 1857, at the conclusion of which von Graeffe announced a revolutionary operation, broad iridectomy, which could cure some cases of glaucoma. Medical treatment with eserine became possible in 1876. Bjerrum defined the characteristic visual fields defects in 1889. The introduction of the slit lamp in 1911 permitted the development of gonioscopy and allowed acute angle closure and primary open-angle glaucoma (POAG) to be clearly separated in 1938 by Barkan. The introduction of trabeculectomy by Watson in 1970 greatly advanced the surgical treatment of glaucoma. The advent of beta blockers in 1976 and prostaglandins in 1996 redefined the medical management.The major causes of blindness in developed countries have changed mightily over the last century although comparisons can only be approximate as data are often presented as a percentage of those blind and the population structures have changed greatly. One hundred years ago, over half of the blindness was due to corneal disease, 50 years ago half was due to untreated cataract, whereas today half the blindness is due to age-related macular degeneration. However, over this time, glaucoma has consistently caused about one tenth (8%–12%) of blindness in most studies in most countries. Why should this be so? Why has the proportion of blindness caused by glaucoma changed so little over time, especially as we have this new understanding and these wonderful new drugs and surgical alternatives?One reason is the ageing demographics of most societies means more people are living to a much older age and more older people means more glaucoma. The prevalence of glaucoma (and here I refer to POAG that causes almost over 95% of the glaucoma seen in developed countries) increases with age. However, this rate does not reach 100% as it does for lens opacities, nor does it increase exponentially over the age of 80 as it does for age-related macular degeneration. Rather, we found in the Melbourne Visual Impairment Project (VIP) that the prevalence leveled off at about 10% older than age 80.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar This suggests that only something like 10% or so of people are at risk of developing glaucoma, provided they live long enough. This study examined people of all ages; the oldest was 104, although there were only small numbers of the most elderly. It would be most interesting to have this observation confirmed by other studies, but unfortunately most of the population-based studies so far have not examined many people over age 85.Another reason glaucoma blindness rates remain unchanged is that half of those who have glaucoma have not been diagnosed and so are not being treated.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar, 2Dielemans I. Vingerling J.R. Wolfs R.C. et al.The prevalence of primary open-angle glaucoma in a population-based study in the Netherlands The Rotterdam Eye Study.Ophthalmology. 1994; 101: 1851-1855Abstract Full Text PDF PubMed Scopus (469) Google Scholar What was most disturbing was the finding in the Melbourne VIP that half of those who had undiagnosed glaucoma had had an eye examination in the previous year and the diagnosis of glaucoma had been missed.3Wong E.Y. Keeffe J.E. Rait J.L. et al.Detection of undiagnosed glaucoma by eye health professionals.Ophthalmology. 2004; 111: 1508-1514Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Every one of those missed had a field defect that presumably had not been tested for, or not detected. Mandating visual field testing on every routine eye examination may be too much, but more careful testing of anyone with a family history would achieve a lot.At present, the strongest risk factor for glaucoma is to have a first-degree relative who has glaucoma.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar, 4Tielsch J.M. Katz J. Sommer A. et al.Family history and risk of primary open angle glaucoma The Baltimore Eye Survey.Arch Ophthalmol. 1994; 112: 69-73Crossref PubMed Scopus (328) Google Scholar Not unexpectedly, asking about a family history of glaucoma is not a particularly reliable indicator; most people don't know.5McNaught A.I. Allen J.G. Healey D.L. et al.Accuracy and implications of a reported family history of glaucoma: experience from the Glaucoma Inheritance Study in Tasmania.Arch Ophthalmol. 2000; 118: 900-904PubMed Google Scholar Most people with glaucoma have not been advised to warn their relatives, and people do not usually go home and announce to the family, “Hey, guess what? I was told today I have glaucoma.” Although family linkage and heritability of glaucoma have been shown to be very strong, to date the hunt for specific genes for glaucoma has been disappointing and slow after the promising start with myocillin. This is clearly a fertile area for more research.The observed increase in risk of glaucoma in African Americans, and in some parts of the Caribbean and Africa itself, most likely reflects genetic heterogeneity of high-risk genes. Dark pigmentation itself is not a risk factor as such. For example, POAG is very rare in traditional heavily pigmented Aboriginal Australians, even when they have pseudoexfoliation.6Taylor H.R. Pseudoexfoliation, an environmental disease?.Trans Ophthalmol Soc UK. 1979; 99: 302-307PubMed Google ScholarThe interesting paper in this issue by Rein et al7Rein D.B. Wittenborn J.S. Lee P.P. et al.The cost-effectiveness of routine office-based identification and subsequent medical treatment of primary open-angle glaucoma in the United States.Ophthalmology. 2009; 116: 823-832Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar sets out the results of a computer model that exams the economic impact in the US of diagnosing and treating glaucoma. They have taken as the standard of care the American Academy of Ophthalmology (AAO) Preferred Practice Pattern and followed a conventional treatment progression using different topical medications then laser trabeculoplasty and trabeculectomy. They used the results of clinical trials to model the response to treatment. Their findings indicate that the diagnosis and treatment of POAG would reduce the percentage of those who would develop mild field loss (≥16 decibels [dB]) from 27% to 5%–12% and the number of years that people would have visual impairment (or blindness) would be reduced from 5.2 years to 1.0-2.6 years. These changes would cost between $28,000 and $46,000/QALY Quality Adjusted Life Year (QALY). These gains would be regarded to be quite highly cost-effective. Their model was shown to be sensitive to the cost of treatment; a doubling in these costs changed the ratio to about $90,000/QALY. It was also sensitive to the value given to a QALY, if the value of a QALY were halved, the ratio became $93,000/QALY.An analysis we performed in Australia asked slightly different questions and found somewhat different answers.8Taylor H.R. Crowston J. Keeffe J. et al.Tunnel Vision: The Economic Impact of Primary Open Angle Glaucoma–A Dynamic Economic Model. Centre for Eye Research Australia, Melbourne2008www.cera.org.auGoogle Scholar We found that increasing the number of diagnosed and treated people with glaucoma was quite expensive at $AU153,000–167,000/QALY and at this cost not very cost effective. This analysis included caregiver and employment costs that the Rein model did not, but also differed in a number of other ways. In addition the Australian Study looked at the order in which treatment modifications were used. A change to initial laser trabeculoplasty followed by topical medication and then trabulectomy was surprisingly cost-effective and was actually cost savings, returning $2.50 for every $1.00 spent. Even if the cost of laser treatment increased 4-fold, it still returned $1.74 for each $1.00 spent. One can only guess at the impact that the lack of well-funded champions to promote laser trabeculoplasty over available pharmaceutical products may have had on our prescribing habits and the costs of managing glaucoma.To my mind, a key to reducing blindness from glaucoma is first and most simply to remind every patient with glaucoma that it is a hereditary disease and that they need to inform their first-degree relatives so that their relatives in turn can say during their own eye examinations, “You should know that glaucoma runs in my family.”Second from a health economics perspective, much more consideration should be given to laser trabeculoplasty as the initial treatment. It should be considered as “a first drop,” and additional medications introduced as needed. However, for as long as laser trabeculoplasty controls glaucoma, it would seem to do so 24 hours a day (or 24/7), it has 100% “compliance” and is a “one-time” cost.I hope that addressing these 2 issues and convincing health program funders of the health economic implications of untreated glaucoma will go a long way toward reducing the vision and economic impact of glaucoma. Glaucoma, or the sea-colored blindness, is a disease we still have much to learn about. It was described by Hippocrates in ancient Greece and differentiated from cataract, the white blindness (in cataract the pupil became white like broken whitewater; in glaucoma the blind pupil had the blue-green haze from a clear lens). The importance of increased intraocular pressure was recognized and accepted only in the early 1800s. The invention of the ophthalmoscope by Helmholtz in 1850 led to the recognition of disc cupping and a greater understanding of glaucoma. This new instrument was one of the main topics at the first International Congress of Ophthalmology in 1857, at the conclusion of which von Graeffe announced a revolutionary operation, broad iridectomy, which could cure some cases of glaucoma. Medical treatment with eserine became possible in 1876. Bjerrum defined the characteristic visual fields defects in 1889. The introduction of the slit lamp in 1911 permitted the development of gonioscopy and allowed acute angle closure and primary open-angle glaucoma (POAG) to be clearly separated in 1938 by Barkan. The introduction of trabeculectomy by Watson in 1970 greatly advanced the surgical treatment of glaucoma. The advent of beta blockers in 1976 and prostaglandins in 1996 redefined the medical management. The major causes of blindness in developed countries have changed mightily over the last century although comparisons can only be approximate as data are often presented as a percentage of those blind and the population structures have changed greatly. One hundred years ago, over half of the blindness was due to corneal disease, 50 years ago half was due to untreated cataract, whereas today half the blindness is due to age-related macular degeneration. However, over this time, glaucoma has consistently caused about one tenth (8%–12%) of blindness in most studies in most countries. Why should this be so? Why has the proportion of blindness caused by glaucoma changed so little over time, especially as we have this new understanding and these wonderful new drugs and surgical alternatives? One reason is the ageing demographics of most societies means more people are living to a much older age and more older people means more glaucoma. The prevalence of glaucoma (and here I refer to POAG that causes almost over 95% of the glaucoma seen in developed countries) increases with age. However, this rate does not reach 100% as it does for lens opacities, nor does it increase exponentially over the age of 80 as it does for age-related macular degeneration. Rather, we found in the Melbourne Visual Impairment Project (VIP) that the prevalence leveled off at about 10% older than age 80.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar This suggests that only something like 10% or so of people are at risk of developing glaucoma, provided they live long enough. This study examined people of all ages; the oldest was 104, although there were only small numbers of the most elderly. It would be most interesting to have this observation confirmed by other studies, but unfortunately most of the population-based studies so far have not examined many people over age 85. Another reason glaucoma blindness rates remain unchanged is that half of those who have glaucoma have not been diagnosed and so are not being treated.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar, 2Dielemans I. Vingerling J.R. Wolfs R.C. et al.The prevalence of primary open-angle glaucoma in a population-based study in the Netherlands The Rotterdam Eye Study.Ophthalmology. 1994; 101: 1851-1855Abstract Full Text PDF PubMed Scopus (469) Google Scholar What was most disturbing was the finding in the Melbourne VIP that half of those who had undiagnosed glaucoma had had an eye examination in the previous year and the diagnosis of glaucoma had been missed.3Wong E.Y. Keeffe J.E. Rait J.L. et al.Detection of undiagnosed glaucoma by eye health professionals.Ophthalmology. 2004; 111: 1508-1514Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Every one of those missed had a field defect that presumably had not been tested for, or not detected. Mandating visual field testing on every routine eye examination may be too much, but more careful testing of anyone with a family history would achieve a lot. At present, the strongest risk factor for glaucoma is to have a first-degree relative who has glaucoma.1Weih L.M. Nanjan M. McCarty C.A. Taylor H.R. Prevalence and predictors of open-angle glaucoma; Results from the Visual Impairment Project.Ophthalmology. 2001; 108: 1966-1972Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar, 4Tielsch J.M. Katz J. Sommer A. et al.Family history and risk of primary open angle glaucoma The Baltimore Eye Survey.Arch Ophthalmol. 1994; 112: 69-73Crossref PubMed Scopus (328) Google Scholar Not unexpectedly, asking about a family history of glaucoma is not a particularly reliable indicator; most people don't know.5McNaught A.I. Allen J.G. Healey D.L. et al.Accuracy and implications of a reported family history of glaucoma: experience from the Glaucoma Inheritance Study in Tasmania.Arch Ophthalmol. 2000; 118: 900-904PubMed Google Scholar Most people with glaucoma have not been advised to warn their relatives, and people do not usually go home and announce to the family, “Hey, guess what? I was told today I have glaucoma.” Although family linkage and heritability of glaucoma have been shown to be very strong, to date the hunt for specific genes for glaucoma has been disappointing and slow after the promising start with myocillin. This is clearly a fertile area for more research. The observed increase in risk of glaucoma in African Americans, and in some parts of the Caribbean and Africa itself, most likely reflects genetic heterogeneity of high-risk genes. Dark pigmentation itself is not a risk factor as such. For example, POAG is very rare in traditional heavily pigmented Aboriginal Australians, even when they have pseudoexfoliation.6Taylor H.R. Pseudoexfoliation, an environmental disease?.Trans Ophthalmol Soc UK. 1979; 99: 302-307PubMed Google Scholar The interesting paper in this issue by Rein et al7Rein D.B. Wittenborn J.S. Lee P.P. et al.The cost-effectiveness of routine office-based identification and subsequent medical treatment of primary open-angle glaucoma in the United States.Ophthalmology. 2009; 116: 823-832Abstract Full Text Full Text PDF PubMed Scopus (66) Google Scholar sets out the results of a computer model that exams the economic impact in the US of diagnosing and treating glaucoma. They have taken as the standard of care the American Academy of Ophthalmology (AAO) Preferred Practice Pattern and followed a conventional treatment progression using different topical medications then laser trabeculoplasty and trabeculectomy. They used the results of clinical trials to model the response to treatment. Their findings indicate that the diagnosis and treatment of POAG would reduce the percentage of those who would develop mild field loss (≥16 decibels [dB]) from 27% to 5%–12% and the number of years that people would have visual impairment (or blindness) would be reduced from 5.2 years to 1.0-2.6 years. These changes would cost between $28,000 and $46,000/QALY Quality Adjusted Life Year (QALY). These gains would be regarded to be quite highly cost-effective. Their model was shown to be sensitive to the cost of treatment; a doubling in these costs changed the ratio to about $90,000/QALY. It was also sensitive to the value given to a QALY, if the value of a QALY were halved, the ratio became $93,000/QALY. An analysis we performed in Australia asked slightly different questions and found somewhat different answers.8Taylor H.R. Crowston J. Keeffe J. et al.Tunnel Vision: The Economic Impact of Primary Open Angle Glaucoma–A Dynamic Economic Model. Centre for Eye Research Australia, Melbourne2008www.cera.org.auGoogle Scholar We found that increasing the number of diagnosed and treated people with glaucoma was quite expensive at $AU153,000–167,000/QALY and at this cost not very cost effective. This analysis included caregiver and employment costs that the Rein model did not, but also differed in a number of other ways. In addition the Australian Study looked at the order in which treatment modifications were used. A change to initial laser trabeculoplasty followed by topical medication and then trabulectomy was surprisingly cost-effective and was actually cost savings, returning $2.50 for every $1.00 spent. Even if the cost of laser treatment increased 4-fold, it still returned $1.74 for each $1.00 spent. One can only guess at the impact that the lack of well-funded champions to promote laser trabeculoplasty over available pharmaceutical products may have had on our prescribing habits and the costs of managing glaucoma. To my mind, a key to reducing blindness from glaucoma is first and most simply to remind every patient with glaucoma that it is a hereditary disease and that they need to inform their first-degree relatives so that their relatives in turn can say during their own eye examinations, “You should know that glaucoma runs in my family.” Second from a health economics perspective, much more consideration should be given to laser trabeculoplasty as the initial treatment. It should be considered as “a first drop,” and additional medications introduced as needed. However, for as long as laser trabeculoplasty controls glaucoma, it would seem to do so 24 hours a day (or 24/7), it has 100% “compliance” and is a “one-time” cost. I hope that addressing these 2 issues and convincing health program funders of the health economic implications of untreated glaucoma will go a long way toward reducing the vision and economic impact of glaucoma." @default.
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