Age-Related Macular Degeneration de Jong, Paulus T.V.M
The New England journal of medicine,
10/2006, Volume:
355, Issue:
14
Journal Article
Peer reviewed
This review describes the mechanisms entailed in the leading cause of blindness in the United States.
This review describes the mechanisms entailed in the leading cause of blindness in the United ...States.
Since 1874, when it was first described in the medical literature as “symmetrical central choroido-retinal disease occurring in senile persons,”
1
age-related macular degeneration has also been referred to as senile, or diskiform, macular degeneration, among many other terms. About 25 years ago, the term “age-related maculopathy” was coined and its end stage was acknowledged as age-related macular degeneration. In this review, I use the commonly accepted age-related macular degeneration, although I have reservations about its appropriateness. After briefly describing the clinical features of age-related macular degeneration, I turn to the physiology of the aging macula and to mechanisms implicated in . . .
Open-angle glaucoma (OAG) is the commonest cause of irreversible blindness worldwide. Apart from an increased intraocular pressure (IOP), oxidative stress and an impaired ocular blood flow are ...supposed to contribute to OAG. The aim of this study was to determine whether the dietary intake of nutrients that either have anti-oxidative properties (carotenoids, vitamins, and flavonoids) or influence the blood flow (omega fatty acids and magnesium) is associated with incident OAG. We investigated this in a prospective population-based cohort, the Rotterdam Study. A total of 3502 participants aged 55 years and older for whom dietary data at baseline and ophthalmic data at baseline and follow-up were available and who did not have OAG at baseline were included. The ophthalmic examinations comprised measurements of the IOP and perimetry; dietary intake of nutrients was assessed by validated questionnaires and adjusted for energy intake. Cox proportional hazard regression analysis was applied to calculate hazard ratios of associations between the baseline intake of nutrients and incident OAG, adjusted for age, gender, IOP, IOP-lowering treatment, and body mass index. During an average follow-up of 9.7 years, 91 participants (2.6%) developed OAG. The hazard ratio for retinol equivalents (highest versus lowest tertile) was 0.45 (95% confidence interval 0.23—0.90), for vitamin B1 0.50 (0.25—0.98), and for magnesium 2.25 (1.16—4.38). The effects were stronger after the exclusion of participants taking supplements. Hence, a low intake of retinol equivalents and vitamin B1 (in line with hypothesis) and a high intake of magnesium (less unambiguous to interpret) appear to be associated with an increased risk of OAG.
The caliber of the retinal vessels has been shown to be associated with stroke events. However, the consistency and magnitude of association, and the changes in predicted risk independent of ...traditional risk factors, are unclear. To determine the association between retinal vessel caliber and the risk of stroke events, the investigators combined individual data from 20,798 people, who were free of stroke at baseline, in 6 cohort studies identified from a search of the Medline (National Library of Medicine, Bethesda, Maryland) and EMBASE (Elsevier B.V., Amsterdam, the Netherlands) databases. During follow-up of 5–12 years, 945 (4.5%) incident stroke events were recorded. Wider retinal venular caliber predicted stroke (pooled hazard ratio = 1.15, 95% confidence interval: 1.05, 1.25 per 20-μm increase in caliber), but the caliber of retinal arterioles was not associated with stroke (pooled hazard ratio = 1.00, 95% confidence interval: 0.92, 1.08). There was weak evidence of heterogeneity in the hazard ratio for retinal venular caliber, which may be attributable to differences in follow-up strategies across studies. Inclusion of retinal venular caliber in prediction models containing traditional stroke risk factors reassigned 10.1% of people at intermediate risk into different, mostly lower, risk categories.
The direct visualization of retinal vessels provides a unique opportunity to study cerebral small vessel disease, because these vessels share many features. It was reported that persons with smaller ...retinal arteriolar-to-venular ratio tended to have more white matter lesions on MRI. It is unclear whether this is due to arteriolar narrowing or venular dilatation. We investigated whether smaller arteriolar or larger venular diameters or both were related to severity and progression of cerebral small vessel disease. We studied 490 persons (60–90 years) without dementia from a population-based cohort study. At baseline (1990–1993), retinal arteriolar and venular diameters were measured on digitized images of one eye of each participant. In 1995–1996, participants underwent cerebral MRI scanning. We rated the severity of periventricular white matter lesions on a 9-point scale, approximated a total subcortical white matter lesion volume (range: 0–29.5 ml) and rated the presence of lacunar infarcts. On average 3.3 years later, 279 persons had a second MRI. Changes in periventricular and subcortical white matter lesions were rated with a semi-quantitative scale, and progression was classified as no, minor and marked. An incident infarct was a new infarct on the follow-up MRI. Neither venular nor arteriolar diameters were related to the severity of cerebral small vessel disease. Larger venular diameters were, however, associated with a marked progression of cerebral small vessel disease. Age and gender adjusted odds ratios (ORs) per standard deviation increase were 1.71 95% confidence interval (CI): 1.11–2.61 for periventricular, 1.72 (95% CI: 1.09–2.71) for subcortical white matter lesion progression and 1.59 (95% CI: 1.06–2.39) for incident lacunar infarcts. These associations were independent of other cardiovascular risk factors. Only the OR for incident lacunar infarcts was attenuated (1.24; 95% CI: 0.72–2.12). No association was observed between arteriolar diameters and progression of cerebral small vessel disease. In conclusion, retinal venular dilatation was related to progression of cerebral small vessel disease. The mechanisms underlying venular dilatation deserve more attention, as they may provide new clues into the pathophysiology of cerebral small vessel disease.
After going into the etymology of the word "optotype", this article covers some tasks in ancient times that required good visual acuity (VA). Around 300 BCE, Euclid formulated the existence of a ...visual cone with a minimal visual angle at its tip. Trials to test VA appeared AD 1754. Around that time, texts were introduced by opticians in order to be able to prescribe more reliably. In the early nineteenth century, the need for VA tests in ophthalmology resulted in German and English test charts. Numerous variants emerged after the first edition of Snellen's optotypes in 1862 in The Netherlands. However, 100 years later there was still no standard optotype to reliably test VA. Multidisciplinary approaches between ophthalmology, linguistics, psychology and psychophysics improved optotypes and VA testing, which led to the more reliable LogMAR charts. Recent advances in aids and therapies for the blind and severely visually handicapped, necessitate further development of new and standardized VA tests.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
7.
An eternal hunt for glaucoma de Jong, Paulus T. V. M.
Graefe's archive for clinical and experimental ophthalmology,
07/2024, Volume:
262, Issue:
7
Journal Article
Peer reviewed
In the first issue of Graefe’s Archive from 1854, Albrecht von Graefe wrote about glaucoma. Glaucoma comes from the Greek word “glaukos,” gleaming, which was first used by Homer around 800 BCE. Since ...then, glaukos and glaucoma have taken on many different meanings. The terms blindness, cataract and glaucoma were used interchangeably and twisted together in incomprehensible contexts. Over 2500 years of glaucoma theories were upset by the discovery of the ophthalmoscope in 1851. The first reports of increased intraocular pressure appeared in the mid-seventeenth century, but it took over 200 years for this elevated pressure to be accepted by the ophthalmological community. The discovery of glaucoma simplex in 1861 was an important step forward. What did doctors know about glaucoma before 1850 and why did it take so long to classify glaucoma in its various categories? And why is it that we still do not know what the cause is for primary open angle glaucoma? I will try to answer some of these questions after a historical overview.
Full text
Available for:
EMUNI, FIS, FZAB, GEOZS, GIS, IJS, IMTLJ, KILJ, KISLJ, MFDPS, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, SBMB, SBNM, UKNU, UL, UM, UPUK, VKSCE, ZAGLJ
L1 elements are autonomous retrotransposons that can cause hereditary diseases. We have previously identified a full-length L1 insertion in the CHM (choroideremia) gene of a patient with ...choroideremia, an X-linked progressive eye disease. Because this L1 element, designated L1CHM, contains two 3′-transductions, we were able to delineate a retrotransposition path in which a precursor L1 on chromosome 10p15 or 18p11 retrotransposed to chromosome 6p21 and subsequently to the CHM gene on chromosome Xq21. A cell culture retrotransposition assay showed that L1CHM is one of the most active L1 elements in the human genome. Most importantly, analysis of genomic DNA from the CHM patient's relatives indicated somatic and germ-line mosaicism for the L1 insertion in his mother. These findings provide evidence that L1 retrotransposition can occur very early in human embryonic development.
A lower retinal arteriolar-to-venular ratio (AVR) has been suggested to reflect generalized arteriolar narrowing and to predict the risk of cardiovascular diseases. The contribution of the separate ...arteriolar and venular diameters to this AVR is unknown. Thus, associations between retinal arteriolar and venular diameters, and the AVR on the one hand and blood pressure, atherosclerosis, inflammation markers, and cholesterol levels on the other were examined in the Rotterdam Study.
In this cross-sectional population-based study, for one eye of each subject (> or =55 years; n = 5674), retinal arteriolar and venular diameters (in micrometers) of the blood columns were summed on digitized images. At baseline blood pressures, cholesterol levels, and markers of atherosclerosis and inflammation were also measured.
With increasing blood and pulse pressures, retinal arteriolar and venular diameters and the AVR decreased significantly and linearly. Lower arteriolar diameters were associated with increased carotid intima-media thickness. Larger venular diameters were associated with higher carotid plaque score, more aortic calcifications, lower ankle-arm index, higher leukocyte count, higher erythrocyte sedimentation rate, higher total serum cholesterol, lower HDL, higher waist-to-hip ratio, and smoking. A lower AVR was related to increased carotid intima-media thickness, higher carotid plaque score, higher leukocyte count, lower HDL, higher body mass index, higher waist-to-hip ratio, and smoking.
Because larger venular diameters are associated with atherosclerosis, inflammation, and cholesterol levels, the AVR does not depend only on generalized arteriolar narrowing due to the association between smaller arteriolar diameters and higher blood pressures. These data indicate that retinal venular diameters are variable and may play their own independent role in predicting cardiovascular disorders.
PDF
