zeaxanthin and Geographic-Atrophy

Age-related macular degeneration (AMD) is a degenerative condition of the back of the eye that occurs in people over the age of 50 years. Antioxidants may prevent cellular damage in the retina by reacting with free radicals that are produced in the process of light absorption. Higher dietary levels of antioxidant vitamins and minerals may reduce the risk of progression of AMD. This is the third update of the review.. To assess the effects of antioxidant vitamin and mineral supplements on the progression of AMD in people with AMD.. We searched CENTRAL, MEDLINE, Embase, one other database, and three trials registers, most recently on 29 November 2022.. We included randomised controlled trials (RCTs) that compared antioxidant vitamin or mineral supplementation to placebo or no intervention, in people with AMD.. We used standard methods expected by Cochrane.. We included 26 studies conducted in the USA, Europe, China, and Australia. These studies enroled 11,952 people aged 65 to 75 years and included slightly more women (on average 56% women). We judged the studies that contributed data to the review to be at low or unclear risk of bias. Thirteen studies compared multivitamins with control in people with early and intermediate AMD. Most evidence came from the Age-Related Eye Disease Study (AREDS) in the USA. People taking antioxidant vitamins were less likely to progress to late AMD (odds ratio (OR) 0.72, 95% confidence interval (CI) 0.58 to 0.90; 3 studies, 2445 participants; moderate-certainty evidence). In people with early AMD, who are at low risk of progression, this means there would be approximately four fewer cases of progression to late AMD for every 1000 people taking vitamins (one fewer to six fewer cases). In people with intermediate AMD at higher risk of progression, this corresponds to approximately 78 fewer cases of progression for every 1000 people taking vitamins (26 fewer to 126 fewer). AREDS also provided evidence of a lower risk of progression for both neovascular AMD (OR 0.62, 95% CI 0.47 to 0.82; moderate-certainty evidence) and geographic atrophy (OR 0.75, 95% CI 0.51 to 1.10; moderate-certainty evidence), and a lower risk of losing 3 or more lines of visual acuity (OR 0.77, 95% CI 0.62 to 0.96; moderate-certainty evidence). Low-certainty evidence from one study of 110 people suggested higher quality of life scores (measured with the Visual Function Questionnaire) in treated compared with non-treated people after 24 months (mean difference (MD) 12.30, 95% CI 4.24 to 20.36). In exploratory subgroup analyses in the follow-on study to AREDS (AREDS2), replacing beta-carotene with lutein/zeaxanthin gave hazard ratios (HR) of 0.82 (95% CI 0.69 to 0.96), 0.78 (95% CI 0.64 to 0.94), 0.94 (95% CI 0.70 to 1.26), and 0.88 (95% CI 0.75 to 1.03) for progression to late AMD, neovascular AMD, geographic atrophy, and vision loss, respectively. Six studies compared lutein (with or without zeaxanthin) with placebo and one study compared a multivitamin including lutein/zeaxanthin with multivitamin alone. The duration of supplementation and follow-up ranged from six months to five years. Most evidence came from the AREDS2 study in the USA; almost all participants in AREDS2 also took the original AREDS supplementation formula. People taking lutein/zeaxanthin may have similar or slightly reduced risk of progr. Moderate-certainty evidence suggests that antioxidant vitamin and mineral supplementation (AREDS: vitamin C, E, beta-carotene, and zinc) probably slows down progression to late AMD. People with intermediate AMD have a higher chance of benefiting from antioxidant supplements because their risk of progression is higher than people with early AMD. Although low-certainty evidence suggested little effect with lutein/zeaxanthin alone compared with placebo, exploratory subgroup analyses from one large American study support the view that lutein/zeaxanthin may be a suitable replacement for the beta-carotene used in the original AREDS formula.

Topics: Antioxidants; beta Carotene; Dietary Supplements; Female; Geographic Atrophy; Humans; Lutein; Macular Degeneration; Male; Malnutrition; Minerals; Vitamin A; Vitamin K; Vitamins; Zeaxanthins; Zinc

It has been proposed that antioxidants may prevent cellular damage in the retina by reacting with free radicals that are produced in the process of light absorption. Higher dietary levels of antioxidant vitamins and minerals may reduce the risk of progression of age-related macular degeneration (AMD).. The objective of this review was to assess the effects of antioxidant vitamin or mineral supplementation on the progression of AMD in people with AMD.. We searched CENTRAL (2017, Issue 2), MEDLINE Ovid (1946 to March 2017), Embase Ovid (1947 to March 2017), AMED (1985 to March 2017), OpenGrey (System for Information on Grey Literature in Europe, the ISRCTN registry (www.isrctn.com/editAdvancedSearch), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. We last searched the electronic databases on 29 March 2017.. We included randomised controlled trials (RCTs) that compared antioxidant vitamin or mineral supplementation (alone or in combination) to placebo or no intervention, in people with AMD.. Both review authors independently assessed risk of bias in the included studies and extracted data. One author entered data into RevMan 5; the other author checked the data entry. We graded the certainty of the evidence using GRADE.. We included 19 studies conducted in USA, Europe, China, and Australia. We judged the trials that contributed data to the review to be at low or unclear risk of bias.Nine studies compared multivitamins with placebo (7 studies) or no treatment (2 studies) in people with early and moderate AMD. The duration of supplementation and follow-up ranged from nine months to six years; one trial followed up beyond two years. Most evidence came from the Age-Related Eye Disease Study (AREDS) in the USA. People taking antioxidant vitamins were less likely to progress to late AMD (odds ratio (OR) 0.72, 95% confidence interval (CI) 0.58 to 0.90; 2445 participants; 3 RCTs; moderate-certainty evidence). In people with very early signs of AMD, who are at low risk of progression, this would mean that there would be approximately 4 fewer cases of progression to late AMD for every 1000 people taking vitamins (1 fewer to 6 fewer cases). In people at high risk of progression (i.e. people with moderate AMD) this would correspond to approximately 8 fewer cases of progression for every 100 people taking vitamins (3 fewer to 13 fewer). In one study of 1206 people, there was a lower risk of progression for both neovascular AMD (OR 0.62, 95% CI 0.47 to 0.82; moderate-certainty evidence) and geographic atrophy (OR 0.75, 95% CI 0.51 to 1.10; moderate-certainty evidence) and a lower risk of losing 3 or more lines of visual acuity (OR 0.77, 95% CI 0.62 to 0.96; 1791 participants; moderate-certainty evidence). Low-certainty evidence from one study of 110 people suggested higher quality of life scores (National Eye Institute Visual Function Questionnaire) in treated compared with the non-treated people after 24 months (mean difference (MD) 12.30, 95% CI 4.24 to 20.36). Six studies compared lutein (with or without zeaxanthin) with placebo. The duration of supplementation and follow-up ranged from six months to five years. Most evidence came from the AREDS2 study in the USA. People taking lutein or zeaxanthin may have similar or slightly reduced risk of progression to late AMD (RR 0.94, 95% CI 0.87 to 1.01; 6891 eyes; low-certainty evidence), neovascular AMD (RR 0.92, 95% CI 0.84 to 1.02; 6891 eyes; low-certainty evidence), and geographic atrophy (RR 0.92, 95% CI 0.80 to 1.05; 6891 eyes; low-certainty evidence). A similar risk of progression to visual loss of 15 or more letters was seen in the lutein and control groups (RR 0.98, 95% CI 0.91 to 1.05; 6656 eyes; low-certainty evidence). Quality. People with AMD may experience some delay in progression of the disease with multivitamin antioxidant vitamin and mineral supplementation. This finding was largely drawn from one large trial, conducted in a relatively well-nourished American population. We do not know the generalisability of these findings to other populations. Although generally regarded as safe, vitamin supplements may have harmful effects. A systematic review of the evidence on harms of vitamin supplements is needed. Supplements containing lutein and zeaxanthin are heavily marketed for people with age-related macular degeneration but our review shows they may have little or no effect on the progression of AMD.

Topics: Aged; Antioxidants; Dietary Supplements; Disease Progression; Geographic Atrophy; Humans; Lutein; Macular Degeneration; Minerals; Quality of Life; Randomized Controlled Trials as Topic; Vitamin E; Vitamins; Zeaxanthins; Zinc

The discovery of several genetic variants associated with an increased risk for age-related macular degeneration (AMD) has led to a completely new understanding of AMD. In addition to the known modifiable risk factors, genetic risk factors may also help to assess the risk to progress to nonneovascular AMD. Recently published primary studies have indicated that genetic risk analysis may be valuable in the selection of the currently available antioxidant therapy. So far, the best evidence for preventing progression to nonneovascular AMD comes from the Age-Related Eye Disease Studies (AREDS) I and II. These studies indicate that high doses of antioxidants can reduce the risk of progression to the advanced form of the disease. However, the recent evaluation of the addition of either lutein and zeaxanthin, or ω-3 long-chain polyunsaturated fatty acids, or both, to the established AREDS I formulation did not significantly reduce the risk of developing advanced AMD. There is clearly a large unmet medical need for new therapeutic options for nonneovascular AMD. The modulation of the complement cascade is - despite initially disappointing outcomes obtained with blocking complement factor 5 - currently the most promising approach to the treatment of nonneovascular AMD.

Topics: Antioxidants; Fatty Acids, Omega-3; Geographic Atrophy; Humans; Lutein; Zeaxanthins

To examine whether the rate of geographic atrophy (GA) enlargement is influenced by subsequent exudative neovascular age-related macular degeneration (nAMD) and hence, to explore indirectly whether nonexudative nAMD may slow GA enlargement.. Post hoc analysis of a controlled clinical trial cohort.. Age-Related Eye Disease Study 2 participants 50 to 85 years of age.. Baseline and annual stereoscopic color fundus photographs were evaluated for (1) GA presence and area and (2) exudative nAMD presence. Two cohorts were constructed: eyes with GA at study baseline (prevalent cohort) and eyes in which GA developed during follow-up (incident cohort). Mixed-model regression of the square root of GA area was performed according to the presence or absence of subsequent exudative nAMD.. Change over time in square root of GA area.. Of the 757 eyes in the incident GA cohort, over a mean follow-up of 2.3 years (standard deviation [SD], 1.2 years), 73 eyes (9.6%) demonstrated subsequent exudative nAMD. Geographic atrophy enlargement in these eyes was significantly slower (0.20 mm/year; 95% confidence interval [CI], 0.12-0.28 mm/year) compared with the other 684 eyes in which subsequent exudative nAMD did not develop (0.29 mm/year; 95% CI, 0.27-0.30 mm/year; P = 0.037). Of the 456 eyes in the prevalent GA cohort, over a mean follow-up of 4.1 years (SD, 1.4 years), 63 eyes (13.8%) demonstrated subsequent exudative nAMD. Geographic atrophy enlargement in these eyes was similar (0.31 mm/year; 95% CI, 0.24-0.37 mm/year) compared with the other 393 eyes in which subsequent exudative nAMD did not develop (0.28 mm/year; 95% CI, 0.26-0.29 mm/year; P = 0.37).. In eyes with recent GA, GA enlargement before the development of exudative nAMD seems slowed. This association was not observed in eyes with more long-standing GA, which have larger lesion sizes. Hence, perilesional nonexudative choroidal neovascular tissue (presumably present before the development of clinically apparent exudation) may slow enlargement of smaller GA lesions through improved perfusion. This hypothesis warrants further evaluation in prospective studies.

Topics: Aged; Aged, 80 and over; Diagnostic Imaging; Disease Progression; Docosahexaenoic Acids; Drug Therapy, Combination; Eicosapentaenoic Acid; Female; Follow-Up Studies; Geographic Atrophy; Humans; Lutein; Macula Lutea; Male; Middle Aged; Prospective Studies; Treatment Outcome; Wet Macular Degeneration; Zeaxanthins

To analyze the prevalence, incidence, and clinical characteristics of eyes with geographic atrophy (GA) in age-related macular degeneration (AMD), including clinical and genetic factors affecting enlargement.. Prospective cohort study within a controlled clinical trial.. Age-Related Eye Disease Study 2 (AREDS2) participants, aged 50-85 years.. Baseline and annual stereoscopic color fundus photographs were evaluated for GA presence and area. Analyses included GA prevalence and incidence rates, Kaplan-Meier rates, mixed-model regression, and multivariable analysis of the square root of GA, area adjusted for covariates, including clinical/imaging characteristics and genotype.. (1) Presence or development of GA; (2) change in the square root of GA area over time.. At baseline, 517 eyes (6.2%) of 411 participants (9.8%) had pre-existing GA (without neovascular AMD), with the following characteristics: 33% central, 67% noncentral; and the following configurations: 36% small, 26% solid/unifocal, 24% multifocal, 9% horseshoe/ring, and 6% indeterminate. Of the remaining 6530 eyes at risk, 1099 eyes (17.3%) of 883 participants developed incident GA without prior neovascular disease during mean follow-up of 4.4 years. The Kaplan-Meier rate of incident GA was 19% of eyes at 5 years. In eyes with incident GA, 4-year risk of subsequent neovascular AMD was 29%. In eyes with incident noncentral GA, 4-year risk of central involvement was 57%. GA enlargement rate (following square root transformation) was similar in eyes with pre-existing GA (0.29 mm/year; 95% confidence interval 0.27-0.30) and incident GA (0.28 mm/year; 0.27-0.30). In the combined group, GA enlargement was significantly faster with noncentrality, multifocality, intermediate baseline size, and bilateral GA (P < 0.0001 for interaction in each case) but not with AREDS2 treatment assignment (P = 0.33) or smoking status (P = 0.05). Enlargement was significantly faster with ARMS2 risk (P < 0.0001), C3 non-risk (P = 0.0002), and APOE non-risk (P = 0.001) genotypes.. Analyses of AREDS2 data on natural history of GA provide representative data on GA evolution and enlargement. GA enlargement, which was influenced by lesion features, was relentless, resulting in rapid central vision loss. The genetic variants associated with faster enlargement were partially distinct from those associated with risk of incident GA. These findings are relevant to further investigations of GA pathogenesis and clinical trial planning.

Topics: Aged; Aged, 80 and over; Disease Progression; Docosahexaenoic Acids; Drug Therapy, Combination; Eicosapentaenoic Acid; Female; Geographic Atrophy; Humans; Lutein; Macular Degeneration; Male; Middle Aged; Photography; Prospective Studies; Visual Acuity; Zeaxanthins

To compare rates of peripheral retinal changes in Age-Related Eye Disease Study 2 (AREDS2) participants with at least intermediate age-related macular degeneration (AMD) with control subjects without intermediate age-related changes (large drusen).. Cross-sectional evaluation of clinic-based patients enrolled in AREDS2 and a prospective study.. Participants from prospective studies.. The 200° pseudocolor and fundus autofluorescence (FAF) images were captured on the Optos 200 Tx Ultrawide-field device (Optos, Dunfermline, Scotland) by centering on the fovea and then steering superiorly and inferiorly. The montaged images were graded at a reading center with the images divided into 3 zones (zone 1 [posterior pole], zone 2 [midperiphery], and zone 3 [far periphery]) to document the presence of peripheral lesions.. Peripheral retinal lesions: drusen, hypopigmentary/hyperpigmentary changes, reticular pseudodrusen, senile reticular pigmentary changes, cobblestone degeneration, and FAF abnormalities.. A total of 484 (951 eyes) AREDS2 participants with AMD (cases) and 89 (163 eyes) controls without AMD had gradable color and FAF images. In zones 2 and 3, neovascularization and geographic atrophy (GA) were present, ranging from 0.4% to 6% in eyes of cases, respectively, and GA was present in 1% of eyes of controls. Drusen were detected in 97%, 78%, and 64% of eyes of cases and 48%, 21%, and 9% of eyes of controls in zones 2 and 3 superior and 3 inferior, respectively (P < 0.001 for all). Peripheral reticular pseudodrusen were seen in 15%. Senile reticular pigmentary change was the predominant peripheral change seen in 48% of cases and 16% of controls in zone 2 (P < 0.001). Nonreticular pigment changes were less frequent in the periphery than in the posterior pole (46% vs. 76%) and negligible in controls.. Peripheral retinal changes are more prevalent in eyes with AMD than in control eyes. Drusen are seen in a majority of eyes with AMD in both the mid and far periphery, whereas pigment changes and features of advanced AMD are less frequent. Age-related macular degeneration may be more than a "macular" condition but one that involves the entire retina. Future longitudinal studies of peripheral changes in AMD and their impact on visual function may contribute to understanding AMD pathogenesis.

Topics: Aged; Aged, 80 and over; Cross-Sectional Studies; Docosahexaenoic Acids; Eicosapentaenoic Acid; Female; Fluorescein Angiography; Geographic Atrophy; Humans; Lutein; Male; Middle Aged; Optical Imaging; Prospective Studies; Retina; Retinal Drusen; Retinal Pigment Epithelium; Tomography, Optical Coherence; Wet Macular Degeneration; Zeaxanthins

To evaluate the association of statin use with progression of age-related macular degeneration (AMD).. Preplanned, prospective cohort study within a controlled clinical trial of oral supplementation for age-related eye diseases.. Age-Related Eye Disease Study 2 (AREDS2) participants, aged 50 to 85 years.. Factors, including age, gender, smoking status, aspirin use, and history of diabetes, hypertension, heart disease, angina, and stroke-all known to be associated with statin use-were included in a logistic regression model to estimate propensity scores for each participant. Age-adjusted proportional hazards regression models, with and without propensity score matching, were performed to evaluate the association of statin use with progression to late AMD. Analyses adjusting for the competing risk of death were also performed.. Baseline and annual stereoscopic fundus photographs were assessed centrally by masked graders for the development of late AMD, either neovascular AMD or geographic atrophy (GA).. Of the 3791 participants (2462 with bilateral large drusen and 1329 with unilateral late AMD at baseline), 1659 (43.8%) were statin users. The overall analysis, with no matching of propensity scores and no adjustment for death as a competing risk, showed that statin use was not associated with progression to late AMD (hazard ratio [HR], 1.08; 95% confidence interval [CI], 0.83-1.41; P = 0.56). When matched for propensity scores and adjusted for death as a competing risk, the result was not statistically significant (HR, 0.81; 95% CI, 0.55-1.20; P = 0.29). Furthermore, subgroup analyses of persons with or without late AMD at baseline and the various components of late AMD (neovascular AMD, central GA, or any GA) also showed no statistically significant association of statin use with progression to AMD.. Statin use was not statistically significantly associated with progression to late AMD in the AREDS2 participants, and these findings are consistent with findings in the majority of previous studies. Statins have been demonstrated to reduce the risk of cardiovascular disease, but our data do not provide evidence of a beneficial effect on slowing AMD progression.

Topics: Aged; Aged, 80 and over; Cardiovascular Diseases; Dietary Supplements; Disease Progression; Fatty Acids, Omega-3; Female; Follow-Up Studies; Geographic Atrophy; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Incidence; Lutein; Male; Middle Aged; Proportional Hazards Models; Prospective Studies; Risk Factors; Visual Acuity; Wet Macular Degeneration; Zeaxanthins

The Age-Related Eye Disease Study (AREDS) formulation for the treatment of age-related macular degeneration (AMD) contains vitamin C, vitamin E, beta carotene, and zinc with copper. The Age-Related Eye Disease Study 2 (AREDS2) assessed the value of substituting lutein/zeaxanthin in the AREDS formulation because of the demonstrated risk for lung cancer from beta carotene in smokers and former smokers and because lutein and zeaxanthin are important components in the retina.. To further examine the effect of lutein/zeaxanthin supplementation on progression to late AMD.. The Age-Related Eye Disease Study 2 is a multicenter, double-masked randomized trial of 4203 participants, aged 50 to 85 years, at risk for developing late AMD; 66% of patients had bilateral large drusen and 34% had large drusen and late AMD in 1 eye.. In addition to taking the original or a variation of the AREDS supplement, participants were randomly assigned in a factorial design to 1 of the following 4 groups: placebo; lutein/zeaxanthin, 10 mg/2 mg; omega-3 long-chain polyunsaturated fatty 3 acids, 1.0 g; or the combination.. S Documented development of late AMD by central, masked grading of annual retinal photographs or by treatment history. RESULTS In exploratory analysis of lutein/zeaxanthin vs no lutein/zeaxanthin, the hazard ratio of the development of late AMD was 0.90 (95% CI, 0.82-0.99; P = .04). Exploratory analyses of direct comparison of lutein/zeaxanthin vs beta carotene showed hazard ratios of 0.82 (95% CI, 0.69-0.96; P = .02) for development of late AMD, 0.78 (95% CI, 0.64-0.94; P = .01) for development of neovascular AMD, and 0.94 (95% CI, 0.70-1.26; P = .67) for development of central geographic atrophy. In analyses restricted to eyes with bilateral large drusen at baseline, the direct comparison of lutein/zeaxanthin vs beta carotene showed hazard ratios of 0.76 (95% CI, 0.61-0.96; P = .02) for progression to late AMD, 0.65 (95% CI, 0.49-0.85; P = .002) for neovascular AMD, and 0.98 (95% CI, 0.69-1.39; P = .91) for central geographic atrophy.. The totality of evidence on beneficial and adverse effects from AREDS2 and other studies suggests that lutein/zeaxanthin could be more appropriate than beta carotene in the AREDS-type supplements.. clinicaltrials.gov Identifier: NCT00345176.

Topics: Administration, Oral; Aged; Aged, 80 and over; beta Carotene; Diet; Dietary Supplements; Disease Progression; Double-Blind Method; Drug Therapy, Combination; Fatty Acids, Omega-3; Female; Geographic Atrophy; Humans; Lutein; Male; Middle Aged; Retinal Drusen; Trace Elements; Treatment Outcome; Visual Acuity; Vitamins; Wet Macular Degeneration; Xanthophylls; Zeaxanthins

The primary objective of LUTEGA is to determine the long-term effect of a supplementation with fixed combination of lutein, zeaxanthin, omega-3-longchain-polyunsaturated-fatty-acids (O-3-LCPUFAs) and antioxidants on macular pigment optical density (MPOD) in patients with non-exudative age-related macular degeneration (AMD).. The LUTEGA study is a double-blind, placebo-controlled clinical trial. 172 patients with non-exudative AMD were enrolled and randomized to three treatment arms. Supplementation included either once (dosage D1) or twice daily (dosage D2) of 10 mg L / 1 mg Z/ O-3-LCPUFAs (thereof 100 mg DHA, 30 mg EPA)/ antioxidants, or placebo (P). After best-corrected visual acuity (BCVA) test, blood sample was collected and MPOD was measured using the 1-wavelength-reflection method and recording reflection images at 480 nm (modified Visucam(NM/FA), Carl Zeiss Meditec, Germany). During 1 year of intervention, AMD patients were followed up after 1, 3, 6 and 12 months. 145 AMD patients (D1 = 50, D2 = 55, P = 40) completed the study.. After 12 months of intervention, the MPOD parameters (volume, area, maxOD, meanOD) increased significantly in treatment arms D1 and D2 (p < 0.001). Volume of MPOD showed the highest within-group difference and increased significantly in D1 and D2, and decreased significantly in P (p = 0.041). Between-group comparison of absolute changes of all MPOD parameters were significantly different between D1 and P as well as D2 and P with p < 0.001 at end point (t = 12). BCVA, measured in log MAR, improved in D1 and in D2 (p < 0.001). After 12 months of intervention, the mean improvement in BCVA was significant in D2 (p = 0.006) and D1 (p = 0.038) compared to P.. The supplementation of L, Z, O-3-LCPUFAs and antioxidants resulted in considerable increase in MPOD. There was no difference in accumulation of MPOD between both dosages. Thus, we believe that the used supplementation with L and Z seems to reach a saturation level in retinal cell structure. Additionally, the constant supplementation of L, Z, O-3-LCPUFAs and antioxidants in AMD patients seems to be useful, because MPOD reduces without supplementation. We conclude that the supplementation caused an increase of MPOD, which results in an improvement and stabilization in BCVA in AMD patients. Thus, a protective effect on the macula in AMD patients is assumed.

Topics: Aged; Antioxidants; Ascorbic Acid; Dietary Supplements; Double-Blind Method; Drug Combinations; Fatty Acids, Omega-3; Female; Follow-Up Studies; Geographic Atrophy; Humans; Lutein; Male; Middle Aged; Prospective Studies; Retinal Pigments; Visual Acuity; Vitamin E; Xanthophylls; Zeaxanthins; Zinc Compounds

Topics: Administration, Oral; Antioxidants; Ascorbic Acid; Double-Blind Method; Drug Therapy, Combination; Geographic Atrophy; Gluconates; Humans; Lutein; Middle Aged; Trace Elements; Treatment Outcome; Visual Acuity; Vitamin E; Wet Macular Degeneration; Xanthophylls; Zeaxanthins; Zinc Oxide

The non-exudative form of age-related macular degeneration (AMD) is a disease with long-term progression for which effective treatments have not been found. Many studies are being conducted to find effective drugs to prevent the appearance of drusen and increase in RPE atrophy area, which could help avoid this more dangerous form of AMD. The main drugs (nutraceuticals) that are used to treat the dry form of AMD are lutein, zeaxanthin and omega-3 fatty acids. Additionally, treatment may include nanosecond laser therapy for drusen in advanced AMD, panretinal subthreshold micropulse laser exposure for atrophic AMD, as well as microcurrent stimulation. Further research in this area should be aimed at understanding all the pathogenetic mechanisms associated with the development of AMD, and developing new approaches to the treatment of this disease including physiotherapy.. Неэкссудативная форма возрастной макулярной дегенерации (ВМД) является длительно прогрессирующим заболеванием, эффективные методы лечения которого не определены. Проводится много исследований с целью найти эффективные препараты для предотвращения появления друз, предотвращения роста площади атрофии ретинального пигментного эпителия, которые помогут избежать более разрушительной формы ВМД. Основными препаратами (нутрицевтиками), которые применяются для лечения сухой формы ВМД, считаются лютеин, зеаксантин и омега-3-полиненасыщенные жирные кислоты. Используют также наносекундную лазерную терапию друз при развитой стадии ВМД, панретинальное субпороговое микроимпульсное лазерное воздействие при атрофической форме ВМД, микротоковую стимуляцию. Дальнейшие исследования в этой области могут быть нацелены на понимание всех патогенетических механизмов, связанных с развитием ВМД, и разработку новых подходов в терапии этой болезни, в том числе и физиотерапевтических.

Topics: Disease Progression; Geographic Atrophy; Humans; Lutein; Macular Degeneration; Retinal Drusen; Zeaxanthins

To evaluate differences in measurements of macular pigment optical density (MPOD) in patients with dry age-related macular degeneration (AMD) and a group of healthy patients (control group). Short-term repeatability of MPOD measures was also assessed in the control group.. This cross-sectional study included 31 eyes from 31 patients with bilateral dry AMD, 21 eyes from 21 cases with dry AMD in the study eye and exudative AMD in the fellow eye. The control group included 17 eyes from 17 healthy patients of similar age and sex. The MPOD values were measured using a commercially available color perimetry technique (CP). Short-term repeatability of MPOD measurements by the CP technique was assessed in 20 eyes of 20 healthy subjects who were measured 3 times on 3 consecutive days.. The mean values for MPOD were 5.59 ± 2.06 dB in cases in which both eyes had dry AMD, 5.25 ± 2.72 dB in cases in which one eye had wet AMD and the studied eye had dry AMD, and 5.97 ± 2.14 dB in the eyes of the healthy control group. The mean value was lower in cases in which the fellow eye had wet AMD; however, no significant difference in MPOD was found between the three groups (p = 0.659) or between the group with dry AMD in both eyes and the healthy control group (p = 0.977). The intraclass correlation coefficient (ICC) value was 0.664 between day 1 and day 2, and 0.822 between day 2 and day 3.. Our results do not show a direct relation between MPOD and dry AMD. Color perimetry does not provide acceptable short-term repeatability for measuring MPOD. Learning effects may contribute to the measured test-retest variability. Other studies are needed to determine if CP is suitable for repeated measurements during the long term follow-up with the same patient.

Topics: Adult; Aged; Aged, 80 and over; Cross-Sectional Studies; Female; Geographic Atrophy; Healthy Volunteers; Humans; Lutein; Macula Lutea; Macular Pigment; Male; Observer Variation; Reproducibility of Results; Visual Field Tests; Zeaxanthins

To compare the macular pigment optical density (MPOD) of patients with unilateral wet age-related macular degeneration (AMD) with the MPOD of bilateral dry AMD patients and healthy elderly individuals.. The MPOD of 34 patients with unilateral wet AMD was measured in their fellow eye that had the dry form of the disease (study group). The MPOD of the study group was compared with the MPOD of 33 patients with bilateral dry AMD (patients' control group) and 35 elderly subjects without any signs of retinal disease (control group). None of the subjects was under carotenoid supplementation. The MPOD was measured with Heterochromatic Flicker Photometry [QuantifEYE™- MPS 9000 (ZeaVision(©))]. The statistical package SPSS v 17.0 was used for the analysis.. The overall mean MPOD was 0.52 (SD 0.15). Patients with unilateral wet AMD have significantly higher levels of MPOD in their fellow eye compared with patients with bilateral dry AMD (0.58 versus 0.48, p = 0.026). Mean MPOD of patients with bilateral dry AMD does not differ significantly from that of healthy elderly subjects (0.48 versus 0.50, p = 0.865). In this population sample, no correlation with age was observed, while women have slightly but significantly higher levels of MPOD (0.55 versus 0.49, p = 0.029).. In the present study, the mean MPOD at the fellow eye of patients with unilateral wet AMD was found to be significantly higher than that of patients with bilateral dry AMD, while no other significant difference emerged between groups. Further investigation is demanded to clarify the role of macular pigment in AMD progression.

Topics: Aged; Aged, 80 and over; Disease Progression; Female; Geographic Atrophy; Humans; Intraocular Pressure; Lutein; Male; Middle Aged; Photometry; Retinal Pigments; Visual Acuity; Wet Macular Degeneration; Xanthophylls; Zeaxanthins