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Importance 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. Objective To further examine the effect of lutein/zeaxanthin supplementation on progression to late AMD. Design, Setting, Participants 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. Interventions 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. Main Outcomes and Measures 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. Conclusion and Relevance 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. Trial Registration clinicaltrials.gov Identifier:NCT00345176

Oral supplementation with the Age-Related Eye Disease Study (AREDS) formulation (antioxidant vitamins C and E, beta carotene, and zinc) has been shown to reduce the risk of progression to advanced age-related macular degeneration (AMD). Observational data suggest that increased dietary intake of lutein + zeaxanthin (carotenoids), omega-3 long-chain polyunsaturated fatty acids (docosahexaenoic acid [DHA] + eicosapentaenoic acid [EPA]), or both might further reduce this risk.To determine whether adding lutein + zeaxanthin, DHA + EPA, or both to the AREDS formulation decreases the risk of developing advanced AMD and to evaluate the effect of eliminating beta carotene, lowering zinc doses, or both in the AREDS formulation.The Age-Related Eye Disease Study 2 (AREDS2), a multicenter, randomized, double-masked, placebo-controlled phase 3 study with a 2 × 2 factorial design, conducted in 2006-2012 and enrolling 4203 participants aged 50 to 85 years at risk for progression to advanced AMD with bilateral large drusen or large drusen in 1 eye and advanced AMD in the fellow eye.Participants were randomized to receive lutein (10 mg) + zeaxanthin (2 mg), DHA (350 mg) + EPA (650 mg), lutein + zeaxanthin and DHA + EPA, or placebo. All participants were also asked to take the original AREDS formulation or accept a secondary randomization to 4 variations of the AREDS formulation, including elimination of beta carotene, lowering of zinc dose, or both.Development of advanced AMD. The unit of analyses used was by eye.Median follow-up was 5 years, with 1940 study eyes (1608 participants) progressing to advanced AMD. Kaplan-Meier probabilities of progression to advanced AMD by 5 years were 31% (493 eyes [406 participants]) for placebo, 29% (468 eyes [399 participants]) for lutein + zeaxanthin, 31% (507 eyes [416 participants]) for DHA + EPA, and 30% (472 eyes [387 participants]) for lutein + zeaxanthin and DHA + EPA. Comparison with placebo in the primary analyses demonstrated no statistically significant reduction in progression to advanced AMD (hazard ratio [HR], 0.90 [98.7% CI, 0.76-1.07]; P = .12 for lutein + zeaxanthin; 0.97 [98.7% CI, 0.82-1.16]; P = .70 for DHA + EPA; 0.89 [98.7% CI, 0.75-1.06]; P = .10 for lutein + zeaxanthin and DHA + EPA). There was no apparent effect of beta carotene elimination or lower-dose zinc on progression to advanced AMD. More lung cancers were noted in the beta carotene vs no beta carotene group (23 [2.0%] vs 11 [0.9%], nominal P = .04), mostly in former smokers.Addition of lutein + zeaxanthin, DHA + EPA, or both to the AREDS formulation in primary analyses did not further reduce risk of progression to advanced AMD. However, because of potential increased incidence of lung cancer in former smokers, lutein + zeaxanthin could be an appropriate carotenoid substitute in the AREDS formulation.clinicaltrials.gov Identifier: NCT00345176.

Objectives: To describe the histopathologic findings attributable to irradiation in eyes with uveal malignant melanoma treated with iodine I 125 brachytherapy and to compare these findings with those reviewed in a previous study that compared histopathologic findings in eyes enucleated after proton beam teletherapy with those seen in eyes in a nonirradiated control group. Methods: The slides from 22 eyes with uveal melanoma that had undergone enucleation after the administration of 125 I brachytherapy were studied. The histopathologic features of the tumor and the retina were graded. Results were compared with findings from a previously reported group of 47 proton beam-treated eyes and its control group. Results: Patient age, time between irradiation and enucleation, and ciliary body involvement were similar for the 125 I brachytherapy-treated group and the proton beamtreated group and its control group. This allows comparison of the histopathologic findings. Comparing the 125 I brachytherapy- and proton beam-treated groups, most histopathologic features were similar with nominally statistically significant differences only for cell type, number of mitotic figures, and fibrous metaplasia of the retinal pigment epithelium adjacent to the tumor. Conclusions: Irradiation of uveal melanoma induces changes in the tumor and in the surrounding retina. Brachytherapy and charged particle therapy are the 2 principal methods of irradiation. This study demonstrates that similar changes are produced by 125 I plaque irradiation and proton beam irradiation.

In Atlas of Intraocular Tumors , authors Sanborn, Gonder, and Shields have put together a pictorial review of a wide variety of intraocular tumors of the eye. Chapters 1 and 2 cover tumors of the iris and ciliary body, including various types of nevi, cysts, melanocytomas, melanomas, adenomas, and metastatic and lymphoid tumors. The third chapter reviews neoplasms of the retina, including retinoblastoma, retinocytoma, hamartomas of the retina and retinal pigment epithelium (RPE) as well as the whole spectrum of hemangiomas of the retinal vascular system, arteriovenous malformations, and retinal macroaneurysms. Choroidal tumors, including nevi, melanoma, osteomas, hemangiomas, neurilemoma, and metastatic tumors of the choroid, are presented in chapter 4. Chapter 5 presents primary and metastatic optic nerve tumors, ie, melanocytoma, sarcoid, and leukemic infiltration. The last three chapters are devoted to neoplasms and lesions affecting the RPE, vitreous, and sclera, mainly RPE hypertrophy, adenocarcinoma of RPE, leukemic and lymphoid

Practical Atlas of Retinal Diseases and Therapy , edited by William R. Freeman, MD, is a multiauthor effort to present current information in the field of vitreoretinal diseases. Each chapter is written by an internationally renowned authority in the field. The first part of the book deals with the hereditary chorioretinal dystrophies and new devices for retinal function testing. This is followed by inflammatory diseases of the retina and choroid, including uveitis, multifocal chorioretinopathies, and opportunistic retinitis. The last section of the first part discusses the diagnosis and treatment of posterior uveal tumors. The next part of the book covers most of the common retinopathies that involve the retina and choroid, such as vascular occlusions, diabetic retinopathy, macular degeneration, complications of cataract surgery, and peripheral retinal lesions. The last chapters discuss surgical aspects of vitreoretinal disease, including scleral buckling, pneumatic retinopexy, vitreoretinal surgery, proliferative retinopathy and retinopathy of prematurity, and management

Retina and Vitreous , edited by Rudolph M. Franklin, covers the proceedings of the Symposium on Retina and Vitreous, which was organized by the New Orleans Academy of Ophthalmology and held March 12 through March 15,1992, in New Orleans, La. The topics include age-related macular degeneration, diabetic retinopathy, idiopathic macular holes, choroidal melanoma, management of proliferative vitreoretinopathy, conditions after cataract extraction, management of dislocated intraocular lenses, and cystoid macular edema. In addition, various topics such as retinitis pigmentosa, ocular complications of pregnancy, and retinopathy of prematurity are discussed. The authors include Donald Gass, MD, Matthew Davis, MD, Richard Green, MD, Stuart Fine, MD, Alan Bird, MB, Thomas Aaberg, MD, as well as many others. The volume starts with a section on age-related macular degeneration and covers various aspects such as natural course, risk factors, pathophysiology, and management, including laser photocoagulation and subretinal surgery. The discussion includes some of the

In reply We thank Dr Tiedeman for his careful reading of our article and his thoughtful comments. As we emphasized in our discussion, advising whether a particular patient should be treated with laser photocoagulation involves consideration of both short- and long-term effects of the treatment and characteristics of the patient such as the condition of the fellow eye. We and Dr Tiedeman are in agreement that the reason that group B patients are good candidates for immediate treatment is the reduced risk for severe loss of vision that begins at 12 months after treatment and endures for at least 3 additional years. This sustained period of lower risk for loss of vision outweighs, in our opinion, the period of increased risk immediately following treatment. Members of the Macular Photocoagulation Study Group are listed in the April issue of theArchiveson page 482.

Jerry Shields, MD, and Carol Shields, MD, have put together an exhaustive and probably the most comprehensive review of intraocular tumors. It contains considerably more up-to-date material than the previous book, Diagnosis and Management of Intraocular Tumors , written by Jerry Shields alone. The newer book includes over two decades of the experience of Jerry and Carol Shields and the collective thoughts of world experts on the subject. The book reviews all intraocular tumors arising from the uveal tract, the sensory retina, and the pigment epithelium, including miscellaneous and metastatic tumors, and covers clinical and pathologic features as well as current approaches to diagnosis and management. The initial three chapters cover important anatomic considerations and provide an overview of diagnostic and management approaches for ocular tumors in general. Chapter 2 covers in relevant detail modern diagnostic methods such as magnetic resonance imaging, computed tomography, ultrasonography, and fine-needle biopsy. Chapter 3 includes

Objectives. —This report presents information on the effects of aspirin on mortality, the occurrence of cardiovascular events, and the incidence of kidney disease in the patients enrolled in the Early Treatment Diabetic Retinopathy Study (ETDRS). Study Design. —This multicenter, randomized clinical trial of aspirin vs placebo was sponsored by the National Eye Institute. Patients. —Patients (N=3711) were enrolled in 22 clinical centers between April 1980 and July 1985. Men and women between the ages of 18 and 70 years with a clinical diagnosis of diabetes mellitus were eligible. Approximately 30% of all patients were considered to have type I diabetes mellitus, 31% type II, and in 39% type I or II could not be determined definitely. Intervention. —Patients were randomly assigned to aspirin or placebo (two 325-mg tablets once per day). Main Outcome Measures. —Mortality from all causes was specified as the primary outcome measure for assessing the systemic effects of aspirin. Other outcome variables included cause-specific mortality and cardiovascular events. Results. —The estimate of relative risk for total mortality for aspirin-treated patients compared with placebo-treated patients for the entire study period was 0.91 (99% confidence interval, 0.75 to 1.11). Larger differences were noted for the occurrence of fatal and nonfatal myocardial infarction; the estimate of relative risk was 0.83 for the entire follow-up period (99% confidence interval, 0.66 to 1.04). Conclusions. —The effects of aspirin on any of the cardiovascular events considered in the ETDRS were not substantially different from the effects observed in other studies that included mainly nondiabetic persons. Furthermore, there was no evidence of harmful effects of aspirin. Aspirin has been recommended previously for persons at risk for cardiovascular disease. The ETDRS results support application of this recommendation to those persons with diabetes at increased risk of cardiovascular disease. (JAMA. 1992;268:1292-1300)

Data are presented from 27 patients (34 eyes) with central serous choroidopathy who were followed up for an average of 23 months without therapeutic intervention. The detachment completely resolved in all cases. The average duration of detachment was three months. In all eyes, the visual acuity returned to 20/40 or better, and in all but two eyes, the final visual acuity was 20/30 or better. Central serous choroidopathy is essentially a benign and self-limited disorder, and treatment by photocoagulation is seldom needed.

Visual loss from embolization of the ocular circulation is a rare but devastating complication of injections into the cutaneous and mucocutaneous tissues of the face, scalp, and nasopharynx.1,2The mechanism seems to be inadvertent intra-arterial injection into the branches of the ethmoidal arteries, with retrograde flow into the ophthalmic artery. Even though the visual symptoms are transient in most cases, permanent visual loss has been reported.3,4 A 37-year-old woman was treated with methylprednisolone acetate injections of the nasal turbinate for chronic allergic rhinitis. A few minutes after the injection, she became dizzy and described a sensation of seeing bright lights in the left eye, with blurring of vision. Examination revealed a best corrected visual acuity of 20/30 in the affected left eye, with 20/20 in the right eye. A paracentral scotoma was present on Amsler grid testing. Results of examination of the pupil and inspection of the anterior

The effects of 100% oxygen and 10% carbon dioxide on the choroidal circulation were studied by the radioactive krypton desaturation technique in anesthetized cats. One hundred percent oxygen caused an increase in choroidal vascular resistance (CVR) and a decrease in mean arterial pressure (MAP), both of which resulted in a slight decrease in choroidal blood flow (CBF). Ten percent carbon dioxide caused a marked decrease in CVR, a variable change in MAP, with a new increase in CBF.