Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Exudative ARMD

  • Author: F Ryan Prall, MD; Chief Editor: Hampton Roy, Sr, MD  more...
 
Updated: May 20, 2016
 

Practice Essentials

In the wet, or exudative, form of age-related macular degeneration (AMD), pathologic choroidal neovascular membranes (CNVM) develop under the retina. The CNVM can leak fluid and blood and, if left untreated, ultimately cause a centrally blinding disciform scar. Approximately 10-20% of patients with nonexudative AMD eventually progress to the exudative form, which is responsible for the majority of the estimated 1.75 million cases of advanced AMD in the United States.[1, 2] See the image below.

Age-related macular degeneration (AMD), exudative. Age-related macular degeneration (AMD), exudative.

Signs and symptoms

AMD occurs bilaterally, but it is often asymmetrical. Patients with exudative AMD present with the following:

  • Subretinal fluid
  • Retinal pigment epithelial (RPE) detachments
  • Subretinal hemorrhage
  • Subretinal lipid deposits (occasionally)

Patients with exudative AMD typically describe painless, progressive blurring of their central visual acuity, which can be acute or insidious in onset.

Patients who develop subretinal hemorrhage from choroidal neovascularization (CNV), for example, typically report an acute onset. Other patients with CNV may experience insidious blurring secondary to shallow subretinal fluid or RPE detachments. They also report relative or absolute central scotomas, metamorphopsia, and difficulty reading.

The natural history of exudative AMD (and occasionally nonexudative AMD) results in a stable central scotoma in which the patient’s visual acuity falls below the reading level and the legal driving level. However, peripheral visual acuity is usually retained.

See Clinical Presentation for more detail.

Diagnosis

After a thorough dilated examination of the fundus with slit lamp biomicroscopy, the following imaging studies are frequently performed on many patients with signs and symptoms of exudative AMD:

  • Color photography of the fundus
  • Fluorescein angiography (FA) - Helps to identify and confirm the source of CNV
  • Optical coherence tomography (OCT) - Can identify soft drusen, RPE detachments, subretinal and intraretinal fluid, CNV, and cystoid macular edema, and can demonstrate the integrity of the photoreceptor and RPE layers

See Workup for more detail.

Management

Antiangiogenic agents

Animal and clinical studies have established vascular endothelial growth factor (VEGF) as a key mediator in ocular angiogenesis.[5, 6] In clinical trials, particular attention has been focused on the development of pharmaceutical agents to block or neutralize VEGF expression. These include the following:

  • Pegaptanib sodium
  • Ranibizumab
  • Bevacizumab
  • Aflibercept

Results from treatment with anti-VEGF agents have been promising, although there continues to be a subset of patients who have disappointing visual outcomes.[7, 8, 9]

Laser treatments

Laser treatments include the following:

  • Thermal laser photocoagulation - Until the advent of anti-VEGF agents, ophthalmologists traditionally used thermal laser destruction of CNV as the primary treatment of exudative AMD.
  • Photodynamic therapy with verteporfin (PDT) - To avoid creating a central, blinding scotoma when treating subfoveal CNV with thermal lasers, clinicians turned to PDT; effective in some forms of CNV, although its use is sometimes limited by cost

See Treatment and Medication for more detail.

Next

Background

Types of macular degeneration

Age-related macular degeneration (AMD) is the leading cause of irreversible vision loss in the industrialized world.[10, 11, 12] See the images below.

Age-related macular degeneration (AMD), exudative. Age-related macular degeneration (AMD), exudative.
Age-related macular degeneration (AMD), exudative. Age-related macular degeneration (AMD), exudative.

Physicians have traditionally recognized two types of macular degeneration: dry and wet. The hallmark of the dry, or nonexudative form, is the deposition of extracellular material beneath the retinal pigment epithelium (RPE) that leads to the formation of drusen. Both atrophic and hypertrophic changes occur in the RPE underlying the central macula and can lead to the loss of retinal photoreceptors.

Patients with nonexudative AMD can progress to the wet, or exudative, form of AMD, in which pathologic choroidal neovascular membranes (CNVM) develop under the retina. The CNVM can leak fluid and blood, and, ultimately, cause a centrally blinding disciform scar over a relatively short time course if left untreated. Approximately 10-20% of patients with nonexudative AMD eventually progress to the exudative form, which is responsible for the majority of the estimated 1.75 million cases of advanced AMD in the United States.[1, 2]

Several classification systems are used to define AMD both clinically and for research purposes. The Wisconsin Age-Related Maculopathy Grading System defined early AMD as the absence of signs of advanced AMD and the presence of (1) soft indistinct or reticular drusen or (2) hard distinct or soft distinct drusen with pigmentary abnormalities (RPE depigmentation or increased retinal pigment). Late AMD was defined as the presence of either (1) geographic atrophy or (2) exudative AMD. Exudative AMD was defined as the presence of any of the following exudative lesions: pigment epithelial detachment or age-related retinal detachment, subretinal hemorrhage, subretinal scar (subretinal fibrous scar), or laser treatment for exudative AMD.[13]

The Age-Related Eye Disease Study Group (AREDS) developed an 11-step scale to document the severity of AMD in fundus photographs. Patients were graded based on the presence or absence of drusen characteristics (size, shape, area); RPE pigmentary abnormalities (hypopigmentation or hyperpigmentation and geographic atrophy); and retinal findings, such as subretinal scar, hemorrhage, or detachment. Steps 4-8 were considered to have early AMD, and steps 9-11 defined advanced AMD. Patients meeting criteria for steps 1-3 did not have AMD.

Based on data from the AREDS, a simplified severity scale was developed that was designed to be used clinically to stratify patients into risk categories. The system assigns one risk factor for the presence of one or more large (>125 microns) drusen and one risk factor for the presence of any pigmentary abnormality. The presence of intermediate-sized drusen in both eyes constitutes one risk factor. These risk factors are added between both eyes and result in a numerical score between 0 and 4. The approximate 5-year risk of developing advanced AMD can then be calculated: 0 factors, 0.5%; 1 factor, 3%; 2 factors, 12%; 3 factors, 25%; and 4 factors, 50%.[14]

Klein et al developed a risk assessment model, again using data from AREDS, but incorporating genetic, environmental, and phenotypic variables. Scores from the simplified severity score were included with patient age, smoking history, age, family history, and genetic information to determine a more precise risk assessment. A risk calculator was developed and is available here.[15]

In 1995, the International ARM Epidemiologic Study Group redefined AMD from the traditional wet and dry designations. The criteria for the diagnosis of AMD subsequently became stricter. Patients with minimal or moderate nonexudative age-related changes in the macula were reclassified as having age-related maculopathy (ARM). By definition, advanced RPE atrophy (ie, geographic atrophy) or choroidal neovascularization (CNV) was required to establish a diagnosis of nonexudative AMD and exudative AMD, respectively.[16] An alternative classification scheme uses a 9-step severity scale to allow for risk stratification and reproducibility of age-related macular changes.[17]

As a result of the International ARM Epidemiologic Study Group efforts, patients with ARM account for 85-90% of individuals with age-related macular changes and have only mild drusen, RPE atrophy, and/or RPE hypertrophy. They tend to be asymptomatic or only minimally symptomatic with mild blurred central vision, color and contrast disturbances, and metamorphopsia (waviness). Conversely, the 10-15% of patients with macular changes defined as AMD tend to report painless, progressive, moderate-to-severe blurring of central vision and moderate-to-severe metamorphopsia, which can be acute or insidious in onset.

Previous
Next

Pathophysiology

AMD is a degenerative retinal disease, presumably caused by both genetic and environmental factors. While age, race, sex, and family history demonstrate a consistently strong association with AMD in large epidemiological studies, smoking, hypertension, obesity, and dietary fat intake are also reported modifiable risk factors contributing to the advancement of AMD.[18, 19, 20, 21, 22, 23, 24]

The exact pathophysiology of AMD is relatively poorly understood; however, recent discoveries are advancing our understanding. Research has concentrated on the RPE/photoreceptor/Bruch's membrane complex. The RPE is a metabolically active layer that supports the function of the retinal photoreceptor. RPE cells phagocytose the shed outer segments of the photoreceptor cells and continually recycle and process the metabolic materials required for photoreceptor function.

As the RPE cells age, they accumulate intracellular residual bodies that contain lipofuscin.[25] This buildup can now be imaged with the advent of autofluorescence imaging.[26] The RPE cells extrude material to be removed by the vascular choriocapillaris; however, decreased RPE function and changes in the permeability of Bruch's membrane may lead to deposition of material between the RPE and Bruch's membrane, accounting for the formation of drusen. Scientists have also found that the choriocapillaris is thin in patients with AMD, and this raises the possibility that decreased clearance of extracellular material may contribute to drusen formation.

Recent findings suggest that drusen formation may initiate an inflammatory cascade that may play a role in AMD progression. Studies in genetics have pointed toward the complement pathway as a primary mechanism. A strong association was discovered between AMD and a single nucleotide polymorphism in the complement factor H (CFH) gene on chromosome 1[27, 28, 18, 29] and the PLEKHA1 and LOC387715 genes on chromosome 10.[30] Conversely, protective effects were reported for polymorphisms in the complement factor B and complement component 2 genes on chromosome 6 and various haplotypes on the CFH gene.[29, 31]

CFH is an inhibitor of the complement pathways; thus, abnormal CFH activity allows for complement cascade activation and subsequent inflammatory response to subretinal tissues.[29] Drusen have been found to contain inflammatory components from the cascade pathway.[32] In addition, smoking, which decreases levels of CFH, significantly increases the odds of developing AMD over nonsmokers with the CFH polymorphism.[33, 34] Similarly, the complement factor B and complement component 2 genes, which are usually involved in the activation of the complement cascade, could limit complement pathway activation with a protective polymorphism and, thus, minimize the degree of chronic inflammation.[31]

Drusen formation is not only a sign of RPE dysfunction but is thought to also be a cause of RPE loss and, in turn, photoreceptor loss. Further degeneration of the RPE can lead to dysfunction in Bruch's membrane, which separates the choriocapillaris from the RPE. Breakdown of Bruch's membrane and a rise in vascular endothelial growth factors can lead to the growth of abnormal choroidal vessels beneath the RPE and potentially under the retina. These vessels go through a period of leakage and occasionally bleed before they eventually involute and result in scar formation. The end-stage of exudative AMD is the formation of a disciform scar in the macula that results in permanent loss of central vision.

Previous
Next

Frequency

United States

AMD is the leading cause of irreversible visual loss in the United States, with variable degrees of age-related macular changes occurring in more than 10% of the population aged 65-74 years and 25% of the population older than 74 years.[35]

Approximately 10%-20% of patients with nonexudative AMD progress to the exudative form.[1] As a result, severe vision loss in many of the 1.75 million individuals with advanced AMD is secondary to the effects of CNV from AMD.[2, 35]

As the population of individuals older than 85 years increases an estimated 107% by the year 2020,[36] the overall prevalence of advanced AMD (geographic atrophy and/or CNV) is expected to increase from 1.75 million individuals to 2.95 million individuals.[2]

Previous
Next

Mortality/Morbidity

AMD leads to an increase in the rate of depression[37, 38] and frequent falls.[39]

Because many activities of daily living require functional central visual acuity, AMD decreases all aspects of the patient's quality of life, including the patient's ability to drive independently.[40] Studies measuring the quality of life in patients with vision loss demonstrate that they hold in high priority treatments that can improve their vision or prevent vision loss. A study from Wills Eye Hospital showed that when it came to an average person with 20/40 vision in the better seeing eye, they were willing to trade 2 of every 10 years of life in order to retain perfect vision (utility value of 0.8), while an average person with counting fingers vision in the better eye would trade roughly 5 of every 10 years of remaining life (utility value of 0.52) to have perfect vision.[41]

Race

Persons of Caucasian ancestry are far more likely to have late ARM and vision loss from AMD than those of African[42] or Hispanic lineage.[43] However, studies have failed to show consistent differences between those of Caucasian and Asian descent.[44, 45]

Sex

Data from several large population-based studies, including the Beaver Dam study,[46] the Third National Health and Nutrition Examination Survey,[47] and the Framingham study[48] have suggested that women are at increased risk for AMD compared with men.

Age

According to the International Classification System, AMD cannot be diagnosed in patients younger than 50 years.[16] Nearly every large population-based study has shown a positive correlation between the prevalence, incidence, and progression of AMD with increasing age.[2, 46, 49, 50, 51]

Previous
Next

Epidemiology

Frequency

United States

AMD is the leading cause of irreversible visual loss in the United States, with variable degrees of age-related macular changes occurring in more than 10% of the population aged 65-74 years and 25% of the population older than 74 years.[35]

Approximately 10%-20% of patients with nonexudative AMD progress to the exudative form.[1] As a result, severe vision loss in many of the 1.75 million individuals with advanced AMD is secondary to the effects of CNV from AMD.[2, 35]

As the population of individuals older than 85 years increases an estimated 107% by the year 2020,[36] the overall prevalence of advanced AMD (geographic atrophy and/or CNV) is expected to increase from 1.75 million individuals to 2.95 million individuals.[2]

Previous
 
 
Contributor Information and Disclosures
Author

F Ryan Prall, MD Assistant Professor of Ophthalmology, Indiana University School of Medicine

F Ryan Prall, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Coauthor(s)

Thomas A Ciulla, MD, MBA Staff Physician and Surgeon, Indiana University Health System, Beltway Surgery Centers, LLC, and St Vincent Hospital; Staff Physician and Retina Specialist, Midwest Eye Institute

Thomas A Ciulla, MD, MBA is a member of the following medical societies: Alpha Omega Alpha, Association for Research in Vision and Ophthalmology, American Academy of Ophthalmology, American Diabetes Association, Indiana Academy of Ophthalmology, Indianapolis Ophthalmological Society, Macula Society, Retina Society, Society of Heed Fellows

Disclosure: Nothing to disclose.

Mark H Criswell, PhD Adjunct Assistant Research Professor, Department of Ophthalmology, Indiana University School of Medicine

Mark H Criswell, PhD is a member of the following medical societies: Association for Research in Vision and Ophthalmology

Disclosure: Nothing to disclose.

Alon Harris, PhD Lois Letzter Professor, Director of Glaucoma Research and Diagnostic Center, Department of Ophthalmology, Indiana University School of Medicine

Alon Harris, PhD is a member of the following medical societies: American College of Sports Medicine, American Physiological Society, American Society for Laser Medicine and Surgery, New York Academy of Sciences

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Steve Charles, MD Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine

Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Macula Society, Retina Society, Club Jules Gonin

Disclosure: Received royalty and consulting fees for: Alcon Laboratories.

Chief Editor

Hampton Roy, Sr, MD Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Hampton Roy, Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, Pan-American Association of Ophthalmology

Disclosure: Nothing to disclose.

Additional Contributors

Brian A Phillpotts, MD, MD 

Brian A Phillpotts, MD, MD is a member of the following medical societies: American Academy of Ophthalmology, American Diabetes Association, American Medical Association, National Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Grant M Comer, MD, to the development and writing of this article.

References
  1. Tielsch JM, Javitt JC, Coleman A, Katz J, Sommer A. The prevalence of blindness and visual impairment among nursing home residents in Baltimore. N Engl J Med. 1995 May 4. 332(18):1205-9. [Medline].

  2. Friedman DS, O'Colmain BJ, Munoz B, Tomany SC, McCarty C, de Jong PT, et al. Prevalence of age-related macular degeneration in the United States. Arch Ophthalmol. 2004 Apr. 122(4):564-72. [Medline].

  3. Hand L. Blood Pressure Meds May Up AMD Risk, 20-Year Study Suggests. Medscape Medical News. June 4 2014. [Full Text].

  4. Klein R, Myers CE, Klein BE. Vasodilators, blood pressure-lowering medications, and age-related macular degeneration: the Beaver Dam Eye Study. Ophthalmology. 2014 Apr 11. [Medline].

  5. Tolentino MJ, Brucker AJ, Fosnot J, Ying GS, Wu IH, Malik G, et al. Intravitreal injection of vascular endothelial growth factor small interfering RNA inhibits growth and leakage in a nonhuman primate, laser-induced model of choroidal neovascularization. Retina. 2004 Feb. 24(1):132-8. [Medline].

  6. Tolentino MJ, Husain D, Theodosiadis P, Gragoudas ES, Connolly E, Kahn J, et al. Angiography of fluoresceinated anti-vascular endothelial growth factor antibody and dextrans in experimental choroidal neovascularization. Arch Ophthalmol. 2000 Jan. 118(1):78-84. [Medline].

  7. Bergers G, Song S, Meyer-Morse N, Bergsland E, Hanahan D. Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors. J Clin Invest. 2003 May. 111(9):1287-95. [Medline]. [Full Text].

  8. Bradley J, Ju M, Robinson GS. Combination therapy for the treatment of ocular neovascularization. Angiogenesis. 2007. 10(2):141-8. [Medline].

  9. Jo N, Mailhos C, Ju M, Cheung E, Bradley J, Nishijima K, et al. Inhibition of platelet-derived growth factor B signaling enhances the efficacy of anti-vascular endothelial growth factor therapy in multiple models of ocular neovascularization. Am J Pathol. 2006 Jun. 168(6):2036-53. [Medline]. [Full Text].

  10. Kahn HA, Leibowitz HM, Ganley JP, Kini MM, Colton T, Nickerson RS, et al. The Framingham Eye Study. I. Outline and major prevalence findings. Am J Epidemiol. 1977 Jul. 106(1):17-32. [Medline].

  11. Attebo K, Mitchell P, Smith W. Visual acuity and the causes of visual loss in Australia. The Blue Mountains Eye Study. Ophthalmology. 1996 Mar. 103(3):357-64. [Medline].

  12. Klaver CC, Wolfs RC, Vingerling JR, Hofman A, de Jong PT. Age-specific prevalence and causes of blindness and visual impairment in an older population: the Rotterdam Study. Arch Ophthalmol. 1998 May. 116(5):653-8. [Medline].

  13. Klein R, Davis MD, Magli YL, Segal P, Klein BE, Hubbard L. The Wisconsin age-related maculopathy grading system. Ophthalmology. 1991 Jul. 98(7):1128-34. [Medline].

  14. Davis MD, Gangnon RE, Lee LY, Hubbard LD, Klein BE, Klein R, et al. The Age-Related Eye Disease Study severity scale for age-related macular degeneration: AREDS Report No. 17. Arch Ophthalmol. 2005 Nov. 123(11):1484-98. [Medline]. [Full Text].

  15. Klein ML, Francis PJ, Ferris FL 3rd, Hamon SC, Clemons TE. Risk assessment model for development of advanced age-related macular degeneration. Arch Ophthalmol. 2011 Dec. 129(12):1543-50. [Medline].

  16. Bird AC, Bressler NM, Bressler SB, Chisholm IH, Coscas G, Davis MD, et al. An international classification and grading system for age-related maculopathy and age-related macular degeneration. The International ARM Epidemiological Study Group. Surv Ophthalmol. 1995 Mar-Apr. 39(5):367-74. [Medline].

  17. Davis MD, Gangnon RE, Lee LY, Hubbard LD, Klein BE, Klein R, et al. The Age-Related Eye Disease Study severity scale for age-related macular degeneration: AREDS Report No. 17. Arch Ophthalmol. 2005 Nov. 123(11):1484-98. [Medline].

  18. Klein R, Peto T, Bird A, Vannewkirk MR. The epidemiology of age-related macular degeneration. Am J Ophthalmol. 2004 Mar. 137(3):486-95. [Medline].

  19. Mares-Perlman JA, Brady WE, Klein R, VandenLangenberg GM, Klein BE, Palta M. Dietary fat and age-related maculopathy. Arch Ophthalmol. 1995 Jun. 113(6):743-8. [Medline].

  20. Chong EW, Kreis AJ, Wong TY, Simpson JA, Guymer RH. Dietary omega-3 fatty acid and fish intake in the primary prevention of age-related macular degeneration: a systematic review and meta-analysis. Arch Ophthalmol. 2008 Jun. 126(6):826-33. [Medline].

  21. Seddon JM, Rosner B, Sperduto RD, Yannuzzi L, Haller JA, Blair NP, et al. Dietary fat and risk for advanced age-related macular degeneration. Arch Ophthalmol. 2001 Aug. 119(8):1191-9. [Medline].

  22. Chong EW, Robman LD, Simpson JA, Hodge AM, Aung KZ, Dolphin TK, et al. Fat consumption and its association with age-related macular degeneration. Arch Ophthalmol. 2009 May. 127(5):674-80. [Medline].

  23. Chua B, Flood V, Rochtchina E, Wang JJ, Smith W, Mitchell P. Dietary fatty acids and the 5-year incidence of age-related maculopathy. Arch Ophthalmol. 2006 Jul. 124(7):981-6. [Medline].

  24. Seddon JM, Cote J, Davis N, Rosner B. Progression of age-related macular degeneration: association with body mass index, waist circumference, and waist-hip ratio. Arch Ophthalmol. 2003 Jun. 121(6):785-92. [Medline].

  25. Okubo A, Rosa RH, Fan JT, et al. RPE residual body content, autofluorescence and aging. Invest Ophthalmol Vis Sci. 1996. 37(suppl):380.

  26. von Ruckmann A, Fitzke FW, Bird AC. In vivo fundus autofluorescence in age-related macular degeneration. Invest Ophthalmol Vis Sci. 1997. 38:478-86.

  27. Edwards AO, Ritter R 3rd, Abel KJ, Manning A, Panhuysen C, Farrer LA. Complement factor H polymorphism and age-related macular degeneration. Science. 2005 Apr 15. 308(5720):421-4. [Medline].

  28. Haines JL, Hauser MA, Schmidt S, Scott WK, Olson LM, Gallins P, et al. Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005 Apr 15. 308(5720):419-21. [Medline].

  29. Hageman GS, Anderson DH, Johnson LV. A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proc Natl Acad Sci USA. 2005. 102:7227-32.

  30. Jakobsdottir J, Conley YP, Weeks DE, Mah TS, Ferrell RE, Gorin MB. Susceptibility genes for age-related maculopathy on chromosome 10q26. Am J Hum Genet. 2005 Sep. 77(3):389-407. [Medline].

  31. Gold B, Merriam JE, Zernant J. Variation in factor B (BF) and complement component 2 (C2)genes is associated with age-related macular degeneration. Nat Genet. 2006. 38:458-62.

  32. Johnson LV, Leitner WP, Staples MK, Anderson DH. Complement activation and inflammatory processes in Drusen formation and age related macular degeneration. Exp Eye Res. 2001 Dec. 73(6):887-96. [Medline].

  33. Esparza-Gordillo J, Soria JM, Buil A, Almasy L, Blangero J, Fontcuberta J. Genetic and environmental factors influencing the human factor H plasma levels. Immunogenetics. 2004 May. 56(2):77-82. [Medline].

  34. Sepp T, Khan JC, Thurlby DA, Shahid H, Clayton DG, Moore AT, et al. Complement factor H variant Y402H is a major risk determinant for geographic atrophy and choroidal neovascularization in smokers and nonsmokers. Invest Ophthalmol Vis Sci. 2006 Feb. 47(2):536-40. [Medline].

  35. Bressler NM, Bressler SB, Congdon NG, Ferris FL 3rd, Friedman DS, et al. Potential public health impact of Age-Related Eye Disease Study results: AREDS report no. 11. Arch Ophthalmol. 2003 Nov. 121(11):1621-4. [Medline].

  36. Thylefors B. A global initiative for the elimination of avoidable blindness. Am J Ophthalmol. 1998 Jan. 125(1):90-3. [Medline].

  37. Brody BL, Gamst AC, Williams RA, et al. Depression, visual acuity, comorbidity, and disability associated with age-related macular degeneration. Ophthalmology. 2001 Oct. 108(10):1893-900; discussion 1900-1. [Medline].

  38. Casten RJ, Rovner BW, Tasman W. Age-related macular degeneration and depression: a review of recent research. Curr Opin Ophthalmol. 2004 Jun. 15(3):181-3. [Medline].

  39. Coleman AL, Stone K, Ewing SK, Nevitt M, Cummings S, Cauley JA, et al. Higher risk of multiple falls among elderly women who lose visual acuity. Ophthalmology. 2004 May. 111(5):857-62. [Medline].

  40. Dong LM, Childs AL, Mangione CM, Bass EB, Bressler NM, Hawkins BS, et al. Health- and vision-related quality of life among patients with choroidal neovascularization secondary to age-related macular degeneration at enrollment in randomized trials of submacular surgery: SST report no. 4. Am J Ophthalmol. 2004 Jul. 138(1):91-108. [Medline].

  41. Vision and quality-of-life. Brown GC. Trans Am Ophthalmol Soc. 1999. 97:473-511.

  42. Sommer A, Tielsch JM, Katz J, Quigley HA, Gottsch JD, Javitt JC, et al. Racial differences in the cause-specific prevalence of blindness in east Baltimore. N Engl J Med. 1991 Nov 14. 325(20):1412-7. [Medline].

  43. Cruickshanks KJ, Klein R, Klein BE. Sunlight and age-related macular degeneration. The Beaver Dam Eye Study. Arch Ophthalmol. 1993 Apr. 111(4):514-8. [Medline].

  44. Das BN, Thompson JR, Patel R, Rosenthal AR. The prevalence of eye disease in Leicester: a comparison of adults of Asian and European descent. J R Soc Med. 1994 Apr. 87(4):219-22. [Medline].

  45. Miyazaki M, Nakamura H, Kubo M, Kiyohara Y, Oshima Y, Ishibashi T, et al. Risk factors for age related maculopathy in a Japanese population: the Hisayama study. Br J Ophthalmol. 2003 Apr. 87(4):469-72. [Medline].

  46. Klein R, Klein BE, Linton KL. Prevalence of age-related maculopathy. The Beaver Dam Eye Study. Ophthalmology. 1992 Jun. 99(6):933-43. [Medline].

  47. Klein R, Rowland ML, Harris MI. Racial/ethnic differences in age-related maculopathy. Third National Health and Nutrition Examination Survey. Ophthalmology. 1995 Mar. 102(3):371-81. [Medline].

  48. Kini MM, Leibowitz HM, Colton T, Nickerson RJ, Ganley J, Dawber TR. Prevalence of senile cataract, diabetic retinopathy, senile macular degeneration, and open-angle glaucoma in the Framingham eye study. Am J Ophthalmol. 1978 Jan. 85(1):28-34. [Medline].

  49. Leibowitz HM, Krueger DE, Maunder LR, Milton RC, Kini MM, Kahn HA, et al. The Framingham Eye Study monograph: An ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration, and visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol. 1980 May-Jun. 24:335-610. [Medline].

  50. Klein R, Klein BE, Jensen SC, Meuer SM. The five-year incidence and progression of age-related maculopathy: the Beaver Dam Eye Study. Ophthalmology. 1997 Jan. 104(1):7-21. [Medline].

  51. Seddon JM, Cote J, Davis N, Rosner B. Progression of age-related macular degeneration: association with body mass index, waist circumference, and waist-hip ratio. Arch Ophthalmol. 2003 Jun. 121(6):785-92. [Medline].

  52. Seddon JM, Ajani UA, Mitchell BD. Familial aggregation of age-related maculopathy. Am J Ophthalmol. 1997 Feb. 123(2):199-206. [Medline].

  53. Seddon JM, Willett WC, Speizer FE, Hankinson SE. A prospective study of cigarette smoking and age-related macular degeneration in women. JAMA. 1996 Oct 9. 276(14):1141-6. [Medline].

  54. Christen WG, Glynn RJ, Manson JE, Ajani UA, Buring JE. A prospective study of cigarette smoking and risk of age-related macular degeneration in men. JAMA. 1996 Oct 9. 276(14):1147-51. [Medline].

  55. Christen WG, Schaumberg DA, Glynn RJ, Buring JE. Dietary {omega}-3 Fatty Acid and Fish Intake and Incident Age-Related Macular Degeneration in Women. Arch Ophthalmol. 2011 Jul. 129(7):921-9. [Medline]. [Full Text].

  56. Seddon JM, George S, Rosner B. Cigarette smoking, fish consumption, omega-3 fatty acid intake, and associations with age-related macular degeneration: the US Twin Study of Age-Related Macular Degeneration. Arch Ophthalmol. 2006 Jul. 124(7):995-1001. [Medline].

  57. Yannuzzi LA. Indocyanine green angiography: a perspective on use in the clinical setting. Am J Ophthalmol. 2011 May. 151(5):745-751.e1. [Medline].

  58. Hee MR, Baumal CR, Puliafito CA, Duker JS, Reichel E, Wilkins JR, et al. Optical coherence tomography of age-related macular degeneration and choroidal neovascularization. Ophthalmology. 1996 Aug. 103(8):1260-70. [Medline].

  59. Ting TD, Oh M, Cox TA, Meyer CH, Toth CA. Decreased visual acuity associated with cystoid macular edema in neovascular age-related macular degeneration. Arch Ophthalmol. 2002 Jun. 120(6):731-7. [Medline].

  60. Sahni J, Stanga P, Wong D, Harding S. Optical coherence tomography in photodynamic therapy for subfoveal choroidal neovascularisation secondary to age related macular degeneration: a cross sectional study. Br J Ophthalmol. 2005 Mar. 89(3):316-20. [Medline].

  61. Piccolino FC, de la Longrais RR, Ravera G, Eandi CM, Ventre L, Abdollahi A, et al. The foveal photoreceptor layer and visual acuity loss in central serous chorioretinopathy. Am J Ophthalmol. 2005 Jan. 139(1):87-99. [Medline].

  62. Rogers AH, Martidis A, Greenberg PB, Puliafito CA. Optical coherence tomography findings following photodynamic therapy of choroidal neovascularization. Am J Ophthalmol. 2002 Oct. 134(4):566-76. [Medline].

  63. Rosenfeld P, Rich RM, Lalwani GA. Ranibizumab: Phase II clinical trial results. Ophthalmology Clinics of North America. 2006. 19:361-72.

  64. Gragoudas ES, Adamis AP, Cunningham ET Jr, Feinsod M, Guyer DR. Pegaptanib for neovascular age-related macular degeneration. N Engl J Med. 2004 Dec 30. 351(27):2805-16. [Medline].

  65. Eyetech Pharmaceuticals. Eyetech announces launch date for Macugen (pegaptanib sodium injection) [Eyetech Web site]. January 20, 2005. Available at: http://media.corporate-ir.net/media_files/irol/13/134799/newspdfs/1-20-05.pdf. Accessed June 27, 2005. [Full Text].

  66. Eyetech Pharmaceuticals. Pfizer and Eyetech provide regulatory update on Macugen (pegaptanib sodium injection) [Eyetech Web site]. September 20, 2004. Available at: http://media.corporate-ir.net/media_files/irol/13/134799/newspdfs/9-20-04-Update.pdf. Accessed October 12, 2004. [Full Text].

  67. Brown DM, Kaiser PK, Michels M, Soubrane G, Heier JS, Kim RY. Ranibizumab versus verteporfin for neovascular age-related macular degeneration. N Engl J Med. 2006 Oct 5. 355(14):1432-44. [Medline].

  68. Genetech Press Release. Preliminary Results from a Phase IIIb Study Showed Patients with Wet AMD Treated with Lucentis Quarterly Experienced a 16-Letter Benefit over the Control Group at One Year. Available at http://www.gene.com/gene/news/press-releases/display.do?method=detail&id=9747. Accessed: 2/21/2008.

  69. Singer MA, Awh CC, Sadda S, Freeman WR, Antoszyk AN, Wong P, et al. HORIZON: An Open-Label Extension Trial of Ranibizumab for Choroidal Neovascularization Secondary to Age-Related Macular Degeneration. Ophthalmology. 2012 Feb 4. [Medline].

  70. Schmidt-Erfurth U, Eldem B, Guymer R, Korobelnik JF, Schlingemann RO, Axer-Siegel R, et al. Efficacy and Safety of Monthly versus Quarterly Ranibizumab Treatment in Neovascular Age-related Macular Degeneration: The EXCITE Study. Ophthalmology. 2011 May. 118(5):831-9. [Medline].

  71. Fung AE, Lalwani GA, Rosenfeld PJ, Dubovy SR, Michels S, Feuer WJ. An optical coherence tomography-guided, variable dosing regimen with intravitreal ranibizumab (Lucentis) for neovascular age-related macular degeneration. Am J Ophthalmol. 2007 Apr. 143(4):566-83. [Medline].

  72. Holz FG, Korobelnik JF, Lanzetta P, Mitchell P, Schmidt-Erfurth U, Wolf S, et al. The effects of a flexible visual acuity-driven ranibizumab treatment regimen in age-related macular degeneration: outcomes of a drug and disease model. Invest Ophthalmol Vis Sci. 2010 Jan. 51(1):405-12. [Medline].

  73. Spaide R. Ranibizumab according to need: a treatment for age-related macular degeneration. Am J Ophthalmol. 2007 Apr. 143(4):679-80. [Medline].

  74. Brown DM, Regillo CD. Anti-VEGF agents in the treatment of neovascular age-related macular degeneration: applying clinical trial results to the treatment of everyday patients. Am J Ophthalmol. 2007 Oct. 144(4):627-37. [Medline].

  75. Gupta OP, Shienbaum G, Patel AH, et al. A treat and extend regimen using ranibizumab for neovascular age-related macular degeneration clinical and economic impact. Ophthalmology. 2010. 117:2134-2140.

  76. Shienbaum G, Gupta OP, Fecarotta C, et al. Management of neovascular age- related macular degeneration using bevacizumab with the treat and extend regimen: clinical results and economic impact. In: ARVO; Fort Lauderdale, Florida; 2010.

  77. Silva R, Axer-Siegel R, Eldem B, Guymer R, Kirchhof B, Papp A, et al. The SECURE Study: Long-Term Safety of Ranibizumab 0.5 mg in Neovascular Age-Related Macular Degeneration. Ophthalmology. 2012 Sep 25. [Medline].

  78. Genentech. Avastin [Genentech Web site]. Available at: http://www.gene.com/gene/products/information/oncology/avastin/index.jsp. Accessed June 28, 2005. [Full Text].

  79. Michels S, Rosenfeld PJ, Puliafito CA, et al. Systemic bevacizumab (Avastin) therapy for neovascular age-related macular degeneration twelve-week results of an uncontrolled open-label clinical study. Ophthalmology. 2005 Jun. 112(6):1035-47. [Medline].

  80. Rosenfeld PJ, Moshfeghi AA, Puliafito CA. Optical coherence tomography findings after an intravitreal injection of bevacizumab (avastin) for neovascular age-related macular degeneration. Ophthalmic Surg Lasers Imaging. 2005 Jul-Aug. 36(4):331-5. [Medline].

  81. Yoganathan P, Deramo VA, Lai JC, Tibrewala RK, Fastenberg DM. Visual improvement following intravitreal bevacizumab (Avastin) in exudative age-related macular degeneration. Retina. 2006 Nov-Dec. 26(9):994-8. [Medline].

  82. Emerson MV, Lauer AK, Flaxel CJ, Wilson DJ, Francis PJ, Stout JT. Intravitreal bevacizumab (Avastin) treatment of neovascular age-related macular degeneration. Retina. 2007 Apr-May. 27(4):439-44. [Medline].

  83. Abraham-Marin ML, Cortes-Luna CF, Alvarez-Rivera G, Hernandez-Rojas M, Quiroz-Mercado H, Morales-Canton V. Intravitreal bevacizumab therapy for neovascular age-related macular degeneration: a pilot study. Graefes Arch Clin Exp Ophthalmol. 2007 May. 245(5):651-5. [Medline].

  84. Bashshur ZF, Schakal A, Hamam RN, El Haibi CP, Jaafar RF, Noureddin BN. Intravitreal bevacizumab vs verteporfin photodynamic therapy for neovascular age-related macular degeneration. Arch Ophthalmol. 2007 Oct. 125(10):1357-61. [Medline].

  85. Lazic R, Gabric N. Verteporfin therapy and intravitreal bevacizumab combined and alone in choroidal neovascularization due to age-related macular degeneration. Ophthalmology. 2007 Jun. 114(6):1179-85. [Medline].

  86. Martin DF, Maguire MG, Ying GS, Grunwald JE, Fine SL, Jaffe GJ. Ranibizumab and bevacizumab for neovascular age-related macular degeneration. N Engl J Med. 2011 May 19. 364(20):1897-908. [Medline].

  87. Martin DF, Maguire MG, Fine SL, Ying GS, Jaffe GJ, Grunwald JE, et al. Ranibizumab and Bevacizumab for Treatment of Neovascular Age-Related Macular Degeneration: Two-Year Results. Ophthalmology. 2012 Apr 26. [Medline].

  88. Cavalcante LL, Cavalcante ML, Murray TG, et al. Intravitreal injection analysis at the Bascom Palmer Eye Institute: evaluation of clinical indications for the treatment and incidence rates of endophthalmitis. Clin Ophthalmol. 2010 May 25. 4:519-24. [Medline]. [Full Text].

  89. Mason JO 3rd, White MF, Feist RM, et al. Incidence of acute onset endophthalmitis following intravitreal bevacizumab (Avastin) injection. Retina. 2008 Apr. 28(4):564-7. [Medline].

  90. Fintak DR, Shah GK, Blinder KJ, et al. Incidence of endophthalmitis related to intravitreal injection of bevacizumab and ranibizumab. Retina. 2008 Nov-Dec. 28(10):1395-9. [Medline].

  91. Pilli S, Kotsolis A, Spaide RF, et al. Endophthalmitis associated with intravitreal anti-vascular endothelial growth factor therapy injections in an office setting. Am J Ophthalmol. 2008 May. 145(5):879-82. [Medline].

  92. Diago T, McCannel CA, Bakri SJ, et al. Infectious endophthalmitis after intravitreal injection of antiangiogenic agents. Retina. 2009 May. 29(5):601-5. [Medline].

  93. McCannel CA. Meta-analysis of endophthalmitis after intravitreal injection of anti-vascular endothelial growth factor agents: causative organisms and possible prevention strategies. Retina. 2011 Apr. 31(4):654-61. [Medline].

  94. Wen JC, McCannel CA, Mochon AB, Garner OB. Bacterial dispersal associated with speech in the setting of intravitreous injections. Arch Ophthalmol. 2011 Dec. 129(12):1551-4. [Medline].

  95. US Food and Drug Administration. FDA alerts health care professionals of infection risk from repackaged Avastin intravitreal injections. Available at http://www.fda.gov/Drugs/DrugSafety/ucm270296.htm. Accessed: August 31, 2011.

  96. Dixon JA, Oliver SC, Olson JL, Mandava N. VEGF Trap-Eye for the treatment of neovascular age-related macular degeneration. Expert Opin Investig Drugs. 2009 Oct. 18(10):1573-80. [Medline].

  97. Regeneron announces FDA approval of Eylea™ (aflibercept) injection for the treatment of wet age-related macular degeneration; 18 November 2011. Available at http://www.multivu.com/mnr/51268-eylea-aflibercept-wet-age-related-macular-degeneration-AMD-FDA-approval. Accessed: 22 November 2011.

  98. Brown DM, Heier JS, Ciulla T, Benz M, Abraham P, Yancopoulos G, et al. Primary Endpoint Results of a Phase II Study of Vascular Endothelial Growth Factor Trap-Eye in Wet Age-related Macular Degeneration. Ophthalmology. 2011 Jun. 118(6):1089-97. [Medline].

  99. Heier JS, Boyer D, Nguyen QD, Marcus D, Roth DB, Yancopoulos G, et al. The 1-year Results of CLEAR-IT 2, a Phase 2 Study of Vascular Endothelial Growth Factor Trap-Eye Dosed As-needed After 12-week Fixed Dosing. Ophthalmology. 2011 Jun. 118(6):1098-106. [Medline].

  100. Gehlbach P, Li T, Hatef E. Statins for age-related macular degeneration. Cochrane Database Syst Rev. 2009 Jul 8. CD006927. [Medline].

  101. Chuo JY, Wiens M, Etminan M, Maberley DA. Use of lipid-lowering agents for the prevention of age-related macular degeneration: a meta-analysis of observational studies. Ophthalmic Epidemiol. 2007 Nov-Dec. 14(6):367-74. [Medline].

  102. MPS Group. Macular Photocoagulation Study Group. Argon laser photocoagulation for senile macular degeneration. Results of a randomized clinical trial. Arch Ophthalmol. 1982 Jun. 100(6):912-8. [Medline].

  103. MPS Group. Macular Photocoagulation Study Group. Argon laser photocoagulation for neovascular maculopathy. Three-year results from randomized clinical trials. Arch Ophthalmol. 1986 May. 104(5):694-701. [Medline].

  104. MPS Group. Argon laser photocoagulation for neovascular maculopathy. Five-year results from randomized clinical trials. Macular Photocoagulation Study Group. Arch Ophthalmol. 1991 Aug. 109(8):1109-14. [Medline].

  105. MPS Group. Macular Photocoagulation Study Group. Five-year follow-up of fellow eyes of patients with age-related macular degeneration and unilateral extrafoveal choroidal neovascularization. Arch Ophthalmol. 1993 Sep. 111(9):1189-99. [Medline].

  106. Freund KB, Yannuzzi LA, Sorenson JA. Age-related macular degeneration and choroidal neovascularization. Am J Ophthalmol. 1993 Jun 15. 115(6):786-91. [Medline].

  107. Moisseiev J, Alhalel A, Masuri R, Treister G. The impact of the macular photocoagulation study results on the treatment of exudative age-related macular degeneration. Arch Ophthalmol. 1995 Feb. 113(2):185-9. [Medline].

  108. Nishijima K, Takahashi M, Akita J, Katsuta H, Tanemura M, Aikawa H, et al. Laser photocoagulation of indocyanine green angiographically identified feeder vessels to idiopathic polypoidal choroidal vasculopathy. Am J Ophthalmol. 2004 Apr. 137(4):770-3. [Medline].

  109. Shiraga F, Ojima Y, Matsuo T, Takasu I, Matsuo N. Feeder vessel photocoagulation of subfoveal choroidal neovascularization secondary to age-related macular degeneration. Ophthalmology. 1998 Apr. 105(4):662-9. [Medline].

  110. Reichel E, Musch DC, Blodi BA. Results from the TTT4CNV clinical trial. Invest Ophthalmol Vis Sci. 2005. 46:E-abstract 2311.

  111. Aveline B, Hasan T, Redmond RW. Photophysical and photosensitizing properties of benzoporphyrin derivative monoacid ring A (BPD-MA). Photochem Photobiol. 1994 Mar. 59(3):328-35. [Medline].

  112. Allison BA, Waterfield E, Richter AM, Levy JG. The effects of plasma lipoproteins on in vitro tumor cell killing and in vivo tumor photosensitization with benzoporphyrin derivative. Photochem Photobiol. 1991 Nov. 54(5):709-15. [Medline].

  113. Hunt DW, Jiang H, Granville DJ, Chan AH, Leong S, Levy JG. Consequences of the photodynamic treatment of resting and activated peripheral T lymphocytes. Immunopharmacology. 1999 Jan. 41(1):31-44. [Medline].

  114. Novartis Ophthalmics. Visudyne launched in Japan for treatment of age-related macular degeneration [Novartis Web site]. May 10, 2004. Available at: http://www.us.novartisophthalmics.com/hcp/press-release/Visodyne_E_10.05.pdf. Accessed October 15, 2004. [Full Text].

  115. Blumenkranz MS, Bressler NM, Bressler SB, Donati G, Fish GE, Haynes LA, et al. Verteporfin therapy for subfoveal choroidal neovascularization in age-related macular degeneration: three-year results of an open-label extension of 2 randomized clinical trials--TAP Report no. 5. Arch Ophthalmol. 2002 Oct. 120(10):1307-14. [Medline].

  116. Dhalla MS, Shah GK, Blinder KJ, Ryan EH Jr, Mittra RA, Tewari A. Combined photodynamic therapy with verteporfin and intravitreal bevacizumab for choroidal neovascularization in age-related macular degeneration. Retina. 2006 Nov-Dec. 26(9):988-93. [Medline].

  117. Augustin AJ, Puls S, Offermann I. Triple therapy for choroidal neovascularization due to age-related macular degeneration: verteporfin PDT, bevacizumab, and dexamethasone. Retina. 2007 Feb. 27(2):133-40. [Medline].

  118. Schmidt-Erfurth U, Schlötzer-Schrehard U, Cursiefen C, Michels S, Beckendorf A, Naumann GO. Influence of photodynamic therapy on expression of vascular endothelial growth factor (VEGF), VEGF receptor 3, and pigment epithelium-derived factor. Invest Ophthalmol Vis Sci. 2003 Oct. 44(10):4473-80. [Medline].

  119. Costagliola C, Romano MR, Rinaldi M, dell'Omo R, Chiosi F, Menzione M, et al. Low fluence rate photodynamic therapy combined with intravitreal bevacizumab for neovascular age-related macular degeneration. Br J Ophthalmol. 2010 Feb. 94(2):180-4. [Medline].

  120. Potter MJ, Claudio CC, Szabo SM. A randomised trial of bevacizumab and reduced light dose photodynamic therapy in age-related macular degeneration: the VIA study. Br J Ophthalmol. 2010 Feb. 94(2):174-9. [Medline].

  121. Lim JY, Lee SY, Kim JG, Lee JY, Chung H, Yoon YH. Intravitreal bevacizumab alone versus in combination with photodynamic therapy for the treatment of neovascular maculopathy in patients aged 50 years or older: 1-year results of a prospective clinical study. Acta Ophthalmol. 2010 Mar 16. [Medline].

  122. Kaiser PK, Boyer DS, Cruess AF, Slakter JS, Pilz S, Weisberger A. Verteporfin plus ranibizumab for choroidal neovascularization in age-related macular degeneration: twelve-month results of the DENALI study. Ophthalmology. 2012 May. 119(5):1001-10. [Medline].

  123. Larsen M, Schmidt-Erfurth U, Lanzetta P, Wolf S, Simader C, Tokaji E, et al. Verteporfin plus ranibizumab for choroidal neovascularization in age-related macular degeneration: twelve-month MONT BLANC study results. Ophthalmology. 2012 May. 119(5):992-1000. [Medline].

  124. Jackson TL, Chakravarthy U, Kaiser PK, Slakter JS, Jan E, Bandello F, et al. Stereotactic Radiotherapy for Neovascular Age-Related Macular Degeneration: 52-Week Safety and Efficacy Results of the INTREPID Study. Ophthalmology. 2013 Mar 12. [Medline].

  125. Bressler NM, Bressler SB, Childs AL, Haller JA, Hawkins BS, Lewis H, et al. Surgery for hemorrhagic choroidal neovascular lesions of age-related macular degeneration: ophthalmic findings: SST report no. 13. Ophthalmology. 2004 Nov. 111(11):1993-2006. [Medline].

  126. Hawkins BS, Bressler NM, Miskala PH, Bressler SB, Holekamp NM, Marsh MJ, et al. Surgery for subfoveal choroidal neovascularization in age-related macular degeneration: ophthalmic findings: SST report no. 11. Ophthalmology. 2004 Nov. 111(11):1967-80. [Medline].

  127. Abraham P, Yue H, Wilson L. Randomized, double-masked, sham-controlled trial of ranibizumab for neovascular age-related macular degeneration: PIER study year 2. Am J Ophthalmol. 2010 Sep. 150(3):315-324.e1. [Medline].

  128. Bressler NM. Photodynamic therapy of subfoveal choroidal neovascularization in age-related macular degeneration with verteporfin: two-year results of 2 randomized clinical trials-tap report 2. Arch Ophthalmol. 2001 Feb. 119(2):198-207. [Medline].

  129. Cho H, Shah CP, Weber M, Heier JS. Aflibercept for exudative AMD with persistent fluid on ranibizumab and/or bevacizumab. Br J Ophthalmol. 2013 Aug. 97(8):1032-5. [Medline].

  130. Drexler W, Sattmann H, Hermann B, Ko TH, Stur M, Unterhuber A, et al. Enhanced visualization of macular pathology with the use of ultrahigh-resolution optical coherence tomography. Arch Ophthalmol. 2003 May. 121(5):695-706. [Medline].

  131. Hageman GS, Luthert PJ, Victor Chong NH, Johnson LV, Anderson DH, et al. An integrated hypothesis that considers drusen as biomarkers of immune-mediated processes at the RPE-Bruch's membrane interface in aging and age-related macular degeneration. Progress in Retinal and Eye Research. November 2001. 20:705-32.

  132. Harrison P. Aflibercept Switch Helps Macular Degeneration. Medscape Medical News. Available at http://www.medscape.com/viewarticle/810212. Accessed: September 1, 2013.

  133. Johnson TM, Glaser BM. Focal laser ablation of retinal angiomatous proliferation. Retina. 2006 Sep. 26(7):765-72. [Medline].

  134. Klein RJ, Zeiss C, Chew EY, Tsai JY, Sackler RS, Haynes C, et al. Complement factor H polymorphism in age-related macular degeneration. Science. 2005 Apr 15. 308(5720):385-9. [Medline].

  135. Matsuyama K, Ogata N, Matsuoka M, Wada M, Takahashi K, Nishimura T. Plasma levels of vascular endothelial growth factor and pigment epithelium-derived factor before and after intravitreal injection of bevacizumab. Br J Ophthalmol. 2010 Sep. 94(9):1215-8. [Medline].

  136. MPS Group. Macular Photocoagulation Study Group. Laser photocoagulation of subfoveal neovascular lesions of age-related macular degeneration. Updated findings from two clinical trials. Arch Ophthalmol. 1993 Sep. 111(9):1200-9. [Medline].

  137. MPS Group. Macular Photocoagulation Study Group. Recurrent choroidal neovascularization after argon laser photocoagulation for neovascular maculopathy. Arch Ophthalmol. 1986 Apr. 104(4):503-12. [Medline].

  138. MPS Group. Macular Photocoagulation Study Group. Subfoveal neovascular lesions in age-related macular degeneration. Guidelines for evaluation and treatment in the macular photocoagulation study. Arch Ophthalmol. 1991 Sep. 109(9):1242-57. [Medline].

  139. National Eye Institute. Comparison of Age-Related Macular Degeneration Treatment Trial (CATT). ClinicalTrials.gov. Available at http://clinicaltrials.gov/ct2/show/NCT00593450. Accessed: 2/21/2008.

  140. Rosenfeld PJ, Brown DM, Heier JS, Boyer DS, Kaiser PK, Chung CY, et al. Ranibizumab for neovascular age-related macular degeneration. N Engl J Med. 2006 Oct 5. 355(14):1419-31. [Medline].

 
Previous
Next
 
Age-related macular degeneration (AMD), exudative.
Age-related macular degeneration (AMD), exudative.
Color photograph of the fundus shows nonexudative age-related macular degeneration (AMD) with geographic atrophy of the retinal pigment epithelium (RPE) and drusen. Absolute atrophy of the RPE occupies the foveal region in this case of nonexudative AMD. The central atrophic region causes a corresponding central scotoma. Note the large choroidal vessels, which are visible through the RPE defect. Drusen surround the region of geographic atrophy. Photo by Tim Steffens.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.