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RETICULAR MACULAR DISEASE IS ASSOCIATED WITH MULTILOBULAR GEOGRAPHIC ATROPHY IN AGE-RELATED MACULAR DEGENERATION

Xu, Luna MD*; Blonska, Anna M. MD*; Pumariega, Nicole M. MS*; Bearelly, Srilaxmi MD, MHS*; Sohrab, Mahsa A. MD*; Hageman, Gregory S. PhD; Smith, R. Theodore MD, PhD

doi: 10.1097/IAE.0b013e31828991b2
Original Study

Purpose: To investigate the incidence of reticular macular disease (RMD), a subphenotype of age-related macular degeneration, in multilobular geographic atrophy (GA) and its relation to GA progression.

Methods: One hundred and fifty-seven eyes of 99 subjects with age-related macular degeneration, primary GA, and good quality autofluorescence, and/or infrared images were classified into unilobular GA (1 lesion) or multilobular GA (≥2 distinct and/or coalescent lesions). Thirty-four subjects (50 eyes) had serial imaging. The authors determined the spatiotemporal relationships of RMD to GA and GA progression rates in five macular fields.

Results: 91.7% eyes (144 of 157) had multilobular GA, 95.8% of which exhibited RMD. In subjects with serial imaging, the mean GA growth rate significantly differed between the unilobular and multilobular groups (0.40 vs. 1.30 mm2/year, P < 0.001). Of the macular fields in these eyes, 77.1% of fields with RMD at baseline showed subsequent GA progression, while 53.4% of fields without RMD showed progression (P < 0.001). Percentage of fields with RMD significantly correlated with GA progression rate (P = 0.01).

Conclusion: Autofluorescence and infrared imaging demonstrates that RMD is nearly always present with multilobular GA in age-related macular degeneration. Furthermore, GA lobules frequently develop in areas of RMD, suggesting progression of a single underlying disease process.

The association between reticular macular disease (RMD) and multilobular geographic atrophy (GA) in age-related macular degeneration is nearly universal. Furthermore, the extent of RMD is associated with GA progression, suggesting a single underlying disease process.

*Department of Ophthalmology, E.S. Harkness Eye Institute, Columbia University, New York, New York;

Department of Ophthalmology and Visual Sciences, John A. Moran Eye Center, University of Utah, Salt Lake City, Utah; and

Department of Ophthalmology, New York University Langone Medical Center, New York, New York.

Reprints requests: R. Theodore Smith, MD, PhD, Department of Ophthalmology, New York University Langone Medical Center, 462 First Avenue, NBV 5N18, New York, NY 10016; e-mail: roland.smith@nyumc.org

Supported by grants from The New York Community Trust (New York, NY) (R.T.S.); National Eye Institute (Bethesda, MD) grants R01 EY015520 (R.T.S.) and R24 EY017404 (G.S.H.); unrestricted grants to the E.S. Harkness Eye Institute and the University of Utah’s Department of Ophthalmology and Visual Sciences from Research to Prevent Blindness (New York, NY); the Kaplen Foundation (S.B.); and the Doris Duke Clinical Research Fellowship Program (L.X.).

Dr. G. S. Hageman is on the Ophthalmology Clinical Advisory Board of Sequenom, Inc, and has financial interest in Optherion, Inc.

The authors declare no conflict of interest.

© 2013 by Ophthalmic Communications Society, Inc.