Citations 2
Role of Intravitreal Antivascular Endothelial Growth Factor Injections for Choroidal Neovascularization due to Choroidal Osteoma
Mansour, Ahmad M. , Arévalo, J. Fernando , Kahtani, Eman Al, Zegarra, Hernando, Abboud, Emad B. , Anand, Rajiv, Ahmadieh, Hamid , Mirza, Salman, Tuncer, Samuray , Návea, Amparo , Mataix, J. , Ascaso, Francisco J., Pulido, José S. , Guthoff, Rainer , Goebel, Winfried, Banker, Alay , Gentile, Ronald C., Martinez, Isabel Alonso, Morris, Rodney J, Panday, Neeraj, Min, Park Jung, Mercé, Emilie, Lai, Timothy Y. Y. , Massoud, Vicky, Ghazi, Nicola G. , Abboud, Emad , Sisk, Robert A. , Roh, Young‐Jung , Martínez, Isabel Alonso, Massoud, Vicky A., Arevalo, Jose Fernando
Journal of Ophthalmology | July 23, 2014 | Volume: 2014 | Issue: No issue available | Pages: 1-8
We treated 26 eyes of 25 young patients having a mean age of 30 years with intravitreal vascular endothelial growth factor (VEGF) inhibitor for choroidal new vessel (CNV) formation overlying choroidal osteoma over a mean follow-up of 26 months. Mean number of injections was 2.4 at 6 months, 3.2 at 12 months, and 5.5 at 24 months. CNV was subfoveal in 14 eyes, juxtafoveal in 5, extrafoveal in 5, and peripapillary in 2. By paired comparison, mean decrease from baseline was 119.7 microns at 6 months (n=15;P=0.001), 105.3 microns at 1 year (n=10;P=0.03), and 157.6 microns at 2 years (n=7;P=0.08). BCVA improved by 3.3 lines at 6 months after therapy (n=26;P<0.001), 2.8 lines (n=20;P=0.01) at 1 year, and 3.1 lines (n=13;P=0.049) at 2 years. We conclude that intravitreal anti-VEGF injections improve vision in majority of eyes with CNV from choroidal osteoma.
Genetic variants near TIMP3 and high-density lipoprotein–associated loci influence susceptibility to age-related macular degeneration
Stambolian, Dwight, Edwards, Albert O., Branham, Kari , Othman, Mohammad , Jakobsdóttir, Jóhanna , Tosakulwong, Nirubol , Pericak‐Vance, Margaret A. , Klein, Michael L. , Tan, Perciliz L. , Kanda, Atsuhiro , Kopplin, Laura J. , Li, Yanming , Augustaitis, Katherine J., Karoukis, Athanasios J., Scott, William K. , Agarwal, Anita , Kovach, Jaclyn L. , Postel, Eric A. , Brooks, Matthew, Baratz, Keith H. , Brown, William L. , Brucker, Alexander J., Orlin, Anton, Brown, Gary C. , Ho, Allen C. , Regillo, Carl D. , Donoso, Larry A., Tian, Lifeng , Kaderli, Brian, Hadley, Dexter , Hagstrom, Stephanie A. , Peachey, Neal S. , Klein, Ronald , Klein, Barbara E.K. , Gotoh, Norimoto, Yamashiro, Kenji , Ferris, Frederick L. , Fagerness, Jesen, Reynolds, Robyn, Farrer, Lindsay A. , Kim, Ivana K. , Miller, Joan W. , Cortón, Marta , Carracedo, Ãngel , Sánchez‐Salorio, Manuel, Pugh, Elizabeth, Doheny, Kimberly F. , Brión, Marı́a , Weeks, Daniel E. , Zack, Donald J. , Heckenlively, John R., Yoshimura, Nagahisa , Iyengar, Sudha K. , Francis, Peter J. , Katsanis, Nicholas , Seddon, Johanna M. , Haines, Jonathan L. , Abecasis, Gonçalo R. , Swaroop, Anand , Johnson, Robert N., Ai, Everett, McDonald, H. Richard , Stolarczuk, Margaret, Pavan, Peter R., Billiris, Karina K., Iyer, Mohan , Menosky, Matthew M., Pautler, Scott E. , Millard, Sharon M., Hubbard, G. Baker , Aaberg, Thomas , DuBois, Lindy, Lyon, Alice T., Anderson-Nelson, Susan, Jampol, Lee M. , Muñana, Annie, Rozenbajgier, Zuzanna, Orth, David H., Cohen, Jack, MacCumber, Matthew, Figliulo, Celeste, Porcz, Liz, Folk, James C. , Boldt, H. Culver , Russell, Stephen R. , Ivins, Rachel, Hinz, Connie J., Bloom, Steve, Jaegers, Ken, Kritchman, Brian, Whittington, Greg K., Frederick, Albert R., Morley, Michael G., Topping, Trexler M., Davis, Heather L., Bressler, Susan B., Bressler, Neil M. , Doll, W T Jr, Trese, Michael T. , Garretson, Bruce R., Ruby, Alan, Osentoski, Tammy, Ruszczyk, Margaret, Grand, G., Joseph, Daniel P., Shah, Gaurav K. , Nobel, Ginny, Antoszyk, Andrew N., Stallings, Alison H, Singerman, Lawrence J. , Miller, David T. , Novák, Michael, Pendergast, Scott, Zegarra, Hernando, Schura, Stephanie A., Smith-Brewer, Sheila, Davidorf, Frederick H., Chorich, Louis J., Salerno, Jill, Dreyer, Richard F., Ma, Colin, Kopfer, Marcia, Wilson, David J. , Nolte, Susan K., Grunwald, Juan E. , Dunaief, Josh, Fine, Stuart L., Maguire, Albert M. , Stoltz, Robert A., McRay, Monique, Fish, Gary E., Anand, Rajiv, Spencer, Rand , Arnwine, Jean, Chandra, Suresh R., Blodi, Barbara, Gottlieb, Justin L., Ip, Michael S. , Nork, T. Michael , Perry-Raymond, Jennie, Brightwell-Arnold, Mary, Harkins, Sandra, Peskin, Ellen, Ying, Gui‐Shuang , Kurinij, Natalie, Chen, Wei , Campochiaro, Peter A. , Conley, Yvette P. , Schwartz, Stephen G. , DeAngelis, Margaret M. , Chew, Emily Y. , Gorin, Michael B. , Menosky, Matthew M., Weinberg, David V. , Barr, Charles C. , Heier, Jeffrey S. , Capone, A. , Hassan, T. , McCannel, Colin A. , Blinder, Kevin J. , Holekamp, Nancy M. , Browning, David J. , Chambers, Robert , Altaweel, Michael M. , Maguire, Maureen G. , Weeks, Daniel E , Brion, María , Abecasis, Gonçalo
Proceedings of the National Academy of Sciences | April 12, 2010 | Volume: 107 | Issue: 16 | Pages: 7401-7406
We executed a genome-wide association scan for age-related macular degeneration (AMD) in 2,157 cases and 1,150 controls. Our results validate AMD susceptibility loci near CFH ( P < 10 −75 ), ARMS2 ( P < 10 −59 ), C2/CFB ( P < 10 −20 ), C3 ( P < 10 −9 ), and CFI ( P < 10 −6 ). We compared our top findings with the Tufts/Massachusetts General Hospital genome-wide association study of advanced AMD (821 cases, 1,709 controls) and genotyped 30 promising markers in additional individuals (up to 7,749 cases and 4,625 controls). With these data, we identified a susceptibility locus near TIMP3 (overall P = 1.1 × 10 −11 ), a metalloproteinase involved in degradation of the extracellular matrix and previously implicated in early-onset maculopathy. In addition, our data revealed strong association signals with alleles at two loci ( LIPC , P = 1.3 × 10 −7 ; CETP , P = 7.4 × 10 −7 ) that were previously associated with high-density lipoprotein cholesterol (HDL-c) levels in blood. Consistent with the hypothesis that HDL metabolism is associated with AMD pathogenesis, we also observed association with AMD of HDL-c—associated alleles near LPL ( P = 3.0 × 10 −3 ) and ABCA1 ( P = 5.6 × 10 −4 ). Multilocus analysis including all susceptibility loci showed that 329 of 331 individuals (99%) with the highest-risk genotypes were cases, and 85% of these had advanced AMD. Our studies extend the catalog of AMD associated loci, help identify individuals at high risk of disease, and provide clues about underlying cellular pathways that should eventually lead to new therapies.