Citations 2
DELAYED RHEGMATOGENOUS RETINAL DETACHMENT AFTER MACULAR SURGERY
Singh, Sumit Randhir , Boscia, Giacomo, Ferrara, Mariantonia , Menzio, Sara, Veritti, Daniele , Kuppermann, Baruch D., Singh, Rishi P. , Rezaei, Kourous A., Israilevich, Rachel , Chhablani, Jay, Boscia, Francesco , Boscia, Giacomo, Romano, Mario Rosario , Sarao, Valentina , Lanzetta, Paolo , Arévalo, J. Fernando , Parolini, Barbara , Hassan, T. , Wu, Lihteh , Starr, Matthew R. , Chhablani, Jay
Retina | February 26, 2025 | Volume: 45 | Issue: 6 | Pages: 1050-1055
Purpose: To report the anatomic and visual outcomes of eyes developing delayed rhegmatogenous retinal detachment (RRD) after macular surgery. Methods: This was a retrospective, multicentric study including eyes undergoing RRD repair at least 3 months after macular surgery for either full-thickness macular hole (FTMH) or epiretinal membrane (ERM). Anatomic and functional assessment, i.e., pre- and postoperative best-corrected visual acuity (BCVA), indications and details of macular and RRD surgery, time interval from macular surgery to RRD, intraocular tamponade, location, extent of RRD, and nature of retinal break, was performed. Results: Sixteen out of 2,906 eyes (0.55%) undergoing macular surgery developed RRD after 8.4 ± 5.8 months (mean ± SD). Intraoperative peripheral retina evaluation showed missed/de novo break (11 eyes; 68.75%), no identifiable break i.e., probable microbreak (two eyes; 12.5%), giant retinal tear (two eyes; 12.5%), and retinoschisis related break (one eye; 6.25%). Anatomical success, i.e., attached retina after one surgery, was seen in 14 eyes (87.5%). BCVA worsened from 0.6 ± 0.3 logMAR (Snellen equivalent 20/80) at baseline to 0.9 ± 0.8 logMAR (20/160) through the last visit (P < 0.001). Conclusion: RRD after macular surgery occurs predominantly via missed/de novo retinal breaks. A significant percentage (50%) of eyes showed worse visual acuity compared with baseline despite successful retinal reattachment.
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.