title: Anti-TNF-α agents for refractory cystoid macular edema associated with noninfectious uveitis.
abstract: BACKGROUND
  The use of anti-tumor necrosis factor (TNF)-α agents for uveitis has been increasing since the first efficacy studies in 2004. However, information on their specific role in cystic macular edema remains sparse. The aim of this study was to evaluate the efficacy of anti-TNF-α agents for the treatment of uveitis-related refractory cystoid macular edema.
  
  
  METHODS
  The files of 23 consecutive patients treated for cystoid macular edema at the uveitis services of two tertiary medical centers in 2006-2011 were reviewed for demographic data, visual acuity, and optical coherence tomography measurements at baseline and 3, 6, and 12 months after treatment. Changes in mean visual acuity and macular thickness were analyzed. Findings were compared between patients treated with a conventional immunosuppressive regimen only (n = 18, 27 eyes) and patients treated with an anti-TNF-α agent after proving refractory to conventional treatment (n = 9, 15 eyes).
  
  
  RESULTS
  Mean duration of cystoid macular edema before initiation of anti-TNF-α therapy was 12 ± 8 months. The two groups had similar baseline values of mean central macular thickness and visual acuity. Significant improvement in macular thickness was noted at 3 months in both groups, with a maximal effect at 6 months for the anti-TNF-α group (p = 0.002). Maximal improvement in visual acuity was achieved at 3 months in both groups, with a reduced effect towards 12 months. Mean visual acuity at 12 months was similar in both groups.
  
  
  CONCLUSIONS
  Anti-TNF-α agents may serve as an effective lasting treatment for long-standing refractory uveitis-related cystoid macular edema. Their role as first-line therapy in this setting warrants further investigation.
authors.affiliation: Department of Ophthalmology, Rabin Medical Center, Beilinson Campus, Petach Tikva, 49100, Israel.
authors.forename: Michal
authors.initials: M
authors.lastname: Schaap-Fogler
authors.forename: Radgonde
authors.initials: R
authors.lastname: Amer
authors.forename: Ronit
authors.initials: R
authors.lastname: Friling
authors.forename: Ethan
authors.initials: E
authors.lastname: Priel
authors.forename: Michal
authors.initials: M
authors.lastname: Kramer
mesh_terms: D000068879:Adalimumab; D000293:Adolescent; D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D002648:Child; D002675:Child, Preschool; D004351:Drug Resistance; D005260:Female; D006801:Humans; D000069285:Infliximab; D008266:Macula Lutea / Q000473:pathology; D008269:Macular Edema / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012008:Recurrence; D041623:Tomography, Optical Coherence; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014605:Uveitis / Q000188:drug therapy* / Q000503:physiopathology; D014792:Visual Acuity / Q000502:physiology; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab