gms | German Medical Science

25th Annual Meeting of the German Retina Society

German Retina Society

01.06. - 02.06.2012, Münster

Tumor necrosis factor α in neovascular age-related macular degenration (AMD)

Meeting Abstract

  • Alireza Mirshahi - Universitäts-Augenklinik Mainz
  • N. Boehm - Universitäts-Augenklinik Mainz
  • K. Korb - Universitäts-Augenklinik Mainz
  • K. Lorenz - Universitäts-Augenklinik Mainz
  • E. Schader - Universitäts-Augenklinik Mainz
  • N. Pfeiffer - Universitäts-Augenklinik Mainz
  • F. Grus - Universitäts-Augenklinik Mainz

German Retina Society. 25th Annual Conference of the German Retina Society. Münster, 01.-02.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12rg48

doi: 10.3205/12rg48, urn:nbn:de:0183-12rg487

This is the English version of the article.
The German version can be found at: http://www.egms.de/de/meetings/rg2012/12rg48.shtml

Published: May 30, 2012

© 2012 Mirshahi et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

Text

Purpose: To compare the concentration of tumor necrosis factor α (TNF) in the vitreous humour of eyes with neovascular age-related macular degeneration (AMD) vs. in eyes with a non-proliferative and non-angiogenic retinal disease, namely idiopathic macular hole. TNF is a pro-inflammatory cytokine produced by macrophages and T-cells playing an important role in both inflammation and apoptosis.

Methods: We measured the concentration of TNF in 39 specimens of vitreous humour obtained from 39 patients undergoing pars plana vitrectomy either for the treatment of a macular hole (22) or for subretinal hemorrhage secondary to neovascular AMD (17), respectively. All eyes were treatment-naive for any intravitreal injection or photodynamic therapy. For the proteomic mapping, we applied a customized antibody-microarray approach. 5 µg protein of each sample were incubated on microarray slides. For detection of bound proteins samples were labeled with a fluorescent dye prior to the incubation and slides were scanned using a confocal microarray scanner subsequent to the incubation. Analysis of experimental data was performed using statistical techniques incl. ANOVA, t-test and Post-hoc testing.

Results: The mean intensity of TNF (5023±3179 SD) in the samples of vitreous humour from patients with neovascular AMD was higher than in samples from patients with idiopathic macular hole (3297±1367; p=0.002).

Conclusion: Our data suggest that TNF α is involved in the pathogenesis of active choroidal neovascularization secondary to AMD. However, there was a wide range in the concentration of TNF in the AMD group.