May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Alfa–interferon treatment of refractory cystoid macular edema in uveitis
Author Affiliations & Notes
  • C.M. Deuter
    Department of Ophthalmology I, University of Tuebingen, Tuebingen, Germany
  • I. Koetter
    Department of Internal Medicine II, University of Tuebingen, Tuebingen, Germany
  • T. Daikeler
    Department of Internal Medicine II, University of Tuebingen, Tuebingen, Germany
  • I. Guenaydin
    Department of Internal Medicine II, University of Tuebingen, Tuebingen, Germany
  • N. Stuebiger
    Department of Ophthalmology I, University of Tuebingen, Tuebingen, Germany
  • K. Siepmann
    Department of Ophthalmology I, University of Tuebingen, Tuebingen, Germany
  • M. Zierhut
    Department of Ophthalmology I, University of Tuebingen, Tuebingen, Germany
  • Footnotes
    Commercial Relationships  C.M. Deuter, None; I. Koetter, None; T. Daikeler, None; I. Guenaydin, None; N. Stuebiger, None; K. Siepmann, None; M. Zierhut, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2674. doi:
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      C.M. Deuter, I. Koetter, T. Daikeler, I. Guenaydin, N. Stuebiger, K. Siepmann, M. Zierhut; Alfa–interferon treatment of refractory cystoid macular edema in uveitis . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2674.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Cystoid macular edema (CME) is the main cause for an irreversible loss of visual acuity in uveitis patients. Medical treatment of CME usually consists of systemic steroids, acetazolamide and immunosuppressive drugs. Unfortunately not in all patients CME responses to this therapeutic options or remains dry after withdrawal of this therapy. The purpose of our study was to investigate the therapeutical effect of interferon alfa–2a (IFN alfa–2a) on CME in endogenous uveitis. Methods: Seven patients (two male, five female; 13 eyes) with CME due to non–infectious intermediate or posterior uveitis received IFN alfa–2a at an initial dosage of 3 million IU or 6 million IU per day (depending on body weight). Characteristically the uveitis was completely quiet in all patients but CME was highly active and did respond neither to the combination of systemic steroids and acetazolamide (all patients) nor to at least one additional immunosuppressive drug (five patients). Control of treatment efficacy was performed by optical coherence tomography (OCT). Results: Only one patient, who developed antibodies against IFN alfa, did not respond. In all other six patients a response to IFN alfa–2a was seen within three days and CME completely resolved between two to four weeks in all 11 eyes of these patients. The mean retinal thickness of the fovea (normal value 150–180 µm) was 551 µm (SD 101 µm) before, 293 µm (SD 98 µm) three days, 165 µm (SD 40 µm) two weeks and 156 µm (SD 31 µm) four weeks after initiation of IFN alfa–2a treatment. Conclusions: To our knowledge this is the first description of treating refractory CME in endogenous uveitis with IFN alfa. This substance seems to have an extremely strong anti–exsudative effect which was not known before and which seems to be superior to conventional anti–inflammatory drugs like steroids or immunosuppressants. IFN alfa may become a new option for the therapy of CME in uveitis patients. However further studies in larger populations of uveitis patients are needed to investigate both mechanisms and duration of the anti–exsudative effect of IFN alfa in CME.

Keywords: inflammation • macula/fovea • drug toxicity/drug effects 
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