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Ocul Immunol Inflamm. 1993;1(1):87-98. doi: 10.3109/09273949309086543.

Topical diclofenac sodium, dexamethasone and placebo compared in a model of immunogenic uveitis in rabbits.

Ocular immunology and inflammation

R Neumann, N S Jabbur, F Vickers, S C Foster

Affiliations

  1. Hilles Immunology Laboratory, Harvard Medical School, Massachusetts Eye & Ear Infirmary, Boston MA; Ciba Geigy, General Drugs Dept, Summit, NJ, 07901, USA, 908-277-7631, 908-277-3840.

PMID: 22827198 DOI: 10.3109/09273949309086543

Abstract

Unacceptable side effects involved in topical steroid usage for uveitis have prompted the search for alternative antiinflammatory drugs for the treatment of ocular inflammation. Cyclooxygenase inhibitors have been widely used for systemic inflammatory conditions over the last two decades and are therefore natural candidates to be studied for uveitis therapy. Previous studies of cyclooxygenase inhibitors in uveitis models yielded inconclusive and sometimes contradicting results. The authors compared the clinical effect of topical dexamethasone, diclofenac and placebo in an immunogenic uveitis model produced in ovalbumin immunized NZW rabbits challenged with ovalbumin in the vitreous. Nine clinical parameters of inflammation were compared employing a double blind placebo controlled protocol. Three groups of 16 eyes each, were assigned for each preparation and were followed for nine days with biomicroscopic examinations. Diclofenac was superior or equal to dexamethasone for iris hyperemia (p=0.059) and conjunctival injection (p=0.02), equal for corneal haziness and AC fibrin, yet inferior for corneal endothelial debris, iris fibrin and AC cells and flare (p<0.05). Placebo was inferior (p<0.05) to the other groups for the above mentioned parameters excluding fibrin precipitation on the iris that was greater in diclofenac treated eyes. While some clinical criteria of inflammation responded better to steroids than to diclofenac, the results of this study show that others responded better or equal to diclofenac. The authors hypothesize that although diclofenac reduces prostaglandin levels it may induce high levels of leukotrienes that maintain cellular exudation.

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