Clinical outcome and cyclo‐oxygenase‐2 expression in five dogs with solar dermatitis/actinic keratosis treated with firocoxib. Issue 6 (15th October 2013)

• Record Type: Journal Article
• Authors: Albanese, Francesco; Abramo, Francesca; Caporali, Chiara; Vichi, Gaia; Millanta, Francesca
• Is Part Of: Veterinary dermatology. Volume 24:Issue 6(2013:Dec.)
• Page Start: 606
• Page End: e147
• Publication Date: 2013-10-15
• Subjects: Veterinary dermatology -- Periodicals; Pet medicine -- Periodicals; 636.08965
• DOI: 10.1111/vde.12082
• Languages: English
• ISSNs: 0959-4493

Abstract

<abstract abstract-type="main" id="vde12082-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="vde12082-sec-0001" sec-type="section"> <title>Background</title> <p>The conversion of arachidonic acid into prostaglandin is catalysed by the cyclo‐oxygenases (COX‐1/COX‐2). Several studies indicate that COX‐2 is overexpressed in actinic keratosis in humans and dogs. Firocoxib is a COX‐2‐selective inhibitor that blocks the biochemical activity of COX‐2.</p> </sec> <sec id="vde12082-sec-0002" sec-type="section"> <title>Hypothesis/Objectives</title> <p>To evaluate the efficacy of firocoxib (5 mg/kg orally once daily) for the treatment of dogs with solar dermatitis/actinic keratosis.</p> </sec> <sec id="vde12082-sec-0003" sec-type="section"> <title>Methods</title> <p>Firocoxib 5 mg/kg was given orally once daily for 180 days to five dogs with clinical signs and histopathological lesions consistent with solar dermatitis/actinic keratosis. On days 0, 50 and 180, the severity of erythema, skin shine, induration and the number of comedones were evaluated by a clinical scoring system. On the same days, samples were collected for histopathology from 'target lesions' and COX‐2 expression was evaluated by immunohistochemistry.</p> </sec> <sec id="vde12082-sec-0004" sec-type="section"> <title>Results</title> <p>The clinical follow‐up showed that four of five dogs improved with the treatment; improvement in terms of histological findings was correlated with the regularization of the epidermal proliferation rather than the recovery of dermal changes.</p> </sec> <sec id="vde12082-sec-0005" sec-type="section"> <title>Conclusions and clinical importance</title> <p>A role for COX‐2 might thus be hypothesized in the pathogenesis of canine solar dermatitis.</p> </sec> </abstract>