Desonide

Corticosteroids play a role in cellular signaling, immune function, inflammation, and protein regulation; however, the precise mechanism of action in the treatment of atopic dermatitis is unknown.

The contribution to efficacy by individual components of the vehicle has not been established.

In an HPA axis suppression trial, three of 75 (4%) pediatric subjects with mild to moderate atopic dermatitis covering at least 25% body surface area, who applied desonide foam twice daily, experienced reversible suppression of the adrenal glands (as indicated by a 30-minute post-stimulation cortisol level 18 mcg/dL) following 4 weeks of therapy.

The extent of percutaneous absorption of topical corticosteroids is determined by many factors, including the product formulation, the integrity of the epidermal barrier, and age. Occlusion, inflammation, and/or other disease processes in the skin may also increase percutaneous absorption. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. They are metabolized primarily in the liver and are then excreted by the kidneys. Some corticosteroids and their metabolites are also excreted in the bile.