Like other topical corticosteroids, desonide has anti-inflammatory, antipruritic, and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called, lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.

Desonide Ointment, 0.05% is a low potency corticosteroid indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatoses.

Desonide Ointment, 0.05% should be applied to the affected area as a thin film from two to four times daily depending on the severity of the condition.

In controlled clinical trials, the total incidence of adverse reactions associated with the use of Desonide Ointment, 0.05% was approximately 6%. These adverse reactions were erythema, induration, pruritus, irritation, oiliness, and peripheral edema.

Desonide Ointment, 0.05% is contraindicated in those patients with a history of hypersensitivity to any of the components of the preparation.

Systemic absorption of topical corticosteroids can produce reversible hypothalamic-pituitary-adrenal (HPA) axis suppression with the potential for glucocorticosteroid insufficiency after withdrawal of treatment. Manifestations of Cushing's syndrome, hyperglycemia, and glucosuria can also be produced in some patients by systemic absorption of topical corticosteroids while on treatment. (See Full Prescribing Information.)