Amcinonide topical

Corticosteroid-responsive dermatoses

Topical/Cutaneous Corticosteroid-responsive dermatoses Adult: As 0.1% cream/oint/lotion: Apply sparingly in a thin film to affected area bid or tid, depending on the severity of the condition.

Corticosteroid-Responsive Dermatoses Apply sparingly to affected area(s) q12hr Limit to minimum amount necessary for therapeutic efficacy Avoid face

Underlying infection Hypersensitivity Use on groin, face, or axila Ophthalmic use

Chronic therapy may interfere with growth and development in children Use med to very high potency for <2 wk to reduce local and systemic side effects Use low potency for chronic therapy Allergic contact dermatitis may occur Should not use occlusive dressings in presence of infection or weeping lesions Adrenal suppression may occur in younger patients or patients receiving high doses for prolonged periods Development of Kaposi's sarcoma with prolonged use reported (discontinue therapy if it occurs) Avoid medium to very high potency on face, folds, groin because can increase steroid absorption Use lower potency for peds (ie, increase BSA/kg, therefore increase systemic absorption) Monitoring Parameters Perform urinary free cortisol and ACTH stimulation tests to monitor for hypothalamic-pituitary-adrenal (HPA) axis suppression if drug is applied to a large surface area or under an occlusive dressing.

C Pregnancy Category: C Lactation: It is not known whether topical administration of topical corticosteroids could result in sufficient systemic absorption to produce detectable quantities in human milk. Use with caution.

Frequency Not Defined Skin atrophy Striae Burning Dryness Irritation Itching Hypertrichosis Acneform lesions Secondary infection Pigmentation changes HPA suppression (with higher potency used >2 wk)

Amcinonide, a synthetic fluorinated glucocorticoid, has anti-inflammatory, antipruritic, and vasoconstrictive actions. It induces phospholipase A2 inhibitory proteins (lipocortins) and sequentially inhibits the release of arachidonic acid, thereby depressing the formation, release, and activity of endogenous chemical mediators of inflammation.