Desonide is a topical, low-potency synthetic corticosteroid with similar efficacy to hydrocortisone. It is used to relieve the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Low-potency topical corticosteroids have modest antiinflammatory properties and are usually effective in treating acute inflammatory skin conditions. Since the stratum corneum is thin on the face and intertriginous areas, low-potency topical corticosteroids are preferred. Low potency topical corticosteroids are also considered the safest for chronic use and are preferred in elderly or pediatric patients. Commercial products include cream, lotion, foam, gel, and ointment formulations. Desonide was initially FDA-approved in 1972.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Topical Administration
-For topical dermatologic use only. Not for ophthalmic, oral, or intravaginal use.
-Do not use with occlusive dressings.
Cream/Ointment/Lotion Formulations:
Cream or ointment:
-Apply a thin film to the affected areas.
Lotion:
-Shake well before using.
-Apply to the affected areas and massage lightly until the lotion disappears.
-For the most effective and economical use, hold the nozzle of the bottle very close to the affected areas and gently squeeze.
Other Topical Formulations:
Foam:
-Shake well before using.
-Turn the can upside down to dispense.
-For application to the face, dispense into the hands and gently massage into the affected areas until the foam disappears. For areas other than the face, the foam may be dispensed directly onto the affected area.
-Rub in gently until the foam disappears.
-Use only enough medication to cover the affected areas.
-This product is flammable. Keep away from fire, flame, and smoking during and immediately after use.
Gel:
-Apply a thin film to the affected areas and rub in gently.
The following adverse reactions (listed in decreasing order of occurrence) are reported with topical corticosteroids such as desonide and may occur more often when used with an occlusive dressing: skin irritation (including burning, <= 3%), pruritus (< 2%), xerosis (dry skin, < 2%), folliculitis, hypertrichosis, acneiform rash/eruptions, skin hypopigmentation, perioral dermatitis, maceration of the skin, secondary infection, skin atrophy, striae, and miliaria. Erythema (< 2%), telangiectasia, purpura, and maculopapular rash may also occur. Although skin atrophy usually occurs after prolonged use of topical corticosteroids, this effect may occur even with short-term use on intertriginous or flexor areas, or on the face. If irritation develops, discontinue topical corticosteroids and institute appropriate therapy. The anti-inflammatory activity of topical corticosteroids may also mask manifestations of infection. In the presence of dermatological infections, institute the use of an appropriate antifungal or antibacterial agent. If a favorable response does not promptly occur, discontinue the corticosteroid until the infection has been adequately controlled.
Signs and symptoms of corticosteroid withdrawal may occur with desonide dose reduction or discontinuation, and supplemental systemic corticosteroids may be needed. For example, disease flare may occur and HPA axis suppression may be present.
Systemic absorption of topical corticosteroids can produce reversible hypothalamic-pituitary-adrenal (HPA) suppression with possible adrenocortical insufficiency after withdrawal of treatment. In some patients, systemic absorption can produce manifestations of Cushing's syndrome, hypertension, hyperglycemia, and glycosuria. Percutaneous absorption of desonide is dependent on many factors including the vehicle, the integrity of the epidermal barrier, duration of use, and use of an occlusive dressing. Children may be more susceptible to systemic toxicity from equivalent doses due to their larger skin surface to body mass ratios. Cushing's syndrome, HPA axis suppression, and increased intracranial pressure have been reported in children receiving topical corticosteroids. Manifestations of adrenocortical insufficiency in children include linear growth inhibition, delayed weight gain, low plasma cortisol concentrations, and absence of response to ACTH stimulation. Clinical signs of increased intracranial pressure include bulging fontanelle, headache, and bilateral papilledema (i.e., pseudotumor cerebri). Patients applying desonide to a large surface area or to areas under occlusion should be evaluated periodically for evidence of HPA axis suppression (using the ACTH stimulation test, A.M. plasma cortisol test, and urinary free cortisol test). To minimize risk of HPA axis suppression, discontinue therapy when control is achieved. If no improvement is seen within 2 weeks, reassessment of diagnosis may be necessary. If HPA axis suppression is noted, an attempt should be made to withdraw the drug, reduce the frequency of application, or substitute a less potent corticosteroid. Recovery of HPA axis function is generally prompt and complete upon discontinuation of the topical corticosteroid.
Topical corticosteroids have been associated with postmarketing cases of blurred vision, cataracts, glaucoma, ocular hypertension, and central serious chorioretinopathy. Such adverse effects, if they occur, could lead to blindness. Cataracts are usually associated with large doses or therapy longer than 6 months. Any patient who develops visual impairment during topical corticosteroid therapy should be referred to an ophthalmologist for evaluation. Low potency corticosteroids (e.g., hydrocortisone, dexamethasone) have been reported to be safer for short-term use around the eye area.
In general, excessive use of corticosteroids can lead to impaired wound healing. Since desonide is a topical corticosteroid, it should not be applied directly or near healing wounds. A propensity for skin ulcer may develop in patients with markedly impaired circulation who use topical corticosteroids.
Tolerance may occur with the prolonged use of topical corticosteroids, such as desonide. Tolerance is usually described as a decreased acute vasoconstrictive response to the agent after a period of days to weeks. This may explain the dramatic responses noted initially by patients early in topical corticosteroid treatment and an apparent diminished response with time. Tolerance is reversible and may be attenuated by interrupted or cyclic schedules of application (e.g., desonide is given for 2-3 weeks, followed by a 1-week intermission).
Allergic contact dermatitis with corticosteroids such as desonide is usually diagnosed by observing a failure to heal. Appropriate diagnostic patch testing may help with the diagnosis.
Although true corticosteroid hypersensitivity is rare, patients who have demonstrated a prior hypersensitivity reaction to desonide should not receive any form of desonide. It is possible, though also rare, that such patients will display cross-hypersensitivity to other corticosteroids. It is advisable that patients who have a hypersensitivity reaction to any corticosteroid undergo skin testing, which, although not a conclusive predictor, may help to determine if hypersensitivity to another corticosteroid exists. Such patients should be carefully monitored during and following the administration of any corticosteroid.
Desonide is contraindicated in any patient with a history of desonide hypersensitivity or hypersensitivity to any ingredients in the preparation. In addition, desonide should be used with caution in patients with a history of corticosteroid hypersensitivity.
Systemic absorption of topical corticosteroids has produced reversible hypothalamic-pituitary-adrenal (HPA) suppression and/or manifestations of Cushing's syndrome in some patients. Conditions which increase systemic absorption include application of more potent corticosteroids, use over large surface areas, prolonged use, use in areas where the epidermal barrier is disrupted (i.e., skin abrasion), and the use of occlusive dressings. Desonide preparations should not be used with occlusive dressings. Patients receiving large doses of a potent topical corticosteroid applied to a large surface area or under an occlusive dressing should be evaluated periodically for evidence of HPA axis suppression and manifestations Cushing's syndrome. If these effects are noted, an attempt should be made to withdraw the drug, to reduce the frequency of application, or to substitute a less potent corticosteroid.
Topical corticosteroids should be used with caution in patients with diabetes mellitus. Exacerbation of diabetes may occur with systemic absorption of the topical corticosteroid. Use of topical corticosteroids may further delay healing of skin ulcers in diabetic patients.
The safety and efficacy of desonide cream, lotion, and ointment in neonates, infants, children, and adolescents have not been established. The safety and efficacy of desonide foam and gel have not been established in neonates and infants less than 3 months of age. Pediatric patients may absorb proportionally larger amounts of topical corticosteroids and therefore are more susceptible to developing systemic toxicity. Hypothalamic-pituitary-adrenal (HPA) axis suppression, Cushing's syndrome, and increased intracranial pressure have been reported in pediatric patients receiving topical corticosteroids. Chronic corticosteroid therapy in pediatric patients may interfere with growth and development, resulting in growth inhibition. Administration of topical corticosteroids should be limited to the least amount compatible with an effective therapeutic regimen. If children are being treated in the diaper area, tight-fitting diapers or plastic pants should be avoided as these garments may act as an occlusive dressing and increase systemic absorption of the drug.
There are no adequate and well-controlled studies of topical application of desonide during pregnancy. Topical corticosteroids, including desonide, should not be used in large amounts, on large areas, or for prolonged periods of time in pregnant women. Guidelines recommend mild to moderate potency agents, such as desonide, over potent corticosteroids, which should be used in short durations. Fetal growth restriction and a significantly increased risk of low birthweight has been reported with use of potent or very potent topical corticosteroids during the third trimester, particularly when using more than 300 grams. Corticosteroids are generally teratogenic in laboratory animals when administered systemically at relatively low dosage levels. The more potent corticosteroids have been shown to be teratogenic after dermal application in laboratory animals.
According to the manufacturer, it is not known whether topical administration of desonide could result in sufficient systemic absorption to produce detectable quantities in breast milk. However, most dermatologists stress that topical corticosteroids can be safely used during lactation and breast-feeding. If applied topically, care should be used to ensure the infant will not come into direct contact with the area of application, such as the breast. Increased blood pressure has been reported in an infant whose mother applied a high potency topical corticosteroid ointment directly to the nipples. Consider the benefits of breast-feeding, the risk of potential infant drug exposure, and the risk of an untreated or inadequately treated condition. If a breast-feeding infant experiences an adverse effect related to a maternally ingested drug, healthcare providers are encouraged to report the adverse effect to the FDA.
The normal inflammatory response to local infections can be masked by desonide. Application of topical corticosteroids to areas of infection, including tuberculosis of the skin, dermatologic fungal infection, and cutaneous or systemic viral infection (e.g., herpes infection, measles, varicella), should be initiated or continued only if the appropriate antiinfective treatment is instituted. If the infection does not respond to the antimicrobial therapy, the concurrent use of the topical corticosteroid should be discontinued until the infection is controlled. Topical corticosteroids may delay the healing of non-infected wounds, such as venous stasis ulcers. Topical corticosteroids should not be used to treat perioral dermatitis, acne vulgaris, or acne rosacea as they may aggravate these conditions.
Desonide is not indicated for ophthalmic administration. If unintended ocular exposure occurs, the patient should rinse the exposed area well with water. Visual impairment, glaucoma, and posterior subcapsular cataracts have been reported with other topical corticosteroids. Advise patients to report any visual symptoms and consider referral to an ophthalmologist for evaluation.
Topical corticosteroids should be used for brief periods, or under close medical supervision in patients with evidence of pre-existing skin atrophy. Geriatric patients may be more likely to have preexisting skin atrophy secondary to aging. Purpura and skin lacerations that may raise the skin and subcutaneous tissue from deep fascia may be more likely to occur with the use of topical corticosteroids in geriatric patients.
For the treatment of corticosteroid-responsive dermatoses, including atopic dermatitis, localized vitiligo, eczema, lichen planus, localized bullous pemphigoid, phimosis, and psoriasis:
-for the general treatment of corticosteroid-responsive dermatoses:
Topical dosage (cream, lotion, or ointment):
Adults: Apply a thin layer topically to the affected skin area(s) 2 to 3 times daily. If no improvement is seen within 2 weeks, reassess diagnosis.
-for the treatment of atopic dermatitis:
Topical dosage (cream, lotion, or ointment):
Adults: Apply a thin layer topically to the affected skin area(s) 2 times daily until symptoms resolve. If no improvement is seen within 2 weeks, reassess diagnosis. Proactive, intermittent application of topical corticosteroids 1 to 2 times weekly to areas that commonly flare is recommended to help prevent relapses.
Children* and Adolescents*: Apply a thin layer topically to the affected skin area(s) 2 times daily until symptoms resolve. If no improvement is seen within 2 weeks, reassess diagnosis. Proactive, intermittent application of topical corticosteroids 1 to 2 times weekly to areas that commonly flare is recommended to help prevent relapses.
Topical dosage (foam or gel):
Adults: Apply a thin layer topically to the affected skin area(s) 2 times daily until symptoms resolve. If no improvement is seen within 4 weeks, reassess diagnosis. Proactive, intermittent application of topical corticosteroids 1 to 2 times weekly to areas that commonly flare is recommended to help prevent relapses.
Infants, Children, and Adolescents 3 months to 17 years: Apply a thin layer topically to the affected skin area(s) 2 times daily until symptoms resolve. If no improvement is seen within 4 weeks, reassess diagnosis. Proactive, intermittent application of topical corticosteroids 1 to 2 times weekly to areas that commonly flare is recommended to help prevent relapses.
-for the treatment of psoriasis:
Topical dosage (cream, lotion, or ointment):
Adults: Apply as a thin layer topically to the affected skin area(s) 2 to 3 times daily. If no improvement is seen within 2 weeks, reassess diagnosis. The duration of the therapy depends on factors such as the topical corticosteroid potency, disease severity and anatomic location, and age. After improvement, may consider transitioning to lower-potency corticosteroid, using intermittent therapy, and combining treatment with noncorticosteroidal agents. Taper by reducing use to every other day, then twice weekly, then discontinue if adequate control is maintained. Guidelines recommend class 1 to 5 topical corticosteroids for up to 4 weeks for plaque psoriasis not involving intertriginous areas and class 1 to 7 topical corticosteroids for a minimum of up to 4 weeks for scalp psoriasis. Use of topical corticosteroids for more than 12 weeks may be considered under careful supervision.
Maximum Dosage Limits:
While in general corticosteroid dosage must be individualized and is highly variable depending on the nature and severity of the disease and on patient age and response, the area of skin where desonide is applied should be limited.
-Adults
Cream or ointment 4 applications/day topically; Lotion 3 applications/day topically; Foam or gel 2 applications/day topically.
-Elderly
Cream or ointment 4 applications/day topically; Lotion 3 applications/day topically; Foam or gel 2 applications/day topically.
-Adolescents
Cream or ointment 4 applications/day topically; Lotion 3 applications/day topically; Foam or gel 2 applications/day topically.
-Children
Foam or gel 2 applications/day topically.
-Infants
>= 3 months: Foam or gel 2 applications/day topically.
< 3 months: Safety and efficacy have not been established.
Patients with Hepatic Impairment Dosing
Specific guidelines for dosage adjustments in hepatic impairment are not available; it appears that no dosage adjustments are needed.
Patients with Renal Impairment Dosing
Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.
*non-FDA-approved indication
Metyrapone: (Major) Medications which affect pituitary or adrenocortical function, including all corticosteroid therapy, should be discontinued prior to and during testing with metyrapone. Patients taking inadvertent doses of corticosteroids on the test day may exhibit abnormally high basal plasma cortisol levels and a decreased response to the test. Although systemic absorption of topical corticosteroids is minimal, temporary discontinuation of these products should be considered if possible to reduce the potential for interference with the test results.
Topical corticosteroids exhibit anti-inflammatory, antipruritic, and vasoconstrictive properties. At the cellular level, corticosteroids induce peptides called lipocortins. Lipocortins antagonize phospholipase A2, an enzyme which causes the breakdown of leukocyte lysosomal membranes to release arachidonic acid. This action decreases the subsequent formation and release of endogenous inflammatory mediators including prostaglandins, kinins, histamine, liposomal enzymes and the complement system. Early anti-inflammatory effects of topical corticosteroids include the inhibition of macrophage and leukocyte movement and activity in the inflamed area by reversing vascular dilation and permeability. Later inflammatory processes such as capillary production, collagen deposition, keloid (scar) formation also are inhibited by corticosteroids. Clinically, these actions correspond to decreased edema, erythema, pruritus, plaque formation and scaling of the affected skin.
Pharmacokinetics:
Desonide is administered topically to the skin as a cream, lotion, foam, or ointment. Circulating levels of desonide are below the level of detection. Once in the systemic circulation, desonide is metabolized in the liver. Excretion is primarily via the urine.
-Route-Specific Pharmacokinetics
Topical Route
The extent of percutaneous absorption of the topical corticosteroids is dependent on many factors, including the pharmaceutical vehicle and the integrity of the epidermis. Absorption after topical application of desonide is increased in areas that have skin damage, inflammation, or occlusion, or in areas where the stratum corneum is thin such as the eyelids, genitalia, axillae, and face. The use of occlusive dressings with the application of desonide enhances penetration into the skin, and may increase the chance of systemic absorption. Ointments have a hydrating effect, are lipophilic, and enhance the penetration of desonide into the skin. Because desonide contains a substituted 17-hydroxyl group, it is not metabolized in the skin. Repeated application of desonide results in a cumulative depot effect in the skin, which may lead to a prolonged duration of action, increased adverse effects, and increased systemic absorption.