Desoximetasone is a topical medium- to high-potency synthetic fluorinated corticosteroid. It is used for the relief of moderate to severe inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses and for psoriasis. Desoximetasone has anti-inflammatory, antipruritic, and vasoconstrictive properties. Medium- to high-potency topical corticosteroids can be useful for treatment of areas with thicker skin such as the palms and soles. The FDA first approved desoximetasone for topical use in 1977.
General Administration Information
For storage information, see the specific product information within the How Supplied section.
Route-Specific Administration
Topical Administration
-Desoximetasone is for topical/external use. Avoid direct contact to the eyes or mucous membranes.
-Apply a thin film and rub gently. Washing or soaking the area before application may increase drug penetration.
The following adverse reactions (listed in decreasing order of occurrence) are reported with topical corticosteroids such as desoximetasone and may occur more often when used with an occlusive dressing: skin irritation (including burning, 0.3-0.8%), pruritus (0.8%), xerosis (dry skin), folliculitis (0.8%), hypertrichosis, acneiform rash/eruptions, skin hypopigmentation, perioral dermatitis, maceration of the skin, secondary infection, skin atrophy, striae, and miliaria. Erythema (0.8%), 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 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 desoximetasone 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 stopping treatment. In some patients, systemic absorption can produce manifestations of Cushing's syndrome, hypertension, hyperglycemia, and glycosuria. Percutaneous absorption of desoximetasone 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. HPA suppression and increased intracranial pressure have been reported in children receiving topical corticosteroids. In a clinical study, the proportion of subjects demonstrating HPA axis suppression with desoximetasone topical spray was 35% in Cohort 1 (12 years to less than 18 years of age) and 43.3% in Cohort 2 (6 years to less than 12 years of age). The trial enrollment in the youngest cohort (2 years to less than 6 years of age) was discontinued early due to high incidence of HPA axis suppression observed in the 2 oldest cohorts (6 years to less than 18 years of age). Overall, the HPA axis suppression rate was 36% in pediatric patients aged 2 years to less than 18 years. Manifestations of adrenocortical insufficiency in children include linear growth inhibition, delayed weight gain, low plasma cortisol concentrations, increased intracranial pressure, and absence of response to ACTH stimulation. Clinical signs of increased intracranial pressure include bulging fontanelles, headache, and bilateral papilledema (i.e., pseudotumor cerebri). Patients applying desoximetasone 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 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.
Case reports describe visual impairment in patients using topical corticosteroids for eczema of the face. The visual impairment was secondary to the onset of ocular hypertension. Such adverse effects, if they occur, could lead to blindness. Use of topical corticosteroids, including desoximetasone, may increase the risk of posterior subcapsular cataracts and glaucoma. Preexisting glaucoma may be aggravated if desoximetasone is used in the periorbital area. Cataracts have been reported, usually with periorbital application of potent or very potent topical steroids for months to years or application of potent steroids over large surfaces areas of non-periorbital skin for prolonged periods of time. Desoximetasone is generally not recommended for application to the eye area. Any patient who develops changes in vision while applying desoximetasone topically should be evaluated for ocular hypertension. 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 desoximetasone 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 desoximetasone. 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., desoximetasone is given for 2-3 weeks, followed by a 1-week intermission).
Allergic contact dermatitis with corticosteroids such as desoximetasone is usually diagnosed by observing a failure to heal. Appropriate diagnostic patch testing may help with the diagnosis.
Desoximetasone is contraindicated in any patient with a history of hypersensitivity to desoximetasone or any ingredients in the preparation.
In general, desoximetasone preparations should not be applied to the face, groin, or axillae. Care should be taken to avoid use around the eyes; ophthalmic administration should be avoided. Desoximetasone may cause eye irritation. Use of topical corticosteroids, including desoximetasone, may increase the risk of posterior subcapsular cataracts and glaucoma. Visual impairment, ocular hypertension and worsened cataracts have been reported with ocular exposure to other high potency topical corticosteroids. Preexisting glaucoma may be aggravated if desoximetasone is used in the periorbital area. Advise patients to report any visual symptoms and consider referral to an ophthalmologist for evaluation.
Systemic absorption of topical corticosteroids (such as desoximetasone) has produced reversible hypothalamic-pituitary-adrenal (HPA) suppression, manifestations of Cushing's syndrome, hyperglycemia, and glucosuria in some patients. Conditions that increase systemic absorption include 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. Advise patients to use only as directed and to avoid occlusive dressings unless otherwise directed; use of this medication under tight fitting diapers or plastic pants may constitute occlusive dressings. Patients receiving large doses of a topical corticosteroid applied to a large surface area or under an occlusive dressing should be evaluated periodically for evidence of HPA axis suppression. If HPA axis suppression is noted, an attempt should be made to withdraw the drug, to reduce the frequency of application, or to substitute a less potent corticosteroid.
The safety and efficacy of desoximetasone 0.25% ointment in neonates, infants, children less than 10 years of age have not been established. The safety and efficacy of desoximetasone topical spray have not been established in pediatric patients for the treatment of plaque psoriasis. Desoximetasone topical spray is not recommended in patients less than 18 years of age due to high incidence of HPA axis suppression. Chronic corticosteroid therapy in children may interfere with growth and development, resulting in growth inhibition. Given a larger body surface area to weight ratio, children and infants may absorb proportionally larger amounts of topical corticosteroids and therefore are more susceptible to developing systemic toxicity. Conditions which increase systemic absorption include the application of the more potent steroids, use over large surface areas, prolonged use, and the addition of occlusive dressings, which may include tight-fitting diapers or plastic pants. Limit administration to the least amount compatible with an effective therapeutic regimen. Cushing's syndrome, adrenal suppression, and increased intracranial pressure have been reported in children receiving topical corticosteroids. Manifestations of adrenal suppression in pediatric patients include linear growth retardation, delayed weight gain, low plasma cortisol levels, and absence of response to ACTH stimulation. Manifestations of intracranial hypertension include bulging fontanelles, headaches, and bilateral papilledema.
There are no available data on desoximetasone use during pregnancy to evaluate for a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. Topical corticosteroids, including desoximetasone, should not be used in large amounts, on large areas, or for prolonged periods of time during pregnancy. Guidelines recommend mild to moderate potency agents 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. Desoximetasone has been shown to be teratogenic and embryotoxic in mice, rats, and rabbits when given by subcutaneous or dermal routes of administration in doses 3 to 30 times the human dose of desoximetasone 0.25% cream, spray, or ointment and or in doses 15 to 150 times the 0.05% cream or gel. There are no adequate and well-controlled studies of teratogenic effects from topical application of desoximetasone in pregnant women.
There is no information on the presence of topically administered desoximetasone in human milk, the effects on the breastfed infant, or the effects on milk production. It is not known whether topical administration of desoximetasone could result in sufficient systemic absorption to produce detectable quantities in breast milk to cause issues during breast-feeding. However, most dermatologists stress that topical corticosteroids can be safely used during lactation. The use of low to mid-potency topical corticosteroids is recommended in this patient population. 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. Advise patients to avoid application of the topical agent directly to the nipple and areola to prevent direct infant exposure, particularly when using high potency corticosteroids. 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.
Topical corticosteroids (such as desoximetasone) 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. Use of lower potency topical corticosteroids also may be necessary in some patients.
The normal inflammatory response to local infections can be masked by desoximetasone. 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. Potent topical corticosteroids should not be used to treat acne vulgaris, acne rosacea, or perioral dermatitis. Desoximetasone may aggravate these conditions.
Topical corticosteroids (such as desoximetasone) 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.
For the relief of moderate-to-severe inflammatory manifestations, including pruritus, of corticosteroid responsive dermatoses including alopecia areata, atopic dermatitis, contact dermatitis, dermatitis, Rhus dermatitis due to plants like poison ivy, discoid lupus erythematosus, eczema, exfoliative dermatitis, granuloma annulare, keloids, lichen planus, lichen simplex, lichen striatus, necrobiosis lipoidica diabeticorum, pemphigoid, pemphigus, pityriasis rosea, psoriasis, sarcoidosis, seborrheic dermatitis, urticaria, and xerosis:
-for the general treatment of mild to moderate corticosteroid-responsive dermatoses:
Topical dosage (0.25% ointment):
Adults: Apply sparingly to the affected skin area(s) 2 times daily.
Children and Adolescents 10 to 17 years: Apply sparingly to the affected skin area(s) 2 times daily.
Topical dosage (cream, gel, or 0.05% ointment):
Adults: Apply sparingly to the affected skin area(s) 2 times daily.
Children and Adolescents: Apply sparingly to the affected skin area(s) 2 times daily.
-for the treatment of plaque psoriasis:
Topical dosage (0.25% ointment):
Adults: Apply sparingly to the affected skin area(s) 2 times daily. 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.
Children and Adolescents 10 to 17 years: Apply sparingly to the affected skin area(s) 2 times daily. Guidelines recommend topical corticosteroids as monotherapy for short-term treatment of localized psoriasis.
Topical dosage (cream, gel, or 0.05% ointment):
Adults: Apply sparingly to the affected skin area(s) 2 times daily. 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.
Children and Adolescents: Apply sparingly to the affected skin area(s) 2 times daily. Guidelines recommend topical corticosteroids as monotherapy for short-term treatment of localized psoriasis.
Topical dosage (spray):
Adults: Apply sparingly to the affected skin area(s) 2 times daily. Discontinue therapy when control is achieved. Treatment beyond 4 weeks is not recommended. 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:
-Adults
Maximum dosage information not available.
-Elderly
Maximum dosage information not available.
-Adolescents
Maximum dosage information not available.
-Children
>= 10 years: Maximum dosage information not available.
< 10 years: Safety and efficacy have not been established.
-Infants
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.
Desoximetasone is administered topically as a cream, ointment, and gel. Desoximetasone is metabolized in the liver and undergoes conjugation to form the glucuronide and sulfate ester. Desoximetasone and its metabolites are primarily excreted by the kidneys and to a lesser extent by the bile. The half-life of desoximetasone is about 15-17 hours.
-Route-Specific Pharmacokinetics
Topical Route
Desoximetasone is absorbed from normal intact skin. Absorption of desoximetasone is dependent on many factors, including the vehicle, the integrity of the epidermis, and the use of occlusive dressings. Percutaneous absorption is increased by the use of occlusive dressings, which may be useful for treating resistant dermatoses. Absorption of topical corticosteroids is increased in areas that have skin damage, inflammation, or in areas where the stratum corneum is thin such as the eyelids, genitalia, axillae, and face. Pharmacokinetic studies following application of desoximetasone cream 0.25% show no detectable level (limit of sensitivity 0.0005 mcg/mL) in the blood when the cream is applied topically on the back followed by occlusion for 24 hours. No detectable levels or very low levels (0.004-0.006 mcg/mL) are noted in subjects following application of desoximetasone ointment 0.25% on the back followed by occlusion for 24 hours. The extent of systemic ointment absorption is 7% of the total applied dosage based on radioactivity recovered from urine and feces.