Betamethasone - Diprolene
Betatrex®, Beta-Val®, Celestone®, Celestone® IM, Diprolene®, Luxiq® Foam, Maxivate®, Uticort®, Valisone® | Adbeon® | Alphatrex® | Beta Derm™ | Betamethacot™ | Betanate™ | Betastat™ | Celestone® Soluspan® | Del-Beta® | Diprolene® AF | Diprosone® | Sone 4™
Classification:
Biologic Response Modifiers
Dermatological Agents
- Topical Antiinflammatory Agents
Hormones and Hormone Modifiers
Musculoskeletal Agents
Description: Betamethasone and its derivatives, betamethasone sodium phosphate and betamethasone acetate, are synthetic glucocorticoids used as antiinflammatory or immunosuppressive agents. The drug has little mineralocorticoid activity and should be used with a mineralocorticoid to manage adrenal insufficiency. Topical derivatives of the drug, including betamethasone benzoate, betamethasone dipropionate, and betamethasone valerate, are also available and are used for treating inflammation due to corticosteroid-responsive dermatoses. Topical betamethasone preparations are considered medium (betamethasone benzoate or valerate) or high-to-very high (betamethasone dipropionate) potency. Betamethasone was first approved by the FDA in 1961. A foam formulation of betamethasone valerate (Luxiq®) was approved February 28, 1999 for corticosteroid-responsive scalp dermatoses.
Mechanism of Action: 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: Betamethasone is administered orally, while betamethasone sodium phosphate can be administered by IM, IV, intra-articular, intrasynovial, intralesional, or soft-tissue injection. The corticosteroid suspension containing betamethasone sodium phosphate and betamethasone acetate may be administered by IM injection or locally by intrasynovial, intra-arterial, intralesional, or soft-tissue injection. Dosages of betamethasone sodium phosphate and betamethasone acetate are expressed in terms of betamethasone and betamethasone acetate, respectively. Topical preparations are administered in a thin film and rubbed gently into the affected area. Dosages of the topical preparations are expressed in terms of betamethasone.
Betamethasone is rapidly absorbed following an oral dose. Peak effects following oral and IV administration occur within 1-2 hours. The onset and duration of action of betamethasone suspensions are dependent on whether the drug is administered by intra-articular or IM injection and on the extent of the local blood supply. The drug is slowly absorbed into the systemic circulation following intra-articular administration.
The amount of betamethasone absorbed following topical application is dependent on the state of the skin at the application site. Absorption after topical application 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, and face. There may be a small extent of systemic absorption of the topical solutions, especially via the oral mucosa. Topical preparations distribute throughout the area of application, while systemic betamethasone is quickly distributed into the kidneys, intestines, skin, liver, and muscle. Betamethasone binds weakly to plasma proteins, and only the unbound portion of a circulating dose is active. Corticosteroids distribute into the breast milk and cross the placenta.
Topical preparations of betamethasone are metabolized in the skin, while systemic betamethasone is metabolized by the liver to inactive metabolites. These inactive metabolites, as well as a small portion of unchanged drug, are excreted in the urine. The biological half-life of betamethasone is 35-54 hours.
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[ Revised 11/7/2005 2:06:00 PM ]
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