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Pharmacology: Pharmacodynamics: Clotrimazole alters cell membrane permeability by binding with phospholipids in the fungal cell membrane. Alteration of permeability causes the cell membrane unable to function as a selective barrier, and potassium and other cellular constituents are lost, thereby inhibiting growth of fungi.
Following topical application, corticosteroids produce anti-inflammatory, antipruritic, and vasoconstrictor actions. Corticosteroids decrease inflammation by stabilizing leukocyte lysosomal membranes, prevent release of destructive acid hydrolases from leukocytes; inhibiting macrophage accumulation in inflamed areas; reducing leukocyte adhesion to capillary endothelium; reducing capillary wall permeability and edema formation; decreasing complement components; antagonizing histamine activity and release of kinin from substrates; reducing fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.
Pharmacokinetics: Absorption: Very small amounts of clotrimazole appear to be absorbed systemically following topical application to the skin. Percutaneous absorption of betamethasone dipropionate may be increased when applied on the inflamed skin. Occlusive dressings substantially increase the percutaneous absorption of topical betamethasone dipropionate.
Distribution: Following application to the skin, highest concentrations of clotrimazole are present in the stratum corneum; lower drug concentrations occur in the stratum spinosum and the papillary and reticular dermis. Betamethasone dipropionate is bound to plasma proteins.
Metabolism: Clotrimazole is metabolised in the liver to inactive compounds. Betamethasone dipropionate is also metabolised in the liver.
Elimination: Clotrimazole is excreted in the faeces and urine. Corticosteroids are excreted by the kidneys. Some topical corticosteroids and their metabolites are excreted in bile.
