For the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatose.
Like other topical corticosteroids, desonide has anti-inflammatory, antipruritic and vasoconstrictive properties. The drug binds to cytosolic glucocorticoid receptors. This complex migrates to the nucleus and binds to genetic elements on the DNA. This activates and represses various genes. However corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.
Topical corticosteroids can be absorbed from normal intact skin, inflammation and/or other disease processes in the skin may increase percutaneous absorption.
For the treatment of mild to moderate active Crohn's disease. Also for the treatment of asthma, non-infectious rhinitis (including hay fever and other allergies), and for treatment and prevention of nasal polyposis.
The exact mechanism of action of budesonide in the treatment of Crohn's disease is not fully understood. However, being a glucocorticosteroid, budesonide has a high local anti-inflammatory effect.
Single oral doses of 200 and 400 mg/kg were lethal in female and male mice, respectively. The signs of acute toxicity were decreased motor activity, piloerection and generalized edema.
Absorption is complete following oral administration.
2.0 and 3.6 hours
Budesonide is excreted in urine and feces in the form of metabolites.
* 3 L/kg [asthmatic children 4 to 6 years of age]
* 0.5 L/min [Athmatic children 4 to 6 years of age]