Source: Web Search Revision Year: 2020 Publisher: Taro International Ltd., 14 Hakitor St., Haifa Bay 2624761, Israel
Like other topical corticosteroids, triamcinolone acetonide has antiinflammatory, antipruritic, and vasoconstrictive properties. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A 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 A.
The extent of absorption through the oral mucosa is determined by multiple factors including the vehicle, the integrity of the mucosal barrier, the duration of therapy, and the presence of inflammation and/or other disease processes. Once absorbed through the mucous membranes, the disposition of corticosteroids is similar to that of systemically administered corticosteroids. Corticosteroids are bound to the plasma proteins in varying degrees. Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys; some corticosteroids and their metabolites are also excreted into the bile.
A urinary free cortisol test and ACTH stimulation test may be helpful in evaluating HPA axis suppression.
Animal studies have not been performed to evaluate triamcinolone acetonide for potential to induce carcinogenesis, mutagenesis, or impairment of fertility.
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