Corticosteroids mechanism of action inflammation

Desonate was approved by the FDA following two major clinical trials in 2006. Each randomized, double-blind, placebo-controlled study enrolled 582 pediatric patients (between the ages of 3 months and 18 years). [9] The patient was topically administered the drug or placebo two times a day for four weeks. Using the Investigator’s Global Severity Score (IGSS), the treatment was considered successful if at Week 4 there was at least a two (2) point decrease from the patient’s baseline IGSS. In clinical trial 1, 44% of patients succeeded successful treatment of Desonate versus 14% treated with the placebo. In clinical trial 2, 28% of patients succeeded successful treatment of Desonate versus 6% treated with the placebo.

Decreases in bone mineral density (BMD) have been observed with long-term administration of products containing inhaled corticosteroids, including flunisolide. The clinical significance of small changes in BMD with regard to long-term outcomes is unknown. Monitor patients with major risk factors for decreased bone mineral content, such as prolonged immobilization, family history of osteoporosis , postmenopausal status, tobacco use, advanced age, poor nutrition, or chronic use of drugs that can reduce bone mass (., anticonvulsants and corticosteroids) and treat with established standards of care.

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

Corticosteroids mechanism of action inflammation

corticosteroids mechanism of action inflammation

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