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indicationFor the treatment of all conditions in which corticosteroid therapy is indicated except adrenal-deficiency states for which its lack of sodium-retaining properties makes it less suitable than hydrocortisone with supplementary fludrocortisone.
pharmacologyParamethasone is a glucocorticoid with the general properties of corticosteroids. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated.
mechanism of actionGlucocorticoids such as paramethasone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Paramethasone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.
toxicitySide effects include inhibition of bone formation, suppression of calcium absorption delayed wound healing, immune suppression, and hyperglycemia.
route of eliminationCorticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.
drug interactionsAcetylsalicylic acid: The corticosteroid, paramethasone, may decrease the effect of the salicylate, acetylsalicylic acid.
Fosphenytoin: The enzyme inducer, fosphenytoin, may decrease the effect of the corticosteroid, paramethasone.
Midodrine: Increased arterial pressure
Phenobarbital: The barbiturate, phenobarbital, may decrease the effect of the corticosteroid, paramethasone.
Phenytoin: The enzyme inducer, phenytoin, may decrease the effect of the corticosteroid, paramethasone.
Primidone: The barbiturate, primidone, may decrease the effect of the corticosteroid, paramethasone.
Pyridostigmine: The corticosteroid, paramethasone, may decrease the effect of the anticholinesterase, pyridostigmine.
Rifampin: The enzyme inducer, rifampin, may decrease the effect of the corticosteroid, paramethasone.