| Indication | For the treatment of primary or secondary adrenocortical insufficiency, such as congenital adrenal hyperplasia, thyroiditis. Also used to treat psoriatic arthritis, rheumatoid arthritis, ankylosing spondylitis, bursitis, acute gouty arthritis and epicondylitis. Also indicated for treatment of systemic lupus erythematosus, pemphigus and acute rhematic carditis. Can be used in the treatment of leukemias, lymphomas, thrombocytopenia purpura and autoimmune hemolytic anemia. Can be used to treat celiac disease, insulin resistance, ulcerative colitis and liver disorders. |
| Pharmacodynamics | Prednisolone is a synthetic glucocorticoid used as antiinflammatory or immunosuppressive agent. Prednisolone is indicated in the treatment of various conditions, including congenital adrenal hyperplasia, psoriatic arthritis, systemic lupus erythematosus, bullous dermatitis herpetiformis, seasonal or perennial allergic rhinitis, allergic corneal marginal ulcers, symptomatic sarcoidosis, idiopathic thrombocytopenic purpura in adults, leukemias and lymphomas in adults, and ulcerative colitis. Glucocorticoids are adrenocortical steroids and cause profound and varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli. |
| Mechanism of action | Glucocorticoids such as Prednisolone 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. Prednisolone 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. |
| Absorption | Readily absorbed by gastrointestinal tract, peak plasma concentration is reached 1-2 hours after administration. |
| Volume of distribution | Not Available |
| Protein binding | Very high (>90%) |
| Metabolism | Excreted in the urine as either free or glucoconjugate. |
| Route of elimination | Not Available |
| Half life | 2-3 hours |
| Clearance | Not Available |
| Toxicity | LD50=500 mg/kg (oral, rat), short-term side effects include high blood glucose levels and fluid retention. Long term side effects include Cushing's syndrome, weight gain, osteoporosis, glaucoma, type II diabetes and adrenal suppression. |