"Hydrocortisone"@en . . . . "Cortisol"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . "Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-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 the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding."@en . " "@en . "Take with food to reduce irritation. Calcium, phosphorous, potassium, Vitamin A, C, D and zinc needs increased with long term use."@en . . "11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease."@en . . . . . . . "Hydrocortisone"@en . . . . . . "Hidrocortisona"@en . . "approved"@en . . . . . . . . . . . . . . . . . . . . . . "17-Hydroxycorticosterone"@en . . . . . . . . . . . "95%"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "6-8 hours"@en . . . . . . . . . "Kendall's compound F"@en . "# de Weerth C, Zijl RH, Buitelaar JK: Development of cortisol circadian rhythm in infancy. Early Hum Dev. 2003 Aug;73(1-2):39-52. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/12932892 # Palacios R, Sugawara I: Hydrocortisone abrogates proliferation of T cells in autologous mixed lymphocyte reaction by rendering the interleukin-2 Producer T cells unresponsive to interleukin-1 and unable to synthesize the T-cell growth factor. Scand J Immunol. 1982 Jan;15(1):25-31. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/6461917 # KNIGHT RP Jr, KORNFELD DS, GLASER GH, BONDY PK: Effects of intravenous hydrocortisone on electrolytes of serum and urine in man. J Clin Endocrinol Metab. 1955 Feb;15(2):176-81. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/13233328"@en . . " "@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "4-Pregnen-11beta,17alpha,21-triol-3,20-dione"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . "50-23-7"@en . . . "11beta-hydrocortisone"@en . . . . . . . . . . . . . . . . . . . "Reichstein's substance M"@en . "Humans and other mammals"@en . "Manfred Baumgarth, Dieter Orth, Jurgen Harting, Hans Schaefer, Achim Zesch, \"Hydrocortisone orthoesters, pharmaceutical formulations thereof and processes for the preparation thereof.\" U.S. Patent US4264584, issued March, 1974."@en . . . . . . . "11\u03B2-hydrocortisone"@en . . . . . . . . . . . . . . . . "Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing"@en . . . . . . . . . . . . . "The main glucocorticoid secreted by the adrenal cortex. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. [PubChem]"@en . . . . . . . . . . . . . "(11beta)-11,17,21-Trihydroxypregn-4-ene-3,20-dione"@en . . . . . . . . . . . . "Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption."@en . . . . . . . . . . . . . . . . . "Corticosteroids 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."@en . . . . . . . . . . . . . . "Hydrocortisonum"@en . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .