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Statements

Subject Item
n2:DB00741
rdf:type
n3:Drug
n3:description
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]
n3:dosage
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n3:generalReferences
# 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
n3:group
approved
n3:halfLife
6-8 hours
n3:indication
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.
n3:manufacturer
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owl:sameAs
n13:DB00741 n37:DB00741
dcterms:title
Hydrocortisone
adms:identifier
n10:Hydrocortisone n23:0009-0142-01 n24:PDN n25:C00735 n26:D00088 n27:46505089 n28:PA449905 n30:5754 n31:17650 n32:5551 n33:22476 n34:2868 n35:2868 n36:DB00741
n3:mechanismOfAction
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.
n3:packager
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n3:patent
n17:5635497 n17:7378405
n3:routeOfElimination
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.
n3:synonym
Hydrocortisone Cortisol 11beta,17alpha,21-Trihydroxy-4-pregnene-3,20-dione Hidrocortisona 17-Hydroxycorticosterone Kendall's compound F 4-Pregnen-11beta,17alpha,21-triol-3,20-dione 11beta-hydrocortisone Reichstein's substance M 11β-hydrocortisone (11beta)-11,17,21-Trihydroxypregn-4-ene-3,20-dione Hydrocortisonum
n3:toxicity
Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing
n5:hasAHFSCode
n29:84-06-00 n29:68-04-00 n29:52-08-08
n3:foodInteraction
Take with food to reduce irritation. Calcium, phosphorous, potassium, Vitamin A, C, D and zinc needs increased with long term use.
n3:mixture
n22:271B5398-363D-11E5-9242-09173F13E4C5 n22:271B5399-363D-11E5-9242-09173F13E4C5 n22:271B5396-363D-11E5-9242-09173F13E4C5 n22:271B5397-363D-11E5-9242-09173F13E4C5 n22:271B539C-363D-11E5-9242-09173F13E4C5 n22:271B539D-363D-11E5-9242-09173F13E4C5 n22:271B539A-363D-11E5-9242-09173F13E4C5 n22:271B539B-363D-11E5-9242-09173F13E4C5 n22:271B53A0-363D-11E5-9242-09173F13E4C5 n22:271B53A1-363D-11E5-9242-09173F13E4C5 n22:271B539E-363D-11E5-9242-09173F13E4C5 n22:271B539F-363D-11E5-9242-09173F13E4C5 n22:271B53A2-363D-11E5-9242-09173F13E4C5 n22:271B5395-363D-11E5-9242-09173F13E4C5
n3:proteinBinding
95%
n3:salt
n3:synthesisReference
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.
n18:hasConcept
n19:M0010707
foaf:page
n8:hydrocortisone.html n15:hydrocortisone.htm n21:hyd1199.shtml
n3:IUPAC-Name
n14:271B5536-363D-11E5-9242-09173F13E4C5
n3:InChI
n14:271B553C-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n14:271B553B-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n14:271B5538-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n14:271B5539-363D-11E5-9242-09173F13E4C5
n3:SMILES
n14:271B553A-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n14:271B5534-363D-11E5-9242-09173F13E4C5 n14:271B554C-363D-11E5-9242-09173F13E4C5
n3:logP
n14:271B5535-363D-11E5-9242-09173F13E4C5 n14:271B5532-363D-11E5-9242-09173F13E4C5 n14:271B554E-363D-11E5-9242-09173F13E4C5
n3:logS
n14:271B5533-363D-11E5-9242-09173F13E4C5 n14:271B554F-363D-11E5-9242-09173F13E4C5
n5:hasATCCode
n6:D07XA01 n6:D07AA02 n6:S02BA01 n6:C05AA01 n6:H02AB09 n6:S01CB03 n6:A07EA02 n6:S01BA02 n6:A01AC03
n3:H-Bond-Acceptor-Count
n14:271B5542-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n14:271B5543-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n14:271B553D-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n14:271B553E-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n14:271B5540-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n14:271B553F-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n14:271B5541-363D-11E5-9242-09173F13E4C5
n3:absorption
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
n3:affectedOrganism
Humans and other mammals
n3:caco2-Permeability
n14:271B5550-363D-11E5-9242-09173F13E4C5
n3:casRegistryNumber
50-23-7
n3:category
n3:containedIn
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n11:271B54F4-363D-11E5-9242-09173F13E4C5 n11:271B54F5-363D-11E5-9242-09173F13E4C5 n11:271B54F2-363D-11E5-9242-09173F13E4C5 n11:271B54F3-363D-11E5-9242-09173F13E4C5 n11:271B54D9-363D-11E5-9242-09173F13E4C5 n11:271B54F1-363D-11E5-9242-09173F13E4C5 n11:271B5488-363D-11E5-9242-09173F13E4C5 n11:271B5489-363D-11E5-9242-09173F13E4C5 n11:271B54A9-363D-11E5-9242-09173F13E4C5 n11:271B5485-363D-11E5-9242-09173F13E4C5 n11:271B54AA-363D-11E5-9242-09173F13E4C5 n11:271B5486-363D-11E5-9242-09173F13E4C5 n11:271B54A7-363D-11E5-9242-09173F13E4C5 n11:271B54A8-363D-11E5-9242-09173F13E4C5 n11:271B5483-363D-11E5-9242-09173F13E4C5 n11:271B5484-363D-11E5-9242-09173F13E4C5 n11:271B54A5-363D-11E5-9242-09173F13E4C5 n11:271B5481-363D-11E5-9242-09173F13E4C5 n11:271B54A6-363D-11E5-9242-09173F13E4C5 n11:271B5482-363D-11E5-9242-09173F13E4C5 n11:271B54A3-363D-11E5-9242-09173F13E4C5 n11:271B547F-363D-11E5-9242-09173F13E4C5 n11:271B54A4-363D-11E5-9242-09173F13E4C5 n11:271B5480-363D-11E5-9242-09173F13E4C5 n11:271B54A1-363D-11E5-9242-09173F13E4C5 n11:271B54A2-363D-11E5-9242-09173F13E4C5 n11:271B547D-363D-11E5-9242-09173F13E4C5 n11:271B547E-363D-11E5-9242-09173F13E4C5 n11:271B549F-363D-11E5-9242-09173F13E4C5 n11:271B547B-363D-11E5-9242-09173F13E4C5 n11:271B54A0-363D-11E5-9242-09173F13E4C5 n11:271B547C-363D-11E5-9242-09173F13E4C5 n11:271B549D-363D-11E5-9242-09173F13E4C5 n11:271B5479-363D-11E5-9242-09173F13E4C5 n11:271B549E-363D-11E5-9242-09173F13E4C5 n11:271B549B-363D-11E5-9242-09173F13E4C5 n11:271B547A-363D-11E5-9242-09173F13E4C5 n11:271B5498-363D-11E5-9242-09173F13E4C5 n11:271B549C-363D-11E5-9242-09173F13E4C5 n11:271B54D8-363D-11E5-9242-09173F13E4C5 n11:271B5496-363D-11E5-9242-09173F13E4C5 n11:271B5497-363D-11E5-9242-09173F13E4C5 n11:271B5494-363D-11E5-9242-09173F13E4C5 n11:271B5495-363D-11E5-9242-09173F13E4C5 n11:271B5492-363D-11E5-9242-09173F13E4C5 n11:271B5493-363D-11E5-9242-09173F13E4C5 n11:271B5490-363D-11E5-9242-09173F13E4C5 n11:271B5491-363D-11E5-9242-09173F13E4C5 n11:271B548E-363D-11E5-9242-09173F13E4C5 n11:271B548F-363D-11E5-9242-09173F13E4C5 n11:271B548C-363D-11E5-9242-09173F13E4C5 n11:271B548D-363D-11E5-9242-09173F13E4C5 n11:271B548A-363D-11E5-9242-09173F13E4C5 n11:271B548B-363D-11E5-9242-09173F13E4C5 n11:271B54AB-363D-11E5-9242-09173F13E4C5 n11:271B5499-363D-11E5-9242-09173F13E4C5 n11:271B549A-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n14:271B5548-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n14:271B554A-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n14:271B554B-363D-11E5-9242-09173F13E4C5
n3:Melting-Point
n14:271B554D-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n14:271B5547-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n14:271B5546-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n14:271B5549-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n14:271B5537-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n14:271B5544-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n14:271B5545-363D-11E5-9242-09173F13E4C5