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| Names | |
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| Pronunciation | /ˈkɔːrtɪsoʊn/,/ˈkɔːrtɪzoʊn/ ⓘ |
| IUPAC name 17α,21-Dihydroxypregn-4-ene-3,11,20-trione | |
| Systematic IUPAC name (1R,3aS,3bS,9aR,9bS,11aS)-1-Hydroxy-1-(hydroxyacetyl)-9a,11a-dimethyl-2,3,3a,3b,4,5,8,9,9a,9b,11,11a-dodecahydro-7H-cyclopenta[a]phenanthrene-7,10(1H)-dione | |
| Other names 17α,21-Dihydroxy-11-ketoprogesterone; 17α-Hydroxy-11-dehydrocorticosterone | |
| Identifiers | |
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3D model (JSmol) | |
| ChEBI | |
| ChEMBL | |
| ChemSpider |
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| ECHA InfoCard | 100.000.149 |
| KEGG |
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| MeSH | Cortisone |
| UNII | |
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| Properties | |
| C21H28O5 | |
| Molar mass | 360.450 g·mol−1 |
| Melting point | 220 to 224 °C (428 to 435 °F; 493 to 497 K) |
| Pharmacology | |
| H02AB10 (WHO) S01BA03 (WHO) | |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Cortisone is apregnene (21-carbon)steroid hormone. It is a naturally occurringcorticosteroid metabolite that is also used as a pharmaceuticalprodrug.Cortisol is converted by the action of the enzymecorticosteroid 11-beta-dehydrogenase isozyme 2 into the inactive metabolite cortisone, particularly in the kidneys. This is done byoxidizing the alcohol group at carbon 11 (in the six-membered ring fused to the five-membered ring). Cortisone is converted back to the active steroid cortisol bystereospecifichydrogenation at carbon 11 by the enzyme11β-Hydroxysteroid dehydrogenase type 1, particularly in the liver.
The term "cortisone" is frequently misused to mean either anycorticosteroid orhydrocortisone, which is in factcortisol. Many who speak of receiving a "cortisone shot" or taking "cortisone" are more likely receiving hydrocortisone or one of many other, much more potent synthetic corticosteroids.
Cortisone can be administered as a prodrug, meaning it has to be converted by the body (specifically the liver, converting it into cortisol) after administration to be effective. It is used to treat a variety of ailments and can be administeredintravenously,orally,intra-articularly (into a joint), ortranscutaneously. Cortisone suppresses various elements of the immune system, thus reducing inflammation and attendant pain and swelling. Risks exist, in particular in the long-term use of cortisone.[1][2] However, using cortisone only results in very mild activity, and very often more potent steroids are used instead.
Cortisone itself is inactive.[3] It must be converted to cortisol by the action of11β-hydroxysteroid dehydrogenase type 1.[4] This primarily happens in the liver, the main site at which cortisone becomes cortisol after oral or systemic injection, and can thus have a pharmacological effect. After application to the skin or injection into a joint, local cells that express 11β-hydroxysteroid dehydrogenase type 1 instead convert it to active cortisol.
A cortisone injection may provide short-term pain relief and may reduce the swelling frominflammation of ajoint,tendon, orbursa in, for example, the joints of theknee,elbow andshoulder[1] and into a brokencoccyx.[5]
Cortisone is used bydermatologists to treatkeloids,[6] relieve the symptoms ofeczema andatopic dermatitis,[7] and stop the development ofsarcoidosis.[8]
Oral use of cortisone has a number of potential systemic adverse effects, includingasthma,hyperglycemia,insulin resistance,diabetes mellitus,osteoporosis,anxiety,depression,amenorrhoea,cataracts,glaucoma,Cushing's syndrome,increased risk of infections, andimpaired growth.[1][2] Withtopical application, it can lead to thinning of the skin, impairedwound healing,increased skin pigmentation,tendon rupture, andskin infections (includingabscesses).[9]
Cortisone was first identified by the American chemistsEdward Calvin Kendall and Harold L. Mason while researching at theMayo Clinic.[10][11][12] During the discovery process, cortisone was known as compound E (whilecortisol was known as compound F).
In 1949,Philip S. Hench and colleagues discovered that large doses of injected cortisone were effective in the treatment of patients with severerheumatoid arthritis.[13] Kendall was awarded the 1950Nobel Prize for Physiology or Medicine along withPhilip Showalter Hench andTadeusz Reichstein for the discovery of the structure and function ofadrenal cortex hormones including cortisone.[14][15] Both Reichstein and the team of O. Wintersteiner and J. Pfiffner had separately isolated the compound prior to the discovery made by Mason and Kendall, but failed to recognize its biological significance.[11] Mason's contributions to the crystallization and characterization of the compound have generally been forgotten outside of the Mayo Clinic.[11]
Cortisone was first produced commercially byMerck & Co. in 1948 or 1949.[13][16] On September 30, 1949,Percy Julian announced an improvement in the process of producing cortisone frombile acids.[17] This eliminated the need to useosmium tetroxide, a rare, expensive, and dangerous chemical. In the UK in the early 1950s,John Cornforth andKenneth Callow at theNational Institute for Medical Research collaborated withGlaxo to produce cortisone fromhecogenin fromsisal plants.[18]
Cortisone is one of several end-products of a process calledsteroidogenesis. This process starts with the synthesis ofcholesterol, which then proceeds through a series of modifications in theadrenal gland to become any one of many steroid hormones. One end-product of this pathway iscortisol. For cortisol to be released from the adrenal gland, a cascade of signaling occurs.Corticotropin-releasing hormone released from thehypothalamus stimulates corticotrophs in theanterior pituitary to releaseACTH, which relays the signal to the adrenal cortex. Here, thezona fasciculata andzona reticularis, in response to ACTH, secrete glucocorticoids, in particular cortisol. In various peripheral tissues, notably the kidneys, cortisol is inactivated to cortisone by theenzymecorticosteroid 11-beta-dehydrogenase isozyme 2. This is crucial because cortisol is a potentmineralocorticoid and would cause havoc with electrolyte levels (raising blood sodium and lowering blood potassium levels) and raise blood pressure if it were not inactivated in the kidneys.[4]
Because cortisone must be converted to cortisol before being active as aglucocorticoid, its activity is less than simply administering cortisol directly (80–90%).[19]
Abuse and addiction to cortisone was the subject of the 1956 motion pictureBigger Than Life, produced by and starringJames Mason. Though it was a box-office flop upon its initial release,[20] many modern critics hail the film as a masterpiece and brilliant indictment of contemporary attitudes toward mental illness and addiction.[21] In 1963,Jean-Luc Godard named it one of the ten greatest American sound films ever made.[22]
John F. Kennedy was regularly administeredcorticosteroids such as cortisone as a treatment forAddison's disease.[23]
Media related toCortisone at Wikimedia Commons| International | |
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