|Jmol interactive 3D||Image|
|Molar mass||360.45 g·mol−1|
|Melting point||220 to 224 °C (428 to 435 °F; 493 to 497 K)|
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
|what is ?)(|
Cortisone (// or //; 17-hydroxy-11-dehydrocorticosterone) is a 21-carbon steroid hormone. It is one of the main hormones released by the adrenal gland in response to stress. In chemical structure, it is a corticosteroid closely related to cortisol. It is used to treat a variety of ailments and can be administered intravenously, orally, intraarticularly (into a joint), or transcutaneously. Cortisone suppresses the immune system, thus reducing inflammation and attendant pain and swelling at the site of the injury. Risks exist, in particular in the long-term use of cortisone.
Effects and uses
A cortisone injection can also be used to give short-term pain relief and reduce the swelling from inflammation of a joint, tendon, or bursa in, for example, the joints of the knee, elbow, and shoulder  and into a broken coccyx.
Cortisone may also be used to deliberately suppress immune response in persons with autoimmune diseases or following an organ transplant to prevent transplant rejection. The suppression of the immune system may also be important in the treatment of inflammatory conditions.
Cortisone is a common treatment for a severe sore throat that occurs commonly with EBV infectious mononucleosis. Cortisone does not decrease the duration of the viral infection, but is used purely to increase the comfort of a patient with trouble speaking or swallowing as a result of the mononucleosis-induced swollen throat.
Oral use of cortisone has a number of potential systemic side-effects: hyperglycemia, insulin resistance, diabetes mellitus, osteoporosis, anxiety, depression, amenorrhoea, cataracts, Cushing's syndrome and glaucoma, among other problems.
Local side effects are rare but can include: pain, infection, skin pigment changes, loss of fatty tissue, and tendon rupture.
Cortisone was first identified by the American chemists Edward Calvin Kendall and Harold L. Mason while researching at the Mayo Clinic. Kendall was awarded the 1950 Nobel Prize for Physiology or Medicine along with Philip S. Hench and Tadeus Reichstein for the discovery of adrenal cortex hormones, their structures, and their functions. As it turns out, both Reichstein and the team of O. Wintersteiner and J. Pfiffner had separately isolated the compound prior to Mason/Kendall, but failed to recognize its biological significance. Dr. Mason's contributions to the crystallization and characterization of the compound have generally been forgotten outside of the Mayo Clinic.
Cortisone was first produced commercially by Merck & Co. On September 30, 1949, Percy Julian announced an improvement in the process of producing cortisone from bile acids.[chronology citation needed] This eliminated the need to use osmium tetroxide, a rare, expensive, and dangerous chemical. In the UK in the early 1950s, John Cornforth and Kenneth Callow at the National Institute for Medical Research collaborated with Glaxo to produce cortisone from hecogenin from sisal plants.
Cortisone is one of several end-products of a process called steroidogenesis. This process starts with the synthesis of cholesterol, which then proceeds through a series of modifications in the adrenal gland (suprarenal) to become any one of many steroid hormones. One end-product of this pathway is cortisol. For cortisol to be released from the adrenal gland, a cascade of signaling occurs. Corticotropin-releasing hormone released from the hypothalamus stimulates corticotrophs in the anterior pituitary to release ACTH, which relays the signal to the adrenal cortex. Here, the zona fasciculata and zona reticularis, in response to ACTH, secrete glucocorticoids, in particular cortisol. In the peripheral tissues, cortisol is converted to cortisone by the enzyme 11-beta-steroid dehydrogenase. Cortisol has much greater glucocorticoid activity than cortisone, and, thus, cortisone can be considered an inactive metabolite of cortisol. However, 11-beta-steroid dehydrogenase can catalyze the reverse reaction as well, and, thus, cortisone is also the inactive precursor molecule of the active hormone cortisol. Cortisone is activated through hydrogenation of the 11-keto-group, and cortisol is, thus, sometimes referred to as hydrocortisone.
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