Cortisone
IUPAC name	17,21-dihydroxypregn -4-ene-3,11,20-trione
Identifiers
CAS number	53-06-5 Y
MeSH	Cortisone
SMILES	C[C@@](C3)4[C@](CC[C@@](O)4 [C@@](CO)=O)([H])[C@]2([H])CCC1=CC (CC[C@@](C)1[C@]([H])2C3=O)=O
Properties
Molecular formula	C21H28O5
Molar mass	360.46 g/mol
Melting point	220–224 °C
Y (what is this?)  (verify) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Cortisone (pronounced /ˈkɔrtɨsoʊn/ or /ˈkɔrtɨzoʊn/ (ˈkôrtəˌsōn or -zōn)) (17-hydroxy-11-dehydrocorticosterone) is a steroid hormone. Chemically, it is a corticosteroid closely related to corticosterone.

[edit] History

Cortisone was first identified by the American chemist Edward Calvin Kendall while a researcher at the Mayo Clinic.^[1] He 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 functions. 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. This eliminated the need to use osmium tetroxide, a rare and expensive chemical.

[edit] Production

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 fasiculata and zona reticularis in response to ACTH secrete glucocorticoids, in particular cortisol. In the peripheral tissues cortisol is converted to cortisone by an enzyme called 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. ^[2]

[edit] Effects and uses

Cortisol, a glucocorticoid, and adrenaline are the main hormones released by the body as a reaction to stress. They elevate blood pressure and prepare the body for a fight or flight response.

One of cortisone's effects on the body, and a potentially harmful side effect when administered clinically, is the suppression of the immune system. This could be the explanation for the apparent correlation between high stress and sickness.

Cortisone can be used as a drug to treat a variety of ailments. It can be administered intravenously, orally, intraarticularly,^[3] or cutaneously.

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^[4].

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 such as severe IgE-mediated allergies.^[5]

Lastly, cortisone is a common treatment for a severe sore throat which occurs commonly with EBV infectious mononucleosis. It is important to note that cortisone does not help lessen the duration of the virus, and is used purely to increase the comfort of a patient with trouble speaking or swallowing as a result of the mononucleosis-induced swollen throat.

[edit] Side effects

Long-term cortisone use potentially has a number of severe side effects: hyperglycemia, insulin resistance, diabetes mellitus, osteoporosis, anxiety, depression, gastritis, colitis, hypertension, ictus, erectile dysfunction, hypogonadism, hypothyroidism, amenorrhoea and retinopathy among other problems.^{[citation needed]}

[edit] Veterinary use

Because of cortisone's effect on the immune system, dogs treated with even moderate doses show an increase in thirst and urination frequency. The urine that is created is not concentrated. Higher doses increase the likelihood of life-threatening side effects, which include fluid in the abdomen and an increased risk of myocardial arrest.^[6]

[edit] See also

• Central serous retinopathy
• Corticosterol

[edit] References

[edit] Notes

This article needs additional citations for verification. Please help improve this article by adding reliable references. Unsourced material may be challenged and removed. (December 2008)

[edit] Bibliography

• Bonagura J., DVM. et al. (2000). Current Veterinary Therapy. 13. pp. 321–381. 
• Ingle DJ (October 1950). "The biologic properties of cortisone: a review". J. Clin. Endocrinol. Metab. 10 (10): 1312–54. PMID 14794756. http://jcem.endojournals.org/cgi/pmidlookup?view=long&pmid=14794756. 
• Woodward R. B., Sondheimer F., Taub D. (1951). "The Total Synthesis of Cortisone". Journal of the American Chemical Society 73: 4057–4057. doi:10.1021/ja01152a551. 

[edit] External links

• Cortisone: The Wonder Drug