Open Access Articles- Top Results for Prednisone


Systematic (IUPAC) name
Clinical data
AHFS/ monograph
MedlinePlus a601102
  • C
  • Rx Only (US)(AUS)
Oral, Nasal, Rectal, Injection, IV
Pharmacokinetic data
Bioavailability 70%
Metabolism prednisolone (liver)
Half-life 1 hour
Excretion Renal
53-03-2 7pxY
A07EA03 H02AB07
PubChem CID 5865
DrugBank DB00635 7pxY
ChemSpider 5656 7pxY
KEGG C07370 7pxY
ChEBI CHEBI:8382 7pxY
Synonyms Deltasone, Liquid Pred, Orasone, Adasone, Deltacortisone, Prednisonum
Chemical data
Formula C21H26O5
358.428 g/mol
 14pxN (what is this?)  (verify)
File:Periportal hepatosteatosis intermed mag.jpg
Micrograph of fatty liver, as may be seen due to long-term prednisone use. Trichrome stain.

Prednisone is a synthetic corticosteroid drug that is particularly effective as an immunosuppressant drug. It is used to treat certain inflammatory diseases (such as moderate allergic reactions) and (at higher doses) some types of cancer, but has significant adverse effects. Because it suppresses the immune system, it leaves patients more susceptible to infections.

Medical uses

Prednisone is used for many different indications including: asthma, COPD, CIDP, rheumatic disorders, allergic disorders, ulcerative colitis and Crohn's disease, adrenocortical insufficiency, hypercalcemia due to cancer, thyroiditis, laryngitis, severe tuberculosis, urticaria (hives), lipid pneumonitis, pericarditis, multiple sclerosis, nephrotic syndrome, lupus, myasthenia gravis, poison oak exposure, Meniere's disease, and as part of a drug regimen to prevent rejection post organ transplant.[1]

Prednisone has also been used in the treatment of migraine headaches and cluster headaches and for severe aphthous ulcer. Prednisone is used as an antitumor drug.[2] Prednisone is important in the treatment of acute lymphoblastic leukemia, Non-Hodgkin lymphomas, Hodgkin's lymphoma, multiple myeloma and other hormone-sensitive tumors, in combination with other anticancer drugs.

Prednisone is also used for the treatment of the Herxheimer reaction, which is common during the treatment of syphilis, and to delay the onset of symptoms of Duchenne muscular dystrophy and also for uveitis. The mechanism for the delay of symptoms is unknown. Because it suppresses the adrenal glands, it is also sometimes used in the treatment of congenital adrenal hyperplasia. Prednisone is also used to treat sarcoidosis and lupus.

Prednisone can also be used in the treatment of decompensated heart failure to potentiate renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large dose of loop diuretics.[3][4][5][6][7][8] The mechanism is prednisone, as a glucocorticoid, can improve renal responsiveness to atrial natriuretic peptide by increasing the density of natriuretic peptide receptor type A in the renal inner medullary collecting duct, inducing a potent diuresis.[9]


Short-term side-effects, as with all glucocorticoids, include high blood glucose levels (especially in patients with diabetes mellitus or on other medications that increase blood glucose, such as tacrolimus) and mineralocorticoid effects such as fluid retention.[10] The mineralocorticoid effects of prednisone are minor, which is why it is not used in the management of adrenal insufficiency, unless a more potent mineralocorticoid is administered concomitantly.

It can also cause depression or depressive symptoms and anxiety in some individuals.[11][12]

Long-term side-effects include Cushing's syndrome, steroid dementia syndrome, truncal weight gain, osteoporosis, glaucoma and cataracts, type II diabetes mellitus, and depression upon dose reduction or cessation.[citation needed]






Adrenal suppression will begin to occur if prednisone is taken for longer than seven days. Eventually, this may cause the body to temporarily lose the ability to manufacture natural corticosteroids (especially cortisol), which results in dependence on prednisone. For this reason, prednisone should not be abruptly stopped if taken for more than seven days, instead, the dosage should be gradually reduced. This weaning process may be over a few days, if the course of prednisone was short, but may take weeks or months[citation needed] if the patient had been on long-term treatment. Abrupt withdrawal may lead to an Addison crisis. For those on chronic therapy, alternate-day dosing may preserve adrenal function and thereby reduce side-effects.[14]

Glucocorticoids act to inhibit-feedback of both the hypothalamus, decreasing corticotropin-releasing hormone [CRH], and corticotrophs in the anterior pituitary gland, decreasing the amount of adrenocorticotropic hormone [ACTH]. For this reason, glucocorticoid analogue drugs such as prednisone down-regulate the natural synthesis of glucocorticoids. This mechanism leads to dependence in a short time and can be dangerous if medications are withdrawn too quickly. The body must have time to begin synthesis of CRH and ACTH and for the adrenal glands to begin functioning normally again.


The magnitude and speed of dose reduction in corticosteroid withdrawal should be determined on a case-by-case basis, taking into consideration the underlying condition that is being treated, and individual patient factors such as the likelihood of relapse and the duration of corticosteroid treatment. Gradual withdrawal of systemic corticosteroids should be considered in those whose disease is unlikely to relapse and have:
· received more than 40 mg prednisolone (or equivalent) daily for more than 1 week;
· been given repeat doses in the evening;
· received more than 3 weeks' treatment;
· recently received repeated courses (particularly if taken for longer than 3 weeks);
· taken a short course within 1 year of stopping long-term therapy;
· other possible causes of adrenal suppression.
Systemic corticosteroids may be stopped abruptly in those whose disease is unlikely to relapse and who have received treatment for 3 weeks or less and who are not included in the patient groups described above.
During corticosteroid withdrawal the dose may be reduced rapidly down to physiological doses (equivalent to prednisolone 7.5 mg daily) and then reduced more slowly. Assessment of the disease may be needed during withdrawal to ensure that relapse does not occur.[15]


Prednisone has no substantial biological effects until converted via hepatic metabolism to prednisolone.[16]


The pharmaceutical industry uses prednisone tablets for the calibration of dissolution testing equipment according to the United States Pharmacopeia (USP).


The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by Arthur Nobile.[17][18][19] The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became Schering-Plough Corporation, by Arthur Nobile and coworkers.[20] They discovered that cortisone could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. The same process was used to prepare prednisolone from hydrocortisone.[21]

The enhanced adrenocorticoid activity of these compounds over cortisone and hydrocortisone was demonstrated in mice.[22]

Prednisone and prednisolone were introduced in 1955 by Schering and Upjohn, under the brand names Meticorten and Delta-Cortef, respectively.[23] These prescription medicines are now available from a number of manufacturers as generic drugs.


Prednisolone differs from prednisone in that the keto-group at C11 of prednisone is replaced by a hydroxyl group.

Prednisone can be synthesized by dehydrogenation of the C1-C2 bond in hydrocortisone (cortisol) by microbiological fermentation with an organism such as Corynebacterium simplex.[24][25][26][27]

See also


  1. "Prednisone". The American Society of Health-System Pharmacists. Retrieved 3 April 2011. 
  2. [U.S.] National Library of Medicine, Medical Subject Headings. Antineoplastic Agents, Hormonal (2009). Retrieved 9-11-2010
  3. RIEMER, AD (April 1958). "Application of the newer corticosteroids to augment diuresis in congestive heart failure.". The American journal of cardiology 1 (4): 488–96. PMID 13520608. doi:10.1016/0002-9149(58)90120-6. 
  4. NEWMAN, DA (15 February 1959). "Reversal of intractable cardiac edema with prednisone.". New York state journal of medicine 59 (4): 625–33. PMID 13632954. 
  5. Zhang, H; Liu, C; Ji, Z; Liu, G; Zhao, Q; Ao, YG; Wang, L; Deng, B; Zhen, Y; Tian, L; Ji, L; Liu, K (September 2008). "Prednisone adding to usual care treatment for refractory decompensated congestive heart failure.". International heart journal 49 (5): 587–95. PMID 18971570. doi:10.1536/ihj.49.587. 
  6. Liu, C; Liu, G; Zhou, C; Ji, Z; Zhen, Y; Liu, K (September 2007). "Potent diuretic effects of prednisone in heart failure patients with refractory diuretic resistance.". The Canadian journal of cardiology 23 (11): 865–8. PMC 2651362. PMID 17876376. doi:10.1016/s0828-282x(07)70840-1. 
  7. Liu, C; Chen, H; Zhou, C; Ji, Z; Liu, G; Gao, Y; Tian, L; Yao, L; Zheng, Y; Zhao, Q; Liu, K (October 2006). "Potent potentiating diuretic effects of prednisone in congestive heart failure.". Journal of cardiovascular pharmacology 48 (4): 173–6. PMID 17086096. doi:10.1097/01.fjc.0000245242.57088.5b. 
  8. Massari, F; Mastropasqua, F; Iacoviello, M; Nuzzolese, V; Torres, D; Parrinello, G (March 2012). "The glucocorticoid in acute decompensated heart failure: Dr Jekyll or Mr Hyde?". The American journal of emergency medicine 30 (3): 517.e5–10. PMID 21406321. doi:10.1016/j.ajem.2011.01.023. 
  9. Liu, C; Chen, Y; Kang, Y; Ni, Z; Xiu, H; Guan, J; Liu, K (October 2011). "Glucocorticoids improve renal responsiveness to atrial natriuretic peptide by up-regulating natriuretic peptide receptor-A expression in the renal inner medullary collecting duct in decompensated heart failure.". The Journal of Pharmacology and Experimental Therapeutics 339 (1): 203–9. PMID 21737535. doi:10.1124/jpet.111.184796. 
  11. Prednisone Information from
  12. Prednisone: MedlinePlus Drug Information
  13. 13.0 13.1 Mayo Clinic
  14. "Therapeutic and Adverse Effects of Glucocorticoids". Bello CS, Garrett SD. U.S. Pharmacist Continuing Education Program no. 430-000-99-028-H01, August 1999. 
  16. Medline drug information for prednisone
  17. Wainwright, M. "The secret of success: Arthur Nobile's discovery of the steroids prednisone and prednisolone in the 1950s revolutionised the treatment of arthritis". Chemistry in Britain. Retrieved 15 June 2011. 
  18. "National Inventors Hall of Fame". 
  19. "New Jersey Inventors Hall of Fame". 
  20. Merck Index, 14th Edition, p.1327. Published by Merck & Co. Inc.
  21. H.L. Herzog et al. Science, Vol. 121, p 176 (1955).
  22. H.L. Herzog et al[check quotation syntax]" Science, Vol. 121, p 176 (1955).
  23. Drugs@FDA: FDA Approved Drug Products
  24. U.S. Patent 3,134,718
  25. Meystre, Ch. (1956). "Gewinnung von 1;4-Bisdehydro-3-oxo-steroiden. Uber Steroide, 139. Mitteilung". Helvetica Chimica Acta 39 (3): 734–742. doi:10.1002/hlca.19560390314.  edit
  26. DE 1135899 
  27. Nobile, A.; Charney, W.; Perlman, P. L.; Herzog, H. L.; Payne, C. C.; Tully, M. E.; Jevnik, M. A.; Hershberg, E. B. (1955). "Microbiological Transformation of Steroids. I. Δ1,4-Diene-3-Ketosteroids". Journal of the American Chemical Society 77 (15): 4184. doi:10.1021/ja01620a079.  edit

Further reading

  • International Journal of Immunopharmacology, Vol. 7, Issue 5, 1985, pp 731–737

External links