Systematic (IUPAC) name
Clinical data
AHFS/ monograph
MedlinePlus a682794
Licence data US FDA:link
  • AU: A
  • US: C (Risk not ruled out)
Pharmacokinetic data
Half-life 2-3 hours
Excretion Prednisolone is excreted via urine
50-24-8 7pxY
A07EA01 C05AA04, D07AA03, H02AB06, R01AD02, S01BA04, S02BA03, S03BA02
PubChem CID 5755
IUPHAR ligand 2866
DrugBank DB00860 7pxY
ChemSpider 5552 7pxY
KEGG D00472 7pxY
ChEBI CHEBI:8378 7pxY
Synonyms 11,17-dihydroxy-17- (2-hydroxyacetyl)- 10,13-dimethyl-6,7,8,9,10,11,12,13,14,15,16,17- dodecahydrocyclopenta [a]phenanthren-3-one
Chemical data
Formula C21H28O5
360.444 g/mol
 14pxY (what is this?)  (verify)

Prednisolone is a synthetic glucocorticoid, a derivative of cortisol, which is used to treat a variety of inflammatory and auto-immune conditions. It is the active metabolite of the drug prednisone[1] and is used especially in patients with liver failure, as these individuals are unable to metabolise prednisone into prednisolone.


Prednisolone is a corticosteroid drug with predominant glucocorticoid and low mineralocorticoid activity, making it useful for the treatment of a wide range of inflammatory and auto-immune conditions[2] such as asthma,[3] uveitis, pyoderma gangrenosum, rheumatoid arthritis, ulcerative colitis, pericarditis, temporal arteritis and Crohn's disease, Bell's palsy, multiple sclerosis,[4] cluster headaches, vasculitis, acute lymphoblastic leukemia and autoimmune hepatitis,[5] systemic lupus erythematosus, Kawasaki disease[6] and dermatomyositis. It is also used for treatment of sarcoidosis, though the mechanism is unknown.

Prednisolone acetate ophthalmic suspension (eye drops) is an adrenocortical steroid product, prepared as a sterile ophthalmic suspension and used to reduce swelling, redness, itching, and allergic reactions affecting the eye.

Prednisolone can also be used as an immunosuppressive drug for organ transplants and in cases of primary adrenal insufficiency (Addison's disease).

Corticosteroids inhibit the inflammatory response to a variety of inciting agents and, it is presumed, delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation with inflammation.

Mechanism of action

Prednisolone irreversibly binds with glucocorticoid receptors (GR) alpha and beta for which they have a high affinity. AlphaGR and BetaGR are found in virtually all tissues with variable numbers between 3000 and 10000 per cell, depending on the tissue involved. Prednisolone can activate and influence biochemical behaviour of most cells. The steroid/receptor complexes dimerise and interact with cellular DNA in the nucleus, binding to steroid-response elements and modifying gene transcription. They induce synthesis of some proteins, and inhibit synthesis of others.[7][8]

Not all metabolic actions on genes are known. Most mediator proteins are enzymes, e.g., cAMP-dependent kinase

Anti-inflammatory and immunosuppressive actions:

Regulation of gene suppression leads to systemic suppression of inflammation and immune response. This is of clinical usefulness but ultimately leads to gluconeogenesis, proteolysis and lipolysis. Gene transcription returns to normal after cessation, but sudden stoppage can cause Addison's disease. Osteoporosis is permanent.

Adverse effects

Possible side-effects include fluid retention of the face (moon face, Cushing's syndrome), acne, constipation, and mood swings.

A lengthy course of prednisolone can cause bloody or black tarry stools from bleeding into the stomach (this requires urgent medical attention); filling or rounding out of the face; muscle cramps or pain; muscle weakness; nausea; pain in back, hips, ribs, arms, shoulders, or legs; reddish-purple stretch marks on arms, face, legs, trunk, or groin; thin and shiny skin; unusual bruising; urinating at night; rapid weight gain; and wounds that will not heal.

Prolonged use of prednisolone can lead to the development of osteoporosis which makes bones more fragile and susceptible to fractures. One way to help alleviate this side effect is through the use of calcium and vitamin D supplements.[9]

Swelling of the pancreas has also been reported.[10]

Prednisolone can cause increased blood sugar levels for diabetics.

Other effects include decreased or blurred vision, increased eye pressure, increased thirst, cataract formation, confusion, rare cases of dementia in otherwise-healthy elderly patients, and nervousness.

Loteprednol is an analog drug that has reduced adverse ocular effects.

Prednisolone may cause serious mental health problems, these affect around 5% who take such steroids.[10] Symptoms include:

Nasal septum perforation and bowel perforation are also notable adverse effects that restrict steroids' use in some pathologic conditions.[11][12]

Withdrawal from prednisolone can be problematic after taking large doses or over more than two weeks.[13] This is caused by prednisolone inhibiting the natural production of corticosteroids in the "Hypothalamic-Pituitary-Adrenal Axis" (HPAA)[13]

Banned status in athletics

As a glucocorticosteroid, unauthorized or ad-hoc use of prednisolone during competition via oral, intravenous, intramuscular or rectal routes is banned under WADA anti-doping rules.[14] The drug may be used in competition with a TUE (Therapeutic Use Exemption), in compliance with WADA regulations. Local or topical use of prednisolone during competition as well as any use out of competition is not regulated.

See also


  1. ^ Davis M, Williams R, Chakraborty J et al. (June 1978). "Prednisone or prednisolone for the treatment of chronic active hepatitis? A comparison of plasma availability". British Journal of Clinical Pharmacology 5 (6): 501–5. PMC 1429358. PMID 656293. doi:10.1111/j.1365-2125.1978.tb01664.x. 
  2. ^ Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemically administered glucocorticoids. Clin Pharmacokinet. 2005;44(1):61-98. Review. PMID 15634032
  3. ^ Fiel SB, Vincken W. Systemic corticosteroid therapy for acute asthma exacerbations. J Asthma. 2006 Jun-Jul;43(5):321-31. Review. PMID 16801135
  4. ^ Thrower BW. Relapse management in multiple sclerosis. Neurologist. 2009 Jan;15(1):1-5. Review. PMID 19131851
  5. ^ Lambrou GI, Vlahopoulos S, Papathanasiou C, Papanikolaou M, Karpusas M, Zoumakis E, Tzortzatou-Stathopoulou F. Prednisolone exerts late mitogenic and biphasic effects on resistant acute lymphoblastic leukemia cells: Relation to early gene expression. Leuk Res. 2009 May 16. [Epub ahead of print] PMID 19450877
  6. ^ Miura M, Tamame T, Naganuma T, Chinen S, Matsuoka M, & Ohki H. (2011). Steroid pulse therapy for Kawasaki disease unresponsive to additional immunoglobulin therapy. Paediatrics & Child Health. 16(8), 479-84. PMID 23024586
  7. ^ Prednisolone. Australian Medicines Handbook 2010. Adelaide: Australian Medicines handbook Pty Ltd.; 2010. 497, 598.
  8. ^ Rang HP, Dale MM, Ritter JM, Moore PK. The pituitary and the adrenal Cortex. Hunter l, editor. Pharmacology. 5th ed. London: Churchill Livingstone; 2003. 413, 415.
  9. ^ "prednisolone, Pediapred Oral Liquid, Medrol (cont.)". 
  10. ^ a b Drugs Information. "Prednisolone Tablets 1mg, 5mg (Actavis UK Ltd)". Retrieved 13 December 2012. 
  11. ^ "Bowel Perforation in Steroid-Treated Patients"
  12. ^ "Intranasal steroids and septum perforation--an overlooked complication?"
  13. ^ a b Kaminstein, David. "Steroid Withdrawal". medicinenet. Retrieved 23 December 2012. 
  14. ^ "The 2011 Prohibited List".