View source for Prednisone

{{Short description|Steroid medication}}
{{Redirect|Deltra|the fishing trawler in service 1951-57|FV Deltra}}
{{Distinguish|Prednisolone}}
{{Use dmy dates|date=January 2024}}
{{Cs1 config |name-list-style=vanc |display-authors=6}}
{{Infobox drug
| verifiedrevid = 464213538
| Verifiedfields = changed
| image = Prednisone.svg
| image_class = skin-invert-image
| alt = 
| caption = 
| image2 = Prednisone-from-xtal-3D-bs-17.png
| image_class2 = bg-transparent
| alt2 =

<!-- Clinical data -->
| pronounce = 
| tradename = Deltasone, Liquid Pred, Orasone, others
| Drugs.com = {{drugs.com|monograph|prednisone}}
| MedlinePlus = a601102
| DailyMedID = Prednisone
| pregnancy_AU = A
| pregnancy_AU_comment = 
| pregnancy_category =
| routes_of_administration = [[Oral administration|By mouth]]
| class = 
| ATC_prefix = A07
| ATC_suffix = EA03
| ATC_supplemental = {{ATC|H02|AB07}}

<!-- Legal status -->
| legal_AU = S4
| legal_AU_comment = 
| legal_BR = <!-- OTC, A1, A2, A3, B1, B2, C1, C2, C3, C4, C5, D1, D2, E, F -->
| legal_BR_comment = 
| legal_CA = Rx-only
| legal_CA_comment = <ref>{{cite web | title=Product monograph brand safety updates | website=[[Health Canada]] | date=7 July 2016 | url=https://www.canada.ca/en/health-canada/services/drugs-health-products/drug-products/drug-product-database/label-safety-assessment-update/product-monograph-brand-safety-updates.html | access-date=3 April 2024}}</ref>
| legal_DE = <!-- Anlage I, II, III or Unscheduled -->
| legal_DE_comment = 
| legal_NZ = <!-- Class A, B, C -->
| legal_NZ_comment = 
| legal_UK = <!-- GSL, P, POM, CD, CD Lic, CD POM, CD No Reg POM, CD (Benz) POM, CD (Anab) POM or CD Inv POM / Class A, B, C -->
| legal_UK_comment = 
| legal_US = Rx-only
| legal_US_comment = 
| legal_EU = 
| legal_EU_comment = 
| legal_UN = <!-- N I, II, III, IV / P I, II, III, IV -->
| legal_UN_comment = 
| legal_status = <!-- For countries not listed above -->

<!-- Pharmacokinetic data -->
| bioavailability = 70%
| protein_bound = 
| metabolism = [[prednisolone]] ([[liver]])
| metabolites = 
| onset = 
| elimination_half-life = 3 to 4 hours in adults. 1 to 2 hours in children<ref name="pmid378499">{{cite journal | vauthors = Pickup ME | title = Clinical pharmacokinetics of prednisone and prednisolone | journal = Clinical Pharmacokinetics | volume = 4 | issue = 2 | pages = 111–128 | date = 1979 | pmid = 378499 | doi = 10.2165/00003088-197904020-00004 | s2cid = 12218704 }}</ref>
| duration_of_action = 
| excretion = [[Kidney]]

<!-- Identifiers -->
| CAS_number = 53-03-2
| CAS_number_Ref = {{cascite|correct|??}}
| CAS_supplemental = 
| PubChem = 5865
| IUPHAR_ligand = 7096
| DrugBank = DB00635
| DrugBank_Ref = {{drugbankcite|correct|drugbank}}
| ChemSpiderID = 5656
| ChemSpiderID_Ref = {{chemspidercite|correct|chemspider}}
| UNII = VB0R961HZT
| UNII_Ref = {{fdacite|changed|FDA}}
| KEGG = C07370
| KEGG_Ref = {{keggcite|correct|kegg}}
| ChEBI = 8382
| ChEBI_Ref = {{ebicite|correct|EBI}}
| ChEMBL = 635
| ChEMBL_Ref = {{ebicite|correct|EBI}}
| NIAID_ChemDB = 
| PDB_ligand = 
| synonyms =

<!-- Chemical and physical data -->
| IUPAC_name = 17,21-dihydroxypregna-1,4-diene-3,11,20-trione
| C=21 | H=26 | O=5
| SMILES = O=C(CO)[C@@]3(O)CC[C@H]2[C@@H]4CC\C1=C\C(=O)\C=C/[C@]1(C)[C@H]4C(=O)C[C@@]23C
| StdInChI = 1S/C21H26O5/c1-19-7-5-13(23)9-12(19)3-4-14-15-6-8-21(26,17(25)11-22)20(15,2)10-16(24)18(14)19/h5,7,9,14-15,18,22,26H,3-4,6,8,10-11H2,1-2H3/t14-,15-,18+,19-,20-,21-/m0/s1
| StdInChI_Ref = {{stdinchicite|correct|chemspider}}
| StdInChI_comment = 
| StdInChIKey = XOFYZVNMUHMLCC-ZPOLXVRWSA-N
| StdInChIKey_Ref = {{stdinchicite|correct|chemspider}}
| density = 
| density_notes = 
| melting_point = 
| melting_high = 
| melting_notes = 
| boiling_point = 
| boiling_notes = 
| solubility = 
| sol_units = 
| specific_rotation = 
}}

<!-- Definition and medical uses -->
'''Prednisone''' is a [[glucocorticoid]] medication mostly used to [[immunosuppressive drug|suppress the immune system]] and decrease [[inflammation]] in conditions such as [[asthma]], [[COPD]], and [[rheumatologic disease]]s.<ref name=AHFS2018>{{cite web |title=Prednisone Monograph for Professionals |url=https://www.drugs.com/monograph/prednisone.html |website=Drugs.com |publisher=AHFS |access-date=24 December 2018 }}</ref> It is also used to treat [[high blood calcium]] due to [[cancer]] and [[adrenal insufficiency]] along with other [[steroid]]s.<ref name=AHFS2018/> It is taken [[Oral administration|by mouth]].<ref name=AHFS2018/>

<!-- Side effects -->
Common side effects may include [[cataracts]], [[Osteoporosis|bone loss]], easy [[bruising]], muscle weakness, and [[oral candidiasis|thrush]].<ref name=AHFS2018/> Other side effects include weight gain, swelling, [[high blood sugar]], increased risk of infection, and [[psychosis]].<ref name=AHFS2018/><ref name=GG2017>{{cite book | vauthors = Brunton L |title=Goodman & Gilman's the pharmacological basis of therapeutics |date=2017 |publisher=McGraw-Hill Education |isbn=978-1-25-958473-2 |pages=739, 746, 1237|edition=13}}</ref> It is generally considered safe in [[pregnancy]] and low doses appear to be safe while the user is [[breastfeeding]].<ref>{{cite web |title=Prednisone Use During Pregnancy |url=https://www.drugs.com/pregnancy/prednisone.html |website=Drugs.com |access-date=24 December 2018 }}</ref> After prolonged use, prednisone must be stopped gradually.<ref name=AHFS2018/>

<!-- Mechanism -->
Prednisone is a [[prodrug]] and must be converted to [[prednisolone]] by the liver before it becomes active.<ref name=PI2018>{{cite web |title = Product Information Panafcort (prednisone) Panafcortelone (prednisolone) |url= https://www.ebs.tga.gov.au/ebs/picmi/picmirepository.nsf/pdf?OpenAgent&id=CP-2010-PI-06868-3&d=2018063016114622483 |website=TGA eBusiness Services |publisher=Aspen Pharmacare Australia Pty Ltd |access-date=30 June 2018 |location=St Leonards, Australia |pages=1–2 |format=PDF |date=11 July 2017}}</ref><ref>{{cite journal | vauthors = Buttgereit F, Gibofsky A | title = Delayed-release prednisone - a new approach to an old therapy | journal = Expert Opinion on Pharmacotherapy | volume = 14 | issue = 8 | pages = 1097–1106 | date = June 2013 | pmid = 23594208 | doi = 10.1517/14656566.2013.782001 | s2cid = 22720230 }}</ref> Prednisolone then binds to [[glucocorticoid receptor]]s, activating them and triggering changes in [[gene expression]].<ref name=GG2017/> These changes inhibit function and decrease the number of key [[leukocytes]] in the bloodstream.<ref>{{Cite web |last=PMC |first=Europe |title=Europe PMC |url=https://europepmc.org/article/NBK/nbk534809 |access-date=2025-11-14 |website=europepmc.org |language=en}}</ref>

<!-- Society and culture -->
Prednisone was patented in 1954 and approved for medical use in the United States in 1955.<ref name=AHFS2018/><ref name=Fis2006>{{cite book| vauthors = Fischer J, Ganellin CR |title=Analogue-based Drug Discovery |date=2006 |publisher=John Wiley & Sons |isbn=9783527607495 |page=485 |url=https://books.google.com/books?id=FjKfqkaKkAAC&pg=PA485}}</ref> Prednisone is a therapeutic alternative on the [[WHO Model List of Essential Medicines|World Health Organization's List of Essential Medicines]].<ref name="WHO24th">{{cite book | vauthors = ((World Health Organization)) | title = The selection and use of essential medicines, 2025: WHO Model List of Essential Medicines, 24th list | year = 2025 | hdl = 10665/382243 | author-link = World Health Organization | publisher = World Health Organization | location = Geneva | hdl-access=free }}</ref> It is available as a [[generic medication]].<ref name=AHFS2018/> In 2023, it was the 38th most commonly prescribed medication in the United States, with more than 15{{nbsp}}million prescriptions.<ref name="Top300Drugs">{{cite web | title=Top 300 of 2023 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=12 August 2025 | archive-date=12 August 2025 | archive-url=https://web.archive.org/web/20250812130026/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Prednisone Drug Usage Statistics, United States, 2014 - 2023 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/Prednisone | access-date = 13 August 2025 }}</ref>

== Medical uses ==
Prednisone is used for many different [[autoimmune disease]]s and inflammatory conditions, including [[asthma]], [[gout]], [[COPD]], [[CIDP]], [[rheumatic disorders]], [[allergic]] disorders, [[ulcerative colitis]] and [[Crohn's disease]], [[granulomatosis with polyangiitis]], [[adrenocortical insufficiency]], [[hypercalcemia]] due to cancer, [[thyroiditis]], [[laryngitis]], severe [[tuberculosis]], [[urticaria|hives]], [[eczema]], [[lipid pneumonitis]], [[pericarditis]], [[multiple sclerosis]], [[nephrotic syndrome]], [[sarcoidosis]], to relieve the effects of [[shingles]], [[lupus]], [[myasthenia gravis]], [[poison oak]] exposure, [[Ménière's disease]], [[autoimmune hepatitis]], [[giant cell arteritis]], the [[Herxheimer reaction]] that is common during the treatment of [[syphilis]], [[Duchenne muscular dystrophy]], [[uveitis]], and as part of a drug regimen to prevent rejection after [[organ transplant]].<ref>{{EMedicine|article|172356|Autoimmune Hepatitis|treatment}}</ref><ref>{{cite book | chapter=Corticosteroids | date=30 May 2014 | pmid=31643719 | chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK548400/ | title=LiverTox: Clinical and Research Information on Drug-Induced Liver Injury | url=https://www.ncbi.nlm.nih.gov/books/NBK547852/ | access-date=19 March 2020 | id=NBK548400 }}</ref><ref name=AHFS2018/>

Prednisone has also been used in the treatment of [[migraine]] headaches and [[cluster headache]]s and for severe [[aphthous ulcer]].<ref>{{cite book | vauthors = Wackym PA, Snow JB |title=Ballenger's Otorhinolaryngology: Head and Neck Surgery |date=2017 |publisher=PMPH USA |isbn=9781607951773 |page=1185 |url=https://books.google.com/books?id=CFwrAwAAQBAJ&pg=PA1185 }}</ref> Prednisone is used as an [[antitumor drug]].<ref>{{cite web | publisher = U.S. National Library of Medicine | work = Medical Subject Headings. | url = https://meshb.nlm.nih.gov/#/record/ui?name=Antineoplastic+Agents,+Hormonal | title = Antineoplastic Agents, Hormonal | date = 2009 | access-date = 11 November 2010 }}</ref>

Prednisone is often also prescribed as a form of treatment for sudden [[sensorineural hearing loss]] (SSNHL).<ref>{{Cite web |date=22 May 2015 |title=Steroid Treatments Equally Effective Against Sudden Deafness |url=https://www.nih.gov/news-events/nih-research-matters/steroid-treatments-equally-effective-against-sudden-deafness |archive-url=https://web.archive.org/web/20151101163727/http://www.nih.gov/news-events/nih-research-matters/steroid-treatments-equally-effective-against-sudden-deafness |url-status=dead |archive-date=1 November 2015 |access-date=9 May 2022 |website=National Institutes of Health (NIH) |language=EN}}</ref>

Prednisone can be used in the treatment of decompensated [[heart failure]] to increase renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large doses of loop diuretics.<ref>{{cite journal | vauthors = Riemer AD | title = Application of the newer corticosteroids to augment diuresis in congestive heart failure | journal = The American Journal of Cardiology | volume = 1 | issue = 4 | pages = 488–496 | date = April 1958 | pmid = 13520608 | doi = 10.1016/0002-9149(58)90120-6 }}</ref><ref>{{cite journal | vauthors = Newman DA | title = Reversal of intractable cardiac edema with prednisone | journal = New York State Journal of Medicine | volume = 59 | issue = 4 | pages = 625–633 | date = February 1959 | pmid = 13632954 }}</ref><ref>{{cite journal | vauthors = Zhang H, Liu C, Ji Z, Liu G, Zhao Q, Ao YG, Wang L, Deng B, Zhen Y, Tian L, Ji L, Liu K | title = Prednisone adding to usual care treatment for refractory decompensated congestive heart failure | journal = International Heart Journal | volume = 49 | issue = 5 | pages = 587–595 | date = September 2008 | pmid = 18971570 | doi = 10.1536/ihj.49.587 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Liu C, Liu G, Zhou C, Ji Z, Zhen Y, Liu K | title = Potent diuretic effects of prednisone in heart failure patients with refractory diuretic resistance | journal = The Canadian Journal of Cardiology | volume = 23 | issue = 11 | pages = 865–868 | date = September 2007 | pmid = 17876376 | pmc = 2651362 | doi = 10.1016/s0828-282x(07)70840-1 }}</ref><ref>{{cite journal | vauthors = Liu C, Chen H, Zhou C, Ji Z, Liu G, Gao Y, Tian L, Yao L, Zheng Y, Zhao Q, Liu K | title = Potent potentiating diuretic effects of prednisone in congestive heart failure | journal = Journal of Cardiovascular Pharmacology | volume = 48 | issue = 4 | pages = 173–176 | date = October 2006 | pmid = 17086096 | doi = 10.1097/01.fjc.0000245242.57088.5b | s2cid = 45800521 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Massari F, Mastropasqua F, Iacoviello M, Nuzzolese V, Torres D, Parrinello G | title = The glucocorticoid in acute decompensated heart failure: Dr Jekyll or Mr Hyde? | journal = The American Journal of Emergency Medicine | volume = 30 | issue = 3 | pages = 517.e5–517.10 | date = March 2012 | pmid = 21406321 | doi = 10.1016/j.ajem.2011.01.023 }}</ref> In terms of the mechanism of action for this purpose: prednisone, a glucocorticoid, can improve renal responsiveness to atrial [[Natriuresis|natriuretic]] peptide by increasing the density of natriuretic peptide receptor type A in the renal inner medullary collecting duct, thereby inducing a potent diuresis.<ref>{{cite journal | vauthors = Liu C, Chen Y, Kang Y, Ni Z, Xiu H, Guan J, Liu K | title = 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 | journal = The Journal of Pharmacology and Experimental Therapeutics | volume = 339 | issue = 1 | pages = 203–209 | date = October 2011 | pmid = 21737535 | doi = 10.1124/jpet.111.184796 | s2cid = 1892149 }}</ref>

At high doses, it may be used to prevent rejection following an organ transplant.<ref name=AHFS2018/>

== Side effects ==
[[File:Periportal hepatosteatosis intermed mag.jpg|thumb|[[Micrograph]] of [[fatty liver]], as may be seen due to long-term prednisone use. [[Trichrome stain]].]]

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.<ref name=":0">{{Cite news|url=http://www.mayoclinic.org/steroids/art-20045692?pg=2|title=Prednisone and other corticosteroids: Balance the risks and benefits |publisher=Mayo Clinic|access-date=7 April 2017}}</ref> 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 (mood)|depression]] or depressive symptoms and [[anxiety]] in some individuals.<ref>{{cite web | url = https://www.drugs.com/prednisone.html | title = Prednisone Information | work = Drugs.com }}</ref><ref>{{cite web | url = https://www.medlineplus.gov/druginfo/meds/a601102.html#side-effects | title = Prednisone | work = MedlinePlus Drug Information }}</ref>

Long-term side effects include [[Cushing's syndrome]], [[steroid dementia syndrome]],<ref name="WolkowitzLupien2007">{{cite journal | vauthors = Wolkowitz OM, Lupien SJ, Bigler ED | title = The "steroid dementia syndrome": a possible model of human glucocorticoid neurotoxicity | journal = Neurocase | volume = 13 | issue = 3 | pages = 189–200 | date = June 2007 | pmid = 17786779 | doi = 10.1080/13554790701475468 | s2cid = 39340010 }}</ref> [[torso|truncal]] weight gain, [[glaucoma]] and [[cataracts]], diabetes mellitus [[Diabetes mellitus type 2|type 2]], and [[Depression (mood)|depression]] upon dose reduction or cessation.<ref>{{Cite news |url= https://www.betterhealth.vic.gov.au/health/healthyliving/steroids |title=Steroids | date = April 2016 | publisher = Australian Department of Health & Human Services |access-date=14 June 2018 }}</ref> Long-term steroids can also increase the risk of [[osteoporosis]], but research has found that few of these people were taking medications to protect bones.<ref>{{Cite journal |date=21 June 2022 |title=Polymyalgia rheumatica: treatment reviews are needed |url=https://evidence.nihr.ac.uk/alert/polymyalgia-rheumatica-treatment-reviews-and-falls-assessment/ |access-date=5 August 2022 |website=NIHR Evidence |doi=10.3310/nihrevidence_51304 |s2cid=251774691 |language=en-GB|url-access=subscription }}</ref><ref name="pmid34988356">{{cite journal | vauthors = Sokhal BS, Hider SL, Paskins Z, Mallen CD, Muller S | title = Fragility fractures and prescriptions of medications for osteoporosis in patients with polymyalgia rheumatica: results from the PMR Cohort Study | journal = Rheumatology Advances in Practice | volume = 5 | issue = 3 | article-number = rkab094 | date = 2021 | pmid = 34988356 | pmc = 8712242 | doi = 10.1093/rap/rkab094 }}</ref> Prednisone also results in [[leukocytosis]].<ref>{{cite book | vauthors = Miller NR, Walsh FB, Hoyt WF |title=Walsh and Hoyt's Clinical Neuro-ophthalmology |date=2005 |publisher=Lippincott Williams & Wilkins |isbn=9780781748117 |page=1062 |url=https://books.google.com/books?id=9RA2ZOPRuhgC&pg=PA1062 }}</ref>

=== Major ===
'''Source:'''<ref name=":0" />
{{div col}}
* Steroid myopathy
* Increased blood sugar for individuals with diabetes
* Difficulty in regulating emotion
* Difficulty in maintaining linear thinking
* [[Weight gain]] due to increased appetite
* Immunosuppression
* [[Corticosteroid-induced lipodystrophy]] ([[moon face]], [[central obesity]])
* [[Depression (mood)|Depression]], [[mania]], [[psychosis]], or other psychiatric symptoms
* Unusual [[Fatigue (physical)|fatigue]] or [[weakness]]
* [[Mental confusion]]
* Memory and attention dysfunction ([[steroid dementia syndrome]])
* Muscle atrophy<ref>{{cite journal | vauthors = Schakman O, Gilson H, Kalista S, Thissen JP | title = Mechanisms of muscle atrophy induced by glucocorticoids | journal = Hormone Research | volume = 72 | issue = Suppl 1 | pages = 36–41 | date = November 2009 | pmid = 19940494 | doi = 10.1159/000229762 | s2cid = 21997662 }}</ref>
* [[Blurred vision]]
* [[Abdominal pain]]
* [[Peptic ulcer]]
* Painful [[Hip (anatomy)|hips]] or [[shoulders]]
* [[Steroid-induced osteoporosis]]
* [[Stretch marks]]
* [[Osteonecrosis]] – same as avascular necrosis
* Insomnia
* Severe [[joint pain]]
* [[Cataracts]] or [[glaucoma]]
* [[Anxiety]]
* [[Melena|Black stool]]
* [[Abdominal pain|Stomach pain]] or [[bloating]]
* Severe [[Swelling (medical)|swelling]]
* [[Mouth sores]] or [[dry mouth]]
* [[Avascular necrosis]]
* [[Hepatic steatosis]]
* [[Hiccups]] and [[burping]]
* Weakening and breakage of [[tendons]]
{{div col end}}

=== Minor ===
'''Source:'''<ref name=":0" />
{{div col|colwidth=15em}}
* [[anxiety|Nervousness]]
* [[acne vulgaris|Acne]]
* [[Skin rash]]
* [[Appetite]] gain
* [[Hyperactivity]]
* Increased [[thirst]]
* [[Frequent urination]]
* [[Diarrhea]]
* Reduced [[intestinal flora]]
* Leg pain/cramps
* Sensitive teeth
* Headache
* Induced vomiting
{{div col end}}

=== Dependency ===
[[Adrenal gland|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 is short but may take weeks or months<ref>{{Cite news |url=https://www.medicinenet.com/steroid_withdrawal/article.htm |title=Steroid Drug Withdrawal Symptoms, Treatment & Prognosis |work=MedicineNet |access-date=14 June 2018 }}</ref> if the patient had been on long-term treatment. Abrupt withdrawal may lead to an [[Adrenal crisis|Addisonian crisis]]. For those on chronic therapy, alternate-day dosing may preserve adrenal function and thereby reduce side effects.<ref>{{cite web |url=http://www.uspharmacist.com/NewLook/CE/glucocort/lesson.htm |title=Therapeutic and Adverse Effects of Glucocorticoids | vauthors = Bello CS, Garrett SD |work=U.S. Pharmacist Continuing Education Program |archive-url=https://web.archive.org/web/20080711145809/http://www.uspharmacist.com/NewLook/CE/glucocort/lesson.htm |archive-date=11 July 2008}}</ref>

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.

Prednisone may start to result in the suppression of the [[Hypothalamic–pituitary–adrenal axis|hypothalamic–pituitary–adrenal (HPA) axis]] if used at doses 7–10&nbsp;mg or higher for several weeks. This is approximately equal to the amount of endogenous cortisol produced by the body every day. As such, the HPA axis starts to become suppressed and [[atrophy]]. If this occurs the patient should be tapered off prednisone slowly to give the adrenal gland enough time to regain its function and endogenous production of steroids.

=== Withdrawal ===
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 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&nbsp;mg prednisone (or equivalent) daily for more than one week
* been given repeat doses in the evening
* received more than three weeks of treatment
* recently received repeated courses (particularly if taken for longer than three weeks)
* taken a short course within one 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 who have received treatment for three 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&nbsp;mg daily) and then reduced more slowly. Assessment of the disease may be needed during withdrawal to ensure that relapse does not occur.<ref>{{Cite journal | vauthors = Iliopoulou A, Abbas A, Murray R |date=19 May 2013 |title=How to manage withdrawal of glucocorticoid therapy |journal=Prescriber |volume=24 |issue=10 |pages=23–29 |doi=10.1002/psb.1060|s2cid=72082017 }}</ref>

==Pharmacology==
{{see also|Glucocorticoid#Pharmacology}}
Prednisone is a synthetic glucocorticoid used for its anti-inflammatory and immunosuppressive properties.<ref>{{cite journal | vauthors = Becker DE | title = Basic and clinical pharmacology of glucocorticosteroids | journal = Anesthesia Progress | volume = 60 | issue = 1 | pages = 25–31; quiz 32 | date =Spring 2013 | pmid = 23506281 | pmc = 3601727 | doi = 10.2344/0003-3006-60.1.25 }}</ref><ref name="drugbank">{{cite web |title=Prednisone |url=https://www.drugbank.ca/drugs/DB00635 |website=DrugBank |access-date=29 January 2019}}</ref> Prednisone is a prodrug; it is metabolised in the liver by [[11β-Hydroxysteroid dehydrogenase|11-β-HSD]] to prednisolone, the active drug. Prednisone has no substantial biological effects until converted via hepatic metabolism to [[prednisolone]].<ref>{{Cite web |url=https://medlineplus.gov/druginfo/meds/a601102.html |title=Prednisone |work=MedlinePlus |publisher=NIH U.S. National Library of Medicine}}</ref>

===Pharmacokinetics===
Prednisone is absorbed in the gastrointestinal tract and has a half-life of 2–3 hours.<ref name="drugbank"/> It has a volume of distribution of 0.4–1&nbsp;L/kg.<ref name="SchijvensAM">{{cite journal | vauthors = Schijvens AM, Ter Heine R, de Wildt SN, Schreuder MF | title = Pharmacology and pharmacogenetics of prednisone and prednisolone in patients with nephrotic syndrome | journal = Pediatric Nephrology | volume = 34 | issue = 3 | pages = 389–403 | date = March 2019 | pmid = 29549463 | pmc = 6349812 | doi = 10.1007/s00467-018-3929-z | doi-access = free }}</ref> The drug is cleared by hepatic metabolism using [[cytochrome P450]] enzymes. Metabolites are excreted in the bile and urine.<ref name="SchijvensAM"/>

===Lodotra===
"Lodotra" is the brand name of an oral formulation, which releases prednisone four hours after ingestion. It is indicated for rheumatoid arthritis with morning stiffness. Taken at 10&nbsp;p.m., it releases the drug at around&nbsp;2 a.m. The plasmic peak level is reached at 4&nbsp;a.m., which is considered to be the optimal time for relieving morning stiffness. The drug was approved in the [[European Union]], in January 2009.<ref>{{cite web|url=http://www.nelm.nhs.uk/en/NeLM-Area/News/2009---January/08/Delayed-release-prednisone-Lodotra-approved-in-EU-for-treatment-of-rheumatoid-arthritis/|title=Delayed-release prednisone (Lodotra™) approved in EU for treatment of rheumatoid arthritis|vauthors=Wan Y|date=8 January 2009|access-date=22 November 2009|archive-date=9 July 2009|archive-url=https://web.archive.org/web/20090709195015/http://www.nelm.nhs.uk/en/NeLM-Area/News/2009---January/08/Delayed-release-prednisone-Lodotra-approved-in-EU-for-treatment-of-rheumatoid-arthritis/|url-status=dead}}</ref><ref>{{cite journal | vauthors = Buttgereit F, Doering G, Schaeffler A, Witte S, Sierakowski S, Gromnica-Ihle E, Jeka S, Krueger K, Szechinski J, Alten R | title = Efficacy of modified-release versus standard prednisone to reduce duration of morning stiffness of the joints in rheumatoid arthritis (CAPRA-1): a double-blind, randomised controlled trial | journal = Lancet | volume = 371 | issue = 9608 | pages = 205–214 | date = January 2008 | pmid = 18207016 | doi = 10.1016/S0140-6736(08)60132-4 | s2cid = 6197980 }}</ref>

==Industry==
[[File:006035339lg Prednisone 20 MG Oral Tablet.jpg|thumb|Prednisone 20&nbsp;mg oral tablet]]
The pharmaceutical industry uses prednisone tablets for the [[calibration]] of [[dissolution testing]] equipment according to the [[United States Pharmacopeia]] (USP).

==Chemistry==
Prednisone is a [[synthetic compound|synthetic]] [[pregnane]] [[corticosteroid]] and [[chemical derivative|derivative]] of [[cortisone]] and is also known as δ<sup>1</sup>-cortisone or 1,2-dehydrocortisone or as 17α,21-dihydroxypregna-1,4-diene-3,11,20-trione.<ref name="Elks2014">{{cite book| vauthors = Elks J |title=The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies|url=https://books.google.com/books?id=0vXTBwAAQBAJ&pg=PA1013|date=14 November 2014|publisher=Springer|isbn=978-1-4757-2085-3|pages=1013–}}</ref><ref name="IndexNominum2000">{{cite book|title=Index Nominum 2000: International Drug Directory|url=https://books.google.com/books?id=5GpcTQD_L2oC&pg=PA871|date=January 2000|publisher=Taylor & Francis|isbn=978-3-88763-075-1|pages=871–}}</ref>

==History==
The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by [[Arthur Nobile]].<ref>{{cite journal | vauthors = Wainwright M | title = The secret of success: Arthur Nobile's discovery of the steroids prednisone and prednisolone in the 1950s revolutionised the treatment of arthritis | journal = Chemistry in Britain | volume = 34 | issue = 1 | date = 1998 | pages = 46 | oclc = 106716069 }}</ref><ref>{{cite web| title = Inventor Profile: Arthur Nobile |work = National Inventors Hall of Fame|url= http://www.invent.org/hall_of_fame/355.html |url-status=dead |archive-url= https://web.archive.org/web/20120612062323/http://www.invent.org/hall_of_fame/355.html |archive-date=12 June 2012}}</ref><ref>{{cite web | title = Arthur Nobile | work=New Jersey Inventors Hall of Fame |url= http://www.stevens.edu/njinvent/2000/inductees_2000/nobile.html |url-status=dead |archive-url=https://web.archive.org/web/20110901232600/http://www.stevens.edu/njinvent/2000/inductees_2000/nobile.html | archive-date = 1 September 2011}}</ref> The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became [[Schering-Plough|Schering-Plough Corporation]], by Arthur Nobile and coworkers.<ref>{{cite book | title = Merck Index | edition = 14th | page = 1327 | date = 2006 | publisher = Merck & Co. Inc | isbn = 978-0-911910-00-1 }}</ref> 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]].<ref name="Herzog_1955">{{cite journal | vauthors = Herzog HL, Nobile A, Tolksdorf S, Charney W, Hershberg EB, Perlman PL | title = New antiarthritic steroids | journal = Science | volume = 121 | issue = 3136 | pages = 176 | date = February 1955 | pmid = 13225767 | doi = 10.1126/science.121.3136.176 | bibcode = 1955Sci...121..176H }}</ref>

The enhanced adrenocorticoid activity of these compounds over cortisone and hydrocortisone was demonstrated in mice.<ref name="Herzog_1955" />

Prednisone and prednisolone were introduced in 1955 by Schering and Upjohn, under the brand names Meticorten<ref>{{cite web | title = Meticorten: FDA-Approved Drugs | work = U.S. [[Food and Drug Administration]] (FDA) | url = https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=009766 | archive-url = https://web.archive.org/web/20170430051138/https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=009766 | url-status = dead | archive-date = 30 April 2017 }}</ref> and Delta-Cortef,<ref>{{cite web | title = Delta-Cortef: FDA-Approved Drugs | work = U.S. [[Food and Drug Administration]] (FDA) | url = https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=009987 }}</ref> respectively.

== References ==
{{Reflist}}

{{Glucocorticoids}}
{{Antidiarrheals, intestinal anti-inflammatory/anti-infective agents}}
{{Orexigenics}}
{{Glucocorticoid receptor modulators}}
{{Mineralocorticoid receptor modulators}}
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{{Authority control}}

[[Category:Anti-asthmatic agents]]
[[Category:Appetite stimulants]]
[[Category:CYP3A4 inducers]]
[[Category:Glucocorticoids]]
[[Category:Mineralocorticoids]]
[[Category:Prodrugs]]
[[Category:Triketones]]
[[Category:World Health Organization essential medicines]]
[[Category:Wikipedia medicine articles ready to translate]]