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| Clinical data | |
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| Trade names | Deltasone, Liquid Pred, Orasone, others |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a601102 |
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| Routes of administration | By mouth |
| Drug class | Glucocorticoid |
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| Pharmacokinetic data | |
| Bioavailability | 70% |
| Metabolism | prednisolone (liver) |
| Eliminationhalf-life | 3 to 4 hours in adults. 1 to 2 hours in children[2] |
| Excretion | Kidney |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.000.147 |
| Chemical and physical data | |
| Formula | C21H26O5 |
| Molar mass | 358.434 g·mol−1 |
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Prednisone is aglucocorticoid medication mostly used tosuppress the immune system and decreaseinflammation in conditions such asasthma,COPD, andrheumatologic diseases.[3] It is also used to treathigh blood calcium due tocancer andadrenal insufficiency along with othercorticosteroids.[3] It is takenby mouth.[3]
Common side effects may includecataracts,bone loss, easybruising, muscle weakness, andthrush.[3] Other side effects include weight gain, swelling,high blood sugar, increased risk of infection, andpsychosis.[3][4] It is generally considered safe inpregnancy and low doses appear to be safe while the user isbreastfeeding.[5] After prolonged use, prednisone must be stopped gradually.[3]
Prednisone is aprodrug and must be converted toprednisolone by the liver before it becomes active.[6][7] Prednisolone then binds toglucocorticoid receptors, activating them and triggering changes ingene expression.[4] These changes inhibit function and decrease the number of keyleukocytes in the bloodstream.[8]
Prednisone was patented in 1954 and approved for medical use in the United States in 1955.[3][9] Prednisone is a therapeutic alternative on theWorld Health Organization's List of Essential Medicines.[10] It is available as ageneric medication.[3] In 2023, it was the 38th most commonly prescribed medication in the United States, with more than 15 million prescriptions.[11][12]
Prednisone is used for many differentautoimmune diseases and inflammatory conditions, includingasthma,gout,COPD,CIDP,rheumatic disorders,allergic disorders,ulcerative colitis andCrohn's disease,granulomatosis with polyangiitis,adrenocortical insufficiency,hypercalcemia due to cancer,thyroiditis,laryngitis, severetuberculosis,hives,eczema,lipid pneumonitis,pericarditis,multiple sclerosis,nephrotic syndrome,sarcoidosis, to relieve the effects ofshingles,lupus,myasthenia gravis,poison oak exposure,Ménière's disease,autoimmune hepatitis,giant cell arteritis, theHerxheimer reaction that is common during the treatment ofsyphilis,Duchenne muscular dystrophy,uveitis, and as part of a drug regimen to prevent rejection afterorgan transplant.[13][14][3]
Prednisone has also been used in the treatment ofmigraine headaches andcluster headaches and for severeaphthous ulcer.[15] Prednisone is used as anantitumor drug.[16]
Prednisone is often also prescribed as a form of treatment for suddensensorineural hearing loss (SSNHL).[17]
Prednisone can be used in the treatment of decompensatedheart failure to increase renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large doses of loop diuretics.[18][19][20][21][22][23] In terms of the mechanism of action for this purpose: prednisone, a glucocorticoid, can improve renal responsiveness to atrialnatriuretic peptide by increasing the density of natriuretic peptide receptor type A in the renal inner medullary collecting duct, thereby inducing a potent diuresis.[24]
At high doses, it may be used to prevent rejection following an organ transplant.[3]
Short-term side effects, as with all glucocorticoids, include high bloodglucose levels (especially in patients withdiabetes mellitus or on other medications that increase blood glucose, such astacrolimus) andmineralocorticoid effects such as fluid retention.[25] 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 causedepression or depressive symptoms andanxiety in some individuals.[26][27]
Long-term side effects includeCushing's syndrome,steroid dementia syndrome,[28]truncal weight gain,glaucoma andcataracts, diabetes mellitustype 2, anddepression upon dose reduction or cessation.[29] Long-term steroids can also increase the risk ofosteoporosis, but research has found that few of these people were taking medications to protect bones.[30][31] Prednisone also results inleukocytosis.[32]
Source:[25]
Source:[25]
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[34] if the patient had been on long-term treatment. Abrupt withdrawal may lead to anAddisonian crisis. For those on chronic therapy, alternate-day dosing may preserve adrenal function and thereby reduce side effects.[35]
Glucocorticoids act to inhibit feedback of both thehypothalamus, decreasingcorticotropin-releasing hormone (CRH), andcorticotrophs in theanterior pituitary gland, decreasing the amount ofadrenocorticotropic 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 thehypothalamic–pituitary–adrenal (HPA) axis if used at doses 7–10 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 andatrophy. 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.
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:
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 mg daily) and then reduced more slowly. Assessment of the disease may be needed during withdrawal to ensure that relapse does not occur.[36]
Prednisone is a synthetic glucocorticoid used for its anti-inflammatory and immunosuppressive properties.[37][38] Prednisone is a prodrug; it is metabolised in the liver by11-β-HSD to prednisolone, the active drug. Prednisone has no substantial biological effects until converted via hepatic metabolism toprednisolone.[39]
Prednisone is absorbed in the gastrointestinal tract and has a half-life of 2–3 hours.[38] It has a volume of distribution of 0.4–1 L/kg.[40] The drug is cleared by hepatic metabolism usingcytochrome P450 enzymes. Metabolites are excreted in the bile and urine.[40]
"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 p.m., it releases the drug at around 2 a.m. The plasmic peak level is reached at 4 a.m., which is considered to be the optimal time for relieving morning stiffness. The drug was approved in theEuropean Union, in January 2009.[41][42]
The pharmaceutical industry uses prednisone tablets for thecalibration ofdissolution testing equipment according to theUnited States Pharmacopeia (USP).
Prednisone is asyntheticpregnanecorticosteroid andderivative ofcortisone and is also known as δ1-cortisone or 1,2-dehydrocortisone or as 17α,21-dihydroxypregna-1,4-diene-3,11,20-trione.[43][44]
The first isolation and structure identifications of prednisone and prednisolone were done in 1950 byArthur Nobile.[45][46][47] The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later becameSchering-Plough Corporation, by Arthur Nobile and coworkers.[48] They discovered thatcortisone could be microbiologically oxidized to prednisone by the bacteriumCorynebacterium simplex. The same process was used to prepareprednisolone fromhydrocortisone.[49]
The enhanced adrenocorticoid activity of these compounds over cortisone and hydrocortisone was demonstrated in mice.[49]
Prednisone and prednisolone were introduced in 1955 by Schering and Upjohn, under the brand names Meticorten[50] and Delta-Cortef,[51] respectively.
