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Prednisone is a medication mostly used to suppress the immune system and decrease in conditions such as , , and rheumatologic diseases. It is also used to treat high blood calcium due to and adrenal insufficiency along with other . It is taken by mouth.

Common side effects may include , , easy , muscle weakness, and . Other side effects include weight gain, swelling, high blood sugar, increased risk of infection, and .

(2025). 9781259584732, McGraw-Hill Education.
It is generally considered safe in and low doses appear to be safe while the user is . After prolonged use, prednisone must be stopped gradually.

Prednisone is a and must be converted to by the liver before it becomes active. Prednisolone then binds to glucocorticoid receptors, activating them and triggering changes in .

Prednisone was patented in 1954 and approved for medical use in the United States in 1955.

(2025). 9783527607495, John Wiley & Sons. .
It is on the World Health Organization's List of Essential Medicines. It is available as a generic medication. In 2022, it was the 30th most commonly prescribed medication in the United States, with more than 18million prescriptions.


Medical uses
Prednisone is used for many different autoimmune diseases and inflammatory conditions, including , , , , rheumatic disorders, disorders, ulcerative colitis and Crohn's disease, granulomatosis with polyangiitis, adrenocortical insufficiency, due to cancer, , , severe , , , lipid pneumonitis, , multiple sclerosis, nephrotic syndrome, , to relieve the effects of , , myasthenia gravis, exposure, Ménière's disease, autoimmune hepatitis, giant cell arteritis, the Herxheimer reaction that is common during the treatment of , Duchenne muscular dystrophy, , and as part of a drug regimen to prevent rejection after .

Prednisone has also been used in the treatment of headaches and and for severe .

(2025). 9781607951773, PMPH USA. .
Prednisone is used as an .

Prednisone is often also prescribed as a form of treatment for sudden sensorineural hearing loss (SSNHL).

Prednisone can be used in the treatment of decompensated to increase renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large doses of loop diuretics. In terms of the mechanism of action for this purpose: prednisone, a glucocorticoid, can improve renal responsiveness to atrial peptide by increasing the density of natriuretic peptide receptor type A in the renal inner medullary collecting duct, thereby inducing a potent diuresis.

At high doses, it may be used to prevent rejection following an organ transplant.


Side effects
Short-term side effects, as with all glucocorticoids, include high blood levels (especially in patients with diabetes mellitus or on other medications that increase blood glucose, such as ) and mineralocorticoid effects such as fluid retention. 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 in some individuals.

Long-term side effects include Cushing's syndrome, steroid dementia syndrome, weight gain, and , diabetes mellitus type 2, and depression upon dose reduction or cessation. Long-term steroids can also increase the risk of , but research has found that few of these people were taking medications to protect bones. Prednisone also results in .

(2025). 9780781748117, Lippincott Williams & Wilkins. .


Major
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Minor
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Dependency
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 if the patient had been on long-term treatment. Abrupt withdrawal may lead to an . For those on chronic therapy, alternate-day dosing may preserve adrenal function and thereby reduce side effects.

Glucocorticoids act to inhibit feedback of both the , decreasing corticotropin-releasing hormone (CRH), and 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 (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 and . 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 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 mg daily) and then reduced more slowly. Assessment of the disease may be needed during withdrawal to ensure that relapse does not occur.


Pharmacology
Prednisone is a synthetic glucocorticoid used for its anti-inflammatory and immunosuppressive properties. Prednisone is a prodrug; it is metabolised in the liver by 11-β-HSD to prednisolone, the active drug. Prednisone has no substantial biological effects until converted via hepatic metabolism to .


Pharmacokinetics
Prednisone is absorbed in the gastrointestinal tract and has a half-life of 2–3 hours. It has a volume of distribution of 0.4–1 L/kg. The drug is cleared by hepatic metabolism using cytochrome P450 enzymes. Metabolites are excreted in the bile and urine.


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 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 the , in January 2009.


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


Chemistry
Prednisone is a synthetic and derivative of and is also known as δ1-cortisone or 1,2-dehydrocortisone or as 17α,21-dihydroxypregna-1,4-diene-3,11,20-trione.
(2014). 9781475720853, Springer. .
(2000). 9783887630751, Taylor & Francis. .


History
The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by . The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became , by Arthur Nobile and coworkers.
(2025). 9780911910001, Merck & Co. Inc.
They discovered that could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. The same process was used to prepare from .

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

Prednisone and prednisolone were introduced in 1955 by Schering and Upjohn, under the brand names Meticorten and Delta-Cortef, respectively.

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