Prednisone
Prednisone is a glucocorticoid medication mostly used to suppress the immune system and decrease inflammation in conditions such as asthma, COPD, and rheumatologic diseases. It is also used to treat high blood calcium due to cancer and adrenal insufficiency along with other steroids. It is taken by mouth.
Common side effects with long term use include cataracts, bone loss, easy bruising, muscle weakness, and thrush. Other side effects include weight gain, swelling, high blood sugar, increased risk of infection, and psychosis. It is generally considered safe in pregnancy and low doses appear to be safe when breastfeeding. After prolonged use, prednisone needs to be stopped gradually.
Prednisone must be converted to prednisolone by the liver before it becomes active. Prednisolone then binds to glucocorticoid receptors, activating them and triggering changes in gene expression.
Prednisone was patented in 1954 and approved for medical use in the United States in 1955. It is available as a generic medication. In 2017, it was the 22nd most commonly prescribed medication in the United States, with more than 25 million prescriptions.
Medical uses
Prednisone is used for many different autoimmune diseases 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, hives, 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.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. It 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 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 dose of loop diuretics. In terms of the mechanism of action for this purpose: prednisone, 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, thereby inducing a potent diuresis.
At high doses it may be used to prevent rejection following organ transplant.
Side effects
Short-term side effects, as with all glucocorticoids, include high blood glucose levels 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 anxiety in some individuals.
Long-term side effects include Cushing's syndrome, steroid dementia syndrome, truncal weight gain, osteoporosis, glaucoma and cataracts, diabetes mellitus type 2, and depression upon dose reduction or cessation. Prednisone also results in leukocytosis.
Major
- Steroid myopathy
- Increased blood sugar for individuals with diabetes
- Difficulty controlling emotion
- Difficulty in maintaining train of thought
- Weight gain
- Immunosuppression
- Corticosteroid-induced lipodystrophy
- Depression, mania, psychosis, or other psychiatric symptoms
- Unusual fatigue or weakness
- Mental confusion / indecisiveness
- Memory and attention dysfunction
- Muscle atrophy
- Blurred vision
- Abdominal pain
- Peptic ulcer
- Painful hips or shoulders
- Steroid-induced osteoporosis
- Stretch marks
- Osteonecrosis – same as avascular necrosis
- Insomnia
- Severe joint pain
- Cataracts or glaucoma
- Anxiety
- Black stool
- Stomach pain or bloating
- Severe swelling
- Mouth sores or dry mouth
- Avascular necrosis
- Hepatic steatosis
Minor
- Nervousness
- Acne
- Skin rash
- Appetite gain
- Hyperactivity
- Increased thirst
- Frequent urination
- Diarrhea
- Reduced intestinal flora
- Leg pain/cramps
- Sensitive teeth
- Headache
- Induced vomiting
Dependency
Glucocorticoids act to inhibit feedback of both the hypothalamus, decreasing corticotropin-releasing hormone, and corticotrophs in the anterior pituitary gland, decreasing the amount of adrenocorticotropic hormone. 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 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 atrophy. If this occurs the people should be tapered off prednisone slowly to give the adrenal gland enough time to regain its function and endogenous production of steroids. Supplemental doses, or "stress doses" may be required in those with HPA axis suppression who are experiencing a higher degree of stress. Failing to do so in such situations could be life-threatening.
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 daily for more than 1 week
- been given repeat doses in the evening
- received more than 3 weeks of treatment
- recently received repeated courses
- taken a short course within 1 year of stopping long-term therapy
- other possible causes of adrenal suppression
During corticosteroid withdrawal, the dose may be reduced rapidly down to physiological doses 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 prednisolone.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.Industry
The pharmaceutical industry uses prednisone tablets for the calibration of dissolution testing equipment according to the United States Pharmacopeia.Chemistry
Prednisone is a synthetic pregnane corticosteroid and derivative of cortisone and is also known as δ1-cortisone or 1,2-dehydrocortisone or as 17α,21-dihydroxypregna-1,4-diene-3,11,20-trione.History
The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by Arthur Nobile. 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. 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.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. These prescription medicines are now available from a number of manufacturers as generic drugs.