Prednisone is a glucocorticoid prodrug that is converted by 11beta-hydroxysteroid dehydrogenase in the liver into the active form, prednisolone. It is used to treat certain inflammatory diseases (such as severe allergic reactions) and (at higher doses) some types of cancer, but has many significant adverse effects. It is usually taken orally but can be delivered by intramuscular injection or intravenous injection.
Prednisone is used for many different indications including: asthma, COPD, CIDP, rheumatic disorders, allergic disorders, ulcerative colitis and Crohn’s disease, adrenocortical insufficiency, hypercalcemia due to cancer, thyroiditis, laryngitis, severe tuberculosis, lipid pneumonitis, multiple sclerosis, nephrotic syndrome, myasthenia gravis, and as part of a drug regimen to prevent rejection post 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. Prednisone 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 is also used for the treatment of the Herxheimer reaction, which is common during the treatment of syphilis, and to delay the onset of symptoms of Duchenne muscular dystrophy and also for Uveitis. The mechanism for the delay of symptoms is unknown. Because it suppresses the adrenals, it is also sometimes used in the treatment of congenital adrenal hyperplasia. Prednisone is also used to treat sarcoidosis and lupus.
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. It is worth noting, however, that the mineralocorticoid effects of prednisone are very minor; this is why it is not used in the management of adrenal insufficiency, unless a more potent mineralocorticoid is administered concomitantly.
Additional short-term side-effects can include insomnia, euphoria and, rarely, mania (in particular, in those suffering from Bipolar disorders I and II). It can also cause depression or depressive symptoms and anxiety in some individuals.
Long-term side-effects include Cushing’s syndrome, truncal weight gain, osteoporosis, glaucoma and cataracts, type II diabetes mellitus, and depression upon dose reduction or cessation.
- Increased blood sugar for diabetics
- Difficulty controlling emotion
- Difficulty in maintaining train of thought
- Weight gain
- Facial swelling
- Depression, mania, psychosis, or other psychiatric symptoms
- Unusual fatigue or weakness
- Mental confusion / indecisiveness
- Blurred vision
- Abdominal pain
- Peptic ulcer
- Painful hips or shoulders
- Steroid-induced osteoporosis
- Stretch marks
- Long-term migraines
- Severe joint pain
- Cataracts or glaucoma
- Black stool
- Stomach pain or bloating
- Severe swelling
- Mouth sores or dry mouth
- Avascular necrosis
- Hepatic steatosis
- Increased appetite
- Frequent urination
- Removes intestinal flora
- Leg pain/cramps
- Sensitive teeth
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 was short, but may take weeks or months if the patient had been on long-term treatment. Abrupt withdrawal may lead to an Addisonian crisis. 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 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 very 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.