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Medication Safety Issues
Sound-alike/look-alike issues:
PredniSONE may be confused with methylPREDNISolone, Pramosone®, prazosin, prednisoLONE, Prilosec®, primidone, promethazine
Pronunciation
(PRED ni sone)
U.S. Brand Names
Index Terms
Generic Available
Yes
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Treatment of a variety of diseases including adrenocortical insufficiency, hypercalcemia, rheumatic, and collagen disorders; dermatologic, ocular, respiratory, gastrointestinal, and neoplastic diseases; organ transplantation and a variety of diseases including those of hematologic, allergic, inflammatory, and autoimmune in origin; not available in injectable form, prednisolone must be used
Use: Dental
Treatment of a variety of oral diseases of allergic, inflammatory, or autoimmune origin
Use: Unlabeled/Investigational
Investigational: Prevention of postherpetic neuralgia and relief of acute pain in the early stages
Pregnancy Considerations
Crosses the placenta. Immunosuppression reported in 1 infant exposed to high-dose prednisone plus azathioprine throughout gestation. One report of congenital cataracts. Available evidence suggests safe use during pregnancy.
Lactation
Enters breast milk/compatible
Breast-Feeding Considerations
Crosses into breast milk. No data on clinical effects on the infant. AAP considers compatible with breast-feeding.
Contraindications
Hypersensitivity to prednisone or any component of the formulation; serious infections, except tuberculous meningitis; systemic fungal infections; varicella
Warnings/Precautions
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercorticism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully. Particular care is required when patients are transferred from systemic corticosteroids to inhaled products due to possible adrenal insufficiency or withdrawal from steroids, including an increase in allergic symptoms. Patients receiving >20 mg per day of prednisone (or equivalent) may be most susceptible. Fatalities have occurred due to adrenal insufficiency in asthmatic patients during and after transfer from systemic corticosteroids to aerosol steroids; aerosol steroids do not provide the systemic steroid needed to treat patients having trauma, surgery, or infections.
• Immunosuppression: Prolonged use of corticosteroids may also increase the incidence of secondary infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to vaccines. Exposure to chickenpox should be avoided; corticosteroids should not be used to treat ocular herpes simplex. Corticosteroids should not be used for cerebral malaria or viral hepatitis. Close observation is required in patients with latent tuberculosis and/or TB reactivity; restrict use in active TB (only in conjunction with antituberculosis treatment).
• Kaposi's sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi's sarcoma (case reports); if noted, discontinuation of therapy should be considered.
• Myopathy: Acute myopathy has been reported with high dose corticosteroids, usually in patients with neuromuscular transmission disorders; may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed.
• Psychiatric disturbances: Corticosteroid use may cause psychiatric disturbances, including depression, euphoria, insomnia, mood swings, and personality changes. Pre-existing psychiatric conditions may be exacerbated by corticosteroid use.
Disease-related concerns:
• Cardiovascular disease: Use with caution in patients with HF; long-term use has been associated with fluid retention and hypertension.
• Diabetes: Use with caution in patients with diabetes mellitus; may alter glucose production/regulation leading to hyperglycemia.
• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, peptic ulcer, ulcerative colitis) due to perforation risk.
• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.
• Myasthenia gravis: Use with caution in patients with myasthenia gravis; exacerbation of symptoms has occurred especially during initial treatment with corticosteroids.
• Myocardial infarction (MI): Use with caution following acute MI; corticosteroids have been associated with myocardial rupture.
• Osteoporosis: Use with caution in patients with osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.
• Renal impairment: Use with caution in patients with renal impairment; fluid retention may occur.
• Seizure disorders: Use with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid ones.
Special populations:
• Elderly: Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly in the smallest possible effective dose for the shortest duration.
• Pediatrics: May affect growth velocity; growth should be routinely monitored in pediatric patients.
Other warnings/precautions:
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
Adverse Reactions
>10%:
Central nervous system: Insomnia, nervousness
Gastrointestinal: Increased appetite, indigestion
1% to 10%:
Dermatologic: Hirsutism
Endocrine & metabolic: Diabetes mellitus, glucose intolerance, hyperglycemia
Neuromuscular & skeletal: Arthralgia
Ocular: Cataracts, glaucoma
Respiratory: Epistaxis
<1%: Edema, hypertension, vertigo, seizure, psychoses, pseudotumor cerebri, headache, mood swings, delirium, hallucinations, euphoria, acne, skin atrophy, bruising, hyperpigmentation, Cushing's syndrome, pituitary-adrenal axis suppression, growth suppression, glucose intolerance, hypokalemia, alkalosis, amenorrhea, sodium and water retention, hyperglycemia, peptic ulcer, nausea, vomiting, abdominal distention, ulcerative esophagitis, pancreatitis, muscle weakness, osteoporosis, fractures, muscle wasting, hypersensitivity reactions
Metabolism/Transport Effects
Substrate of CYP3A4 (minor); Induces CYP2C19 (weak), 3A4 (weak)
Drug Interactions
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Aminoglutethimide: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Risk C: Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Risk D: Consider therapy modification
Antidiabetic Agents: Corticosteroids (Systemic) may diminish the hypoglycemic effect of Antidiabetic Agents. In some instances, corticosteroid-mediated HPA axis suppression has led to episodes of acute adrenal crisis, which may manifest as enhanced hypoglycemia, particularly in the setting of insulin or other antidiabetic agent use. Risk C: Monitor therapy
Antifungal Agents (Azole Derivatives, Systemic): May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Aprepitant: May increase the serum concentration of Corticosteroids (Systemic). Risk D: Consider therapy modification
Barbiturates: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Calcitriol: Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol. Risk C: Monitor therapy
Calcium Channel Blockers (Nondihydropyridine): May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Corticorelin: Corticosteroids may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor therapy
CycloSPORINE: Corticosteroids (Systemic) may increase the serum concentration of CycloSPORINE. CycloSPORINE may increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Echinacea: May diminish the therapeutic effect of Immunosuppressants. Risk D: Consider therapy modification
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Fluconazole: May decrease the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Fosaprepitant: May increase the serum concentration of Corticosteroids (Systemic). The active metabolite aprepitant is likely responsible for this effect. Risk D: Consider therapy modification
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Macrolide Antibiotics: May decrease the metabolism of Corticosteroids (Systemic). Exceptions: Azithromycin; Dirithromycin [Off Market]; Spiramycin. Risk D: Consider therapy modification
Maraviroc: CYP3A4 Inducers may decrease the serum concentration of Maraviroc. Risk D: Consider therapy modification
Natalizumab: Immunosuppressants may enhance the adverse/toxic effect of Natalizumab. Specifically, the risk of concurrent infection may be increased. Risk X: Avoid combination
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse/toxic effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Risk D: Consider therapy modification
NSAID (COX-2 Inhibitor): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (COX-2 Inhibitor). Risk C: Monitor therapy
NSAID (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of NSAID (Nonselective). Risk C: Monitor therapy
Primidone: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Quinolone Antibiotics: May enhance the adverse/toxic effect of Corticosteroids (Systemic). Risk of tendon-related side effects, including tendonitis and rupture, may be enhanced. Risk C: Monitor therapy
Rifamycin Derivatives: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Risk C: Monitor therapy
Somatropin: May diminish the therapeutic effect of PredniSONE. Growth hormone may reduce the conversion of prednisone to the active prednisolone metabolite. Risk D: Consider therapy modification
Thiazide Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide Diuretics. Risk C: Monitor therapy
Vaccines (Dead Organisms): Immunosuppressants may diminish the therapeutic effect of Vaccines (Dead Organisms). Risk C: Monitor therapy
Vaccines (Live Organisms): Immunosuppressants may enhance the adverse/toxic effect of Vaccines (Live Organisms). Vaccinal infections may develop. Immunosuppressants may also decrease therapeutic response to vaccines. Risk X: Avoid combination
Warfarin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Warfarin. Risk C: Monitor therapy
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may increase gastric mucosal irritation)
Food: Prednisone interferes with calcium absorption, Limit caffeine.
Herb/Nutraceutical: St John's wort may decrease prednisone levels. Avoid cat's claw, echinacea (have immunostimulant properties).
Mechanism of Action
Decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability; suppresses the immune system by reducing activity and volume of the lymphatic system; suppresses adrenal function at high doses. Antitumor effects may be related to inhibition of glucose transport, phosphorylation, or induction of cell death in immature lymphocytes. Antiemetic effects are thought to occur due to blockade of cerebral innervation of the emetic center via inhibition of prostaglandin synthesis.
Pharmacodynamics/Kinetics
Protein binding (concentration dependent): 65% to 91%
Metabolism: Hepatically converted from prednisone (inactive) to prednisolone (active); may be impaired with hepatic dysfunction
Half-life elimination: Normal renal function: 2.5-3.5 hours
See Prednisolone monograph for complete information.
Dosage
Oral: Dose depends upon condition being treated and response of patient; dosage for infants and children should be based on severity of the disease and response of the patient rather than on strict adherence to dosage indicated by age, weight, or body surface area. Consider alternate day therapy for long-term therapy. Discontinuation of long-term therapy requires gradual withdrawal by tapering the dose.
Children:
Anti-inflammatory or immunosuppressive dose: 0.05-2 mg/kg/day divided 1-4 times/day
Acute asthma: 1-2 mg/kg/day in divided doses 1-2 times/day for 3-5 days
Alternatively (for 3- to 5-day “burst”):
<1 year: 10 mg every 12 hours
1-4 years: 20 mg every 12 hours
5-13 years: 30 mg every 12 hours
>13 years: 40 mg every 12 hours
Asthma long-term therapy (alternative dosing by age):
<1 year: 10 mg every other day
1-4 years: 20 mg every other day
5-13 years: 30 mg every other day
>13 years: 40 mg every other day
Nephrotic syndrome:
Initial (first 3 episodes): 2 mg/kg/day or 60 mg/m2/day (maximum: 80 mg/day) in divided doses 3-4 times/day until urine is protein free for 3 consecutive days (maximum: 28 days); followed by 1-1.5 mg/kg/dose or 40 mg/m2/dose given every other day for 4 weeks
Maintenance dose (long-term maintenance dose for frequent relapses): 0.5-1 mg/kg/dose given every other day for 3-6 months
Children and Adults: Physiologic replacement: 4-5 mg/m2/day
Children ?5 years and Adults: Asthma:
Moderate persistent: Inhaled corticosteroid (medium dose) or inhaled corticosteroid (low-medium dose) with a long-acting bronchodilator
Severe persistent: Inhaled corticosteroid (high dose) and corticosteroid tablets or syrup long term: 2 mg/kg/day, generally not to exceed 60 mg/day
Adults:
Immunosuppression/chemotherapy adjunct: Range: 5-60 mg/day in divided doses 1-4 times/day
Allergic reaction (contact dermatitis):
Day 1: 30 mg divided as 10 mg before breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime
Day 2: 5 mg at breakfast, 5 mg at lunch, 5 mg at dinner, 10 mg at bedtime
Day 3: 5 mg 4 times/day (with meals and at bedtime)
Day 4: 5 mg 3 times/day (breakfast, lunch, bedtime)
Day 5: 5 mg 2 times/day (breakfast, bedtime)
Day 6: 5 mg before breakfast
Pneumocystis carinii pneumonia (PCP):
40 mg twice daily for 5 days followed by
40 mg once daily for 5 days followed by
20 mg once daily for 11 days or until antimicrobial regimen is completed
Thyrotoxicosis: Oral: 60 mg/day
Chemotherapy (refer to individual protocols): Oral: Range: 20 mg/day to 100 mg/m2/day
Rheumatoid arthritis: Oral: Use lowest possible daily dose (often ?7.5 mg/day)
Idiopathic thrombocytopenia purpura (ITP): Oral: 60 mg daily for 4-6 weeks, gradually tapered over several weeks
Systemic lupus erythematosus (SLE): Oral:
Acute: 1-2 mg/kg/day in 2-3 divided doses
Maintenance: Reduce to lowest possible dose, usually <1 mg/kg/day as single dose (morning)
Elderly: Use the lowest effective dose
Dosing adjustment in hepatic impairment: Prednisone is inactive and must be metabolized by the liver to prednisolone. This conversion may be impaired in patients with liver disease, however, prednisolone levels are observed to be higher in patients with severe liver failure than in normal patients. Therefore, compensation for the inadequate conversion of prednisone to prednisolone occurs.
Dosing adjustment in hyperthyroidism: Prednisone dose may need to be increased to achieve adequate therapeutic effects
Hemodialysis: Supplemental dose is not necessary
Peritoneal dialysis: Supplemental dose is not necessary
Dosage: Combination Regimens
Note: In the U.S., prednisone is the preferred corticosteroid. However, in the British literature, prednisolone is often used. The oral doses of these two agents are equivalent (ie, 1 mg prednisone = 1 mg prednisolone). Also, early clinical trials gave prednisone only with the first and fourth cycles. Some clinicians give prednisone with every cycle.
Brain tumors:
MOPP (Medulloblastoma)
POC
Breast cancer:
CFP
CMFP
CMFVP (Cooper Regimen, VPCMF)
Leukemia, acute lymphocytic:
DVP
Hyper-CVAD + Imatinib
Hyper-CVAD (Leukemia, Acute Lymphocytic)
Larson Regimen
Linker Protocol
MTX/6-MP/VP (Maintenance)
POMP
PVA (POG 8602)
PVDA
Leukemia, chronic lymphocytic:
CHL + PRED
CP (Leukemia)
CVP (Leukemia)
Lymphoma, Hodgkin's:
BEACOPP
CAD/MOPP/ABV
ChIVPP
COMP
LOPP
MOPP (Lymphoma, Hodgkin's Disease)
MOPP/ABV Hybrid
MOPP/ABVD
MVPP
OPA
OPPA
Stanford V
Lymphoma, non-Hodgkin's:
CEPP(B)
CHOP
CNOP
COP-BLAM
COPP
CVP (Lymphoma, non-Hodgkin's)
EPOCH
MACOP-B
Pro-MACE-CytaBOM
Rituximab-CHOP
R-CVP
Multiple myeloma:
Bortezomib-Melphalan-Prednisone
Bortezomib-Melphalan-Prednisone-Thalidomide
M-2
Melphalan-Prednisone-Thalidomide
MP (Multiple Myeloma)
VBAP
VBMCP
VCAP
Prostate cancer:
Docetaxel-Prednisone
Estramustine + Docetaxel + Prednisone
MP (Prostate Cancer)
Dental Usual Dosing
Anti-inflammatory or immunosuppressive dose: Children: Oral: 0.05-2 mg/kg/day divided 1-4 times/day
Immunosuppression/chemotherapy adjunct: Adults: Oral: Range: 5-60 mg/day in divided doses 1-4 times/day
Administration: Oral
Take with food to decrease GI upset.
Monitoring Parameters
Blood pressure, blood glucose, electrolytes
Test Interactions
Response to skin tests
Dietary Considerations
Should be taken after meals or with food or milk; increase dietary intake of pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus.
Patient Education
Take exactly as directed. Do not take more than prescribed dose and do not discontinue abruptly; consult prescriber. Take with or after meals. Take once-a-day dose with food in the morning. Avoid alcohol. Limit intake of caffeine or stimulants. Maintain adequate nutrition; consult prescriber for possibility of special dietary recommendations. If you have diabetes, monitor serum glucose closely and notify prescriber of changes; this medication can alter glycemic response. Notify prescriber if you are experiencing higher than normal levels of stress; medication may need adjustment. Periodic ophthalmic examinations will be necessary with long-term use. You will be susceptible to infection (avoid crowds and exposure to infection). You may experience insomnia or nervousness; use caution when driving or engaging in tasks requiring alertness until response to drug is known. Report weakness, change in menstrual pattern, vision changes, signs of hyperglycemia, signs of infection (eg, fever, chills, mouth sores, perianal itching, vaginal discharge), other persistent side effects, or worsening of condition.
Geriatric Considerations
Because of the risk of adverse effects, systemic corticosteroids should be used cautiously in the elderly, in the smallest possible dose, and for the shortest possible time.
Additional Information
Tapering of corticosteroids after a short course of therapy (<7-10 days) is generally not required unless the disease/inflammatory process is slow to respond. Tapering after prolonged exposure is dependent upon the individual patient, duration of corticosteroid treatments, and size of steroid dose. Recovery of the HPA axis may require several months. Subtle but important HPA axis suppression may be present for as long as several months after a course of as few as 10-14 days duration. Testing of HPA axis (cosyntropin) may be required, and signs/symptoms of adrenal insufficiency should be monitored in patients with a history of use.
Anesthesia and Critical Care Concerns/Other Considerations
Neuromuscular Effects: ICU-acquired paresis was recently studied in 5 ICUs (3 medical and 2 surgical ICUs) at 4 French hospitals. All ICU patients without pre-existing neuromuscular disease admitted from March 1999 through June 2000 were evaluated (De Jonghe B, 2002). Each patient had to be mechanically ventilated for ?7 days and was screened daily for awakening. The first day the patient was considered awake was Study Day 1. Patients with severe muscle weakness on Study Day 7 were considered to have ICU-acquired paresis. Among the 95 patients who were evaluable, about 25% developed ICU-acquired paresis. Independent predictors included: female gender, the number of days with ?2 organ dysfunction, and administration of corticosteroids. Further studies may be required to verify and characterize the association between the development of ICU-acquired paresis and use of corticosteroids. Concurrent use of a corticosteroid and muscle relaxant appear to increase the risk of certain ICU myopathies; avoid or administer the corticosteroid at the lowest dose possible.
Adrenal Insufficiency: Patients will often have steroid-induced adverse effects on glucose tolerance and lipid profiles. When discontinuing steroid therapy in patients on long-term steroid supplementation, it is important that the steroid therapy be discontinued gradually. Abrupt withdrawal may result in adrenal insufficiency with hypotension and hyperkalemia. Patients on long-term steroid supplementation will require higher corticosteroid doses when subject to stress (ie, trauma, surgery, severe infection). Guidelines for glucocorticoid replacement during various surgical procedures has been published (Coursin, 2002; Salem, 1994).
Septic Shock: A recent randomized, double-blind, placebo controlled trial assessed whether low dose corticosteroid administration could improve 28-day survival in patients with septic shock and relative adrenal insufficiency. Relative adrenal insufficiency was defined as an inappropriate response to corticotropin administration (increase of serum cortisol of ?9 mcg/dL from baseline). Cortisol levels were drawn immediately before corticotropin administration and 30 to 60 minutes afterwards. Three hundred adult septic shock patients requiring mechanical ventilation and vasopressor support were randomized to either hydrocortisone (50 mg IVP every 6 hours) and fludrocortisone (50 mcg tablet daily via nasogastric tube) or matching placebos for 7 days. In patients who did not appropriately respond to corticotropin (nonresponders), there were significantly fewer deaths in the active treatment group. Vasopressor therapy was withdrawn more frequently in this subset of the active treatment group. Adverse events were similar in both groups. Patients who lack adrenal reserve and thus have relative adrenal insufficiency during the stress of septic shock may benefit from physiologic steroid replacement. However, there was a trend for increased mortality in patients who responded to the corticotropin test (increase serum cortisol >9 mcg/dL from baseline). These patients may not benefit from physiologic steroid replacement. Further study is required to better characterize the patient populations who may benefit.
The 2008 Surviving Sepsis Campaign guidelines recommend doses of corticosteroids comparable to >300 mg hydrocortisone daily not be used in severe sepsis or septic shock for the purpose of treating septic shock (Grade 1A). They also recommend corticosteroids not be administered for the treatment of sepsis in the absence of shock. There is, however, no contraindication to continuing maintenance steroid therapy or to using stress dose steroids if the patient's endocrine or corticosteroid administration history warrants (Grade 1D).
Cardiovascular Considerations
Long-term steroid therapy is associated with fluid retention and hypertension. Glucocorticoid agents have some mineralocorticoid activity with consequent hemodynamic effects. Patients will often have steroid-induced adverse effects on glucose tolerance and lipid profiles. In discontinuing steroid therapy in patients on long-term steroid supplementation, it is important that the steroid therapy be discontinued gradually. Abrupt withdrawal may result in adrenal insufficiency with hypotension and hyperkalemia.
Oral and intravenous steroid therapy in patients with heart failure should be administered cautiously with special attention given to signs and symptoms of fluid retention.
Although glucocorticoids can provide relief from pericarditis postmyocardial infarctions, these drugs may cause thinning of the developing scar and myocardial rupture.
Dental Health: Effects on Dental Treatment
No significant effects or complications reported
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
Nervousness and insomnia are common; may rarely cause delirium, mood swings, euphoria, and hallucinations
Mental Health: Effects on Psychiatric Treatment
Barbiturates and carbamazepine may decrease corticosteroid effectiveness
Nursing: Physical Assessment/Monitoring
Assess effectiveness and interactions of other medications patient may be taking. Monitor for effectiveness of therapy and adverse reactions according to dose and length of therapy. Assess knowledge/teach patient appropriate use, possible side effects/interventions, and adverse symptoms to report (ie, opportunistic infection, adrenal suppression). Instruct patients with diabetes to monitor serum glucose levels closely; corticosteroids can alter glucose tolerance. Dose may need to be increased if patient is experiencing higher than normal levels of stress. When discontinuing, taper dose and frequency slowly.
Oncology: Emetic Potential
Very low (<10%)
Oncology: Vesicant
No
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, oral: 1 mg/mL (5 mL, 120 mL, 500 mL) [contains alcohol 5%, sodium benzoate; peppermint vanilla flavor]
Solution, oral [concentrate]:
PredniSONE Intensol™: 5 mg/mL (30 mL) [contains alcohol 30%]
Tablet: 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, 50 mg
Sterapred®: 5 mg [supplied as 21 tablet 6-day unit-dose package or 48 tablet 12-day unit-dose package]
Sterapred® DS: 10 mg [supplied as 21 tablet 6-day unit-dose package or 48 tablet 12-day unit-dose package]
Pricing: U.S. (www.drugstore.com)
Tablets (PredniSONE)
2.5 mg (30): $12.99
5 mg (100): $11.99
10 mg (30): $11.99
20 mg (30): $11.99
50 mg (30): $17.99
Tablets (PredniSONE (Pak))
10 mg (21): $15.99
10 mg (48): $17.99
Tablets (Sterapred DS)
10 mg (21): $59.98
Tablets (Sterapred DS 12 Day)
10 mg (48): $74.36
References
Boot AM, Nauta J, Hokken-Koelega AC, et al, “Renal Transplantation and Osteoporosis,” Arch Dis Child, 1995, 72(6):502-6.
Bowman H and Lennard TW, “Immunosuppressive Drugs,” Br J Hosp Med, 1992, 48(9):570-3.
Dellinger RP, Levy MM, Carlet JM, et al, “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008,” Intensive Care Med, 2008, 34(1): 17-60. Available at http://www.survivingsepsis.org/system/files/images/2008_20International_20SSC_20Guidelines_1_.pdf
Frey BM and Frey FJ, “Clinical Pharmacokinetics of Prednisone and Prednisolone,” Clin Pharmacokinet, 1990, 19(2):126-46.
Gambertoglio JG, Amend WJ Jr, and Benet LZ, "Pharmacokinetics and Bioavailability of Prednisone and Prednisolone in Healthy Volunteers and Patients: A Review,"J Pharmacokinet Biopharm, 1980, 8(1):1-52.
Goedert JJ, Vitale F, Lauria C, et al, “Risk Factors for Classical Kaposi's Sarcoma,” J Natl Cancer Inst, 2002, 94(22):1712-8.
Grotz WH, Mundinger FA, Gugel B, et al, “Bone Mineral Density After Kidney Transplantation: A Cross-Sectional Study in 190-Graft Recipients Up to 20 Years After Transplantation,” Transplantation, 1995, 59(7):982-6.
Gutin PH, “Corticosteroid Therapy in Patients With Brain Tumors,” Natl Cancer Inst Monogr, 1977, 46:151-6.
Jusko WJ and Rose JQ, "Monitoring Prednisone and Prednisolone," Ther Drug Monit, 1980, 2(2):169-76.
Kimberly RP, “Glucocorticoids,” Curr Opin Rheumatol, 1994, 6(3):273-80.
Lowenthal RM and Jestrimski KW, “Corticosteroid Drugs: Their Role in Oncological Practice,” Med J Aust, 1986, 144(2):81-5.
McGee S and Hirschmann J, “Use of Corticosteroids in Treating Infectious Diseases,” Arch Intern Med, 2008, 168(10):1034-46.
Murphy CM, Coonce SL, and Simon PA, “Treatment of Asthma in Children,” Clin Pharm, 1991, 10(9):685-703.
Report of a Workshop by the British Association for Paediatric Nephrology and Research Unit, Royal College of Physicians, “Consensus Statement on Management and Audit Potential for Steroid Responsive Nephrotic Syndrome,” Arch Dis Child, 1994, 70(2):151-7.
Verbeek PR and Geerts WH, “Nontapering Versus Tapering Prednisone in Acute Exacerbations of Asthma: A Pilot Trial,” J Emerg Med, 1995, 13(5):715-9.
Wolkowitz OM, “Long-Lasting Behavioral Changes Following Prednisone Withdrawal,” JAMA, 1989, 261(12):1731-2.
International Brand Names
Lexi-Comp.com
Last full review/revision August 2008
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