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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:
Allergic states (including adjunctive treatment of anaphylaxis)
Autoimmune disorders (including systemic lupus erythematosus [SLE])
Collagen diseases
Dermatologic conditions/diseases
Edematous states (including nephrotic syndrome)
Endocrine disorders
Gastrointestinal diseases
Hematologic disorders (including idiopathic thrombocytopenia purpura [ITP])
Multiple sclerosis exacerbations
Neoplastic diseases
Ophthalmic diseases
Respiratory diseases (including acute asthma exacerbation)
Rheumatic disorders (including rheumatoid arthritis)
Trichinosis with neurologic or myocardial involvement
Tuberculous meningitis
Use: Dental
Treatment of a variety of oral diseases of allergic, inflammatory, or autoimmune origin
Use: Unlabeled/Investigational
Adjunctive therapy for Pneumocystis jiroveci (formerly carinni) pneumonia (PCP); autoimmune hepatitis; adjunctive therapy for pain management in immunocompetent patients with herpes zoster; tuberculosis (severe, paradoxical reactions)
Pregnancy Considerations
Adverse events have been observed with corticosteroids in animal reproduction studies. Prednisone and prednisolone cross the human placenta. In the mother, prednisone is converted to the active metabolite prednisolone by the liver. Prior to reaching the fetus, prednisolone is converted by placental enzymes back to prednisone. As a result, the level of prednisone remaining in the maternal serum and reaching the fetus are similar, however, the amount of prednisolone reaching the fetus is ~8-10 times lower than the maternal serum concentration (healthy women at term). Some studies have shown an association between first trimester prednisone use and oral clefts; adverse events in the fetus/neonate have been noted in case reports following large doses of systemic corticosteroids during pregnancy. Pregnant women exposed to prednisone for antirejection therapy following a transplant may contact the National Transplantation Pregnancy Registry (NTPR) at 215-955-4820. Women exposed to prednisone during pregnancy for the treatment of an autoimmune disease (eg, rheumatoid arthritis) may contact the OTIS Autoimmune Diseases Study at 877-311-8972.
Lactation
Enters breast milk/AAP rates "compatible"
Breast-Feeding Considerations
Prednisone and its metabolite prednisolone are found in low concentrations in breast milk. Peak milk concentrations of both were found ~2 hours after the maternal dose in one case report. In a study which included 6 mother/infant pairs, adverse events were not observed in nursing infants (maternal prednisone dose not provided).
Contraindications
Hypersensitivity to any component of the formulation; systemic fungal infections; administration of live or live attenuated vaccines with immunosuppressive doses of prednisone
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 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 or cerebral malaria. 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.
• Ocular effects: Prolonged use may cause posterior subcapsular cataracts, glaucoma (with possible nerve damage) and may increase the risk for ocular infections.
• 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; effects may be enhanced.
• 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 or who are at risk for osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.
• 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:
• Pediatrics: May affect growth velocity; growth should be routinely monitored in pediatric patients.
Other warnings/precautions:
• Appropriate use: Prior to use, the dose and duration of treatment should be based on the risk versus benefit for each individual patient. In general, use the smallest effective dose for the shortest duration of time to minimize adverse events. A gradual tapering of dose may be required prior to discontinuing therapy.
Adverse Reactions
Frequency not defined.
Cardiovascular: Congestive heart failure (in susceptible patients), hypertension
Central nervous system: Emotional instability, headache, intracranial pressure increased (with papilledema), psychic derangements (including euphoria, insomnia, mood swings, personality changes, severe depression), seizure, vertigo
Dermatologic: Bruising, facial erythema, petechiae, thin fragile skin, urticaria, wound healing impaired
Endocrine & metabolic: Adrenocortical and pituitary unresponsiveness (in times of stress), carbohydrate intolerance, Cushing's syndrome, diabetes mellitus, fluid retention, growth suppression (in children), hypokalemic alkalosis, hypothyroidism enhanced, menstrual irregularities, negative nitrogen balance due to protein catabolism, potassium loss, sodium retention
Gastrointestinal: Abdominal distension, pancreatitis, peptic ulcer (with possible perforation and hemorrhage), ulcerative esophagitis
Hepatic: ALT/AST increased, alkaline phosphatase increased
Neuromuscular & skeletal: Aseptic necrosis of femoral and humeral heads, muscle mass loss, muscle weakness, osteoporosis, pathologic fracture of long bones, steroid myopathy, tendon rupture (particularly Achilles tendon), vertebral compression fractures
Ocular: Exophthalmos, glaucoma, intraocular pressure increased, posterior subcapsular cataracts
Miscellaneous: Allergic reactions, anaphylactic reactions, diaphoresis, hypersensitivity reactions, infections, Kaposi's sarcoma
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
Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Risk C: Monitor therapy
Vaccines (Inactivated): Immunosuppressants may diminish the therapeutic effect of Vaccines (Inactivated). Risk C: Monitor therapy
Vaccines (Live): Immunosuppressants may enhance the adverse/toxic effect of Vaccines (Live). 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
Absorption: 50% to 90% (may be altered in IBS or hyperthyroidism)
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: ~3.5 hours
Excretion: Urine (small portion)
Dosage
Oral:
General dosing range: Children and Adults: Initial: 5-60 mg/day: Note: 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.
Prednisone taper (other regimens also available):
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
Indication-specific dosing:
Children:
Acute asthma (NIH guidelines, 2007):
0-11 years 1-2 mg/kg/day for 3-10 days (maximum 60 mg/day)
?12 years: Refer to Adults dosing
Autoimmune hepatitis (unlabeled use; Czaja 2002): Initial treatment: 2 mg/kg/day for 2 weeks (maximum 60 mg/day), followed by a taper over 6-8 weeks to a dose of 0.1-0.2 mg/kg/day or 5 mg/day
Nephrotic syndrome (Pediatric Nephrology Panel recommendations [Hogg, 2000]): Initial: 2 mg/kg/day or 60 mg/m2/day given every day in 1-3 divided doses (maximum: 80 mg/day) until urine is protein free or for 4-6 weeks; followed by maintenance dose: 2 mg/kg/dose or 40 mg/m2/dose given every other day in the morning; gradually taper and discontinue after 4-6 weeks. Note: No definitive treatment guidelines exist. Dosing is dependant on institution protocols and individual response.
PCP pneumonia (AIDSinfo guidelines, 2008): 1 mg/kg twice daily for 5 days, followed by 0.5-1 mg/kg twice daily for 5 days, followed by 0.5 mg/kg once daily for 11-21 days
Adolescents and Adults:
PCP pneumonia (AIDSinfo guidelines, 2008): Note: Begin within 72 hours of PCP therapy: 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
Adults:
Acute asthma (NIH guidelines, 2007): 40-60 mg per day for 3-10 days; administer as single or 2divided doses
Anaphylaxis, adjunctive treatment (Lieberman 2005): 0.5 mg/kg
Antineoplastic: Usual range: 10 mg/day to 100 mg/m2/day (depending on indication). Note: Details concerning dosing in combination regimens should also be consulted.
Autoimmune hepatitis (unlabeled use; Czaja 2002): Initial treatment: 60 mg/day for 1 week, followed by 40 mg/day for 1 week, then 30 mg/day for 2 weeks, then 20 mg/day. Half this dose should be given when used in combination with azathioprine
Herpes zoster (unlabeled use; Dworkin 2007): 60 mg/day for 7 days, followed by 30 mg/day for 7 days, then 15 mg/day for 7 days
Idiopathic thrombocytopenia purpura (American Society of Hematology 1997): 1-2 mg/kg/day
Rheumatoid arthritis (American College of Rheumatology 2002): ?10 mg/day
Systemic lupus erythematosus (American College of Rheumatology 1999):
Mild SLE: ?10 mg/day
Refractory or severe organ-threatening disease: 20-60 mg/day
Thyrotoxicosis (type II amiodarone induced; unlabeled use): 30-40 mg/day for 7-14 days, gradually taper over 3 months
Tuberculosis, severe, paradoxical reactions (unlabeled use, AIDS info guidelines 2008): 1 mg/kg/day, gradually reduce after 1-2 weeks
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 Regimen
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
Administer with food to decrease GI upset.
Monitoring Parameters
Blood pressure, blood glucose, electrolytes
Following prolonged use: Bone mass density, growth in children, signs and symptoms of infection, cataract formation
Test Interactions
Decreased response to skin tests
Dietary Considerations
Should be taken after meals or with food or milk; may require increased dietary intake of pyridoxine, vitamin C, vitamin D, folate, calcium, and phosphorus; may require decreased dietary intake of sodium
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
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American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines, “Guidelines for the Management of Rheumatoid Arthritis: 2002 Update,” Arthritis Rheum, 2002, 46(2):328-46.
Bartalena L, Brogioni S, Grasso L, et al, “Treatment Of Amiodarone-Induced Thyrotoxicosis, A Difficult Challenge: Results Of A Prospective Study,” J Clin Endocrinol Metab, 1996, 81(8):2930-3.
Basaria S and Cooper DS, “Amiodarone and the Thyroid,” Am J Med, 2005, 118(7):706-14.
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Bogazzi F, Bartalena L, Cosci C, et al, “Treatment of Type II Amiodarone-Induced Thyrotoxicosis by Either Iopanoic Acid or Glucocorticoids: A Prospective, Randomized Study,” J Clin Endocrinol Metab, 2003, 88(5):1999-2002.
Bogazzi F, Bartalena L, Tomisti L, et al, “Glucocorticoid Response in Amiodarone-Induced Thyrotoxicosis Resulting From Destructive Thyroiditis is Predicted by Thyroid Volume and Serum Free Thyroid Hormone Concentrations,” J Clin Endocrinol Metab, 2007, 92(2):556-62.
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.
Czaja AJ and Freese DK, “Diagnosis and Treatment of Autoimmune Hepatitis,” Hepatology, 2002, 36(2):479-97.
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
“Diagnosis And Treatment of Idiopathic Thrombocytopenic Purpura: Recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel,” Ann Intern Med, 1997, 126(4):319-26.
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International Brand Names
Lexi-Comp.com
Last full review/revision September 2008
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