Prednisone - Pediatric Drug Information

11/17/2014
Prednisone: Pediatric drug information
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(For additional information see "Prednisone: Drug information" and see "Prednisone: Patient drug information")
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Brand Names: U.S. PredniSONE Intensol; Rayos

Brand Names: Canada Apo-Prednisone; Novo-Prednisone; Winpred
Therapeutic Category Adrenal Corticosteroid; Anti-inflammatory Agent; Antiasthmatic; Corticosteroid, Systemic; Glucocorticoid
Dosing: Usual
(For additional information see "Prednisone: Drug information")
Dose depends upon condition being treated and response of patient; dosage for infants and children should be based on disease severity and patient response rather
than by rigid adherence to dosage guidelines 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. Oral:
NIH Asthma Guidelines (NAEPP, 2007):
Children <12 years:
Asthma exacerbations (emergency care or hospital doses): 1-2 mg/kg/day in 2 divided doses (maximum: 60 mg/day) until peak expiratory flow is 70% of
predicted or personal best
Short-course burst (acute asthma): 1-2 mg/kg/day in divided doses 1-2 times/day for 3-10 days; maximum dose: 60 mg/day; Note: Burst should be continued
until symptoms resolve or patient achieves peak expiratory flow 80% of personal best; usually requires 3-10 days of treatment (~5 days on average);
longer treatment may be required
Long-term treatment: 0.25-2 mg/kg/day given as a single dose in the morning or every other day as needed for asthma control; maximum dose: 60 mg/day
Children 12 years and Adults:
Asthma exacerbations (emergency care or hospital doses): 40-80 mg/day in divided doses 1-2 times/day until peak expiratory flow is 70% of predicted or
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personal best
Short-course burst (acute asthma): 40-60 mg/day in divided doses 1-2 times/day for 3-10 days; Note: Burst should be continued until symptoms resolve and
peak expiratory flow is at least 80% of personal best; usually requires 3-10 days of treatment (~5 days on average); longer treatment may be required
Long-term treatment: 7.5-60 mg daily given as a single dose in the morning or every other day as needed for asthma control
Children:
Alternative asthma dosing by age:
Short-course burst (acute asthma):
<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
Long-term treatment:
<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
Anti-inflammatory or immunosuppressive: 0.05-2 mg/kg/day divided 1-4 times/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 dose: 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: 6week daily therapy followed by 6-week alternate day therapy may induce a higher rate of long remission compared to the standard of 4 weeks of daily
therapy followed by 4 weeks of alternate day therapy; however, a higher incidence of adverse effects may be seen with the longer regimen and the
clinical benefit may be variable.
Relapse: Use high-dose daily steroid regimen (listed above) until urine is protein free for 3 days; follow with maintenance-tapering course of alternate day
therapy (maintenance dose listed above) for 4-6 weeks; subsequent therapy is determined by individual's response and number of relapses (Hogg,
2000)
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British Pediatric Nephrology Consensus Statement (Report of a Workshop by the British Association for Paediatric Nephrology and Research Unit, 1994):
First 3 episodes: Initial: 2 mg/kg/day or 60 mg/m2/day given every day (maximum dose: 80 mg/day) until urine is protein free for 3 consecutive days
(maximum dose: 28 days); followed by 1-1.5 mg/kg/dose or 40 mg/m2/dose (maximum: 60 mg/dose) given every other day for 4 weeks
Frequent relapses (long-term maintenance dose): 0.5-1 mg/kg/dose given every other day for 3-6 months
Children and Adults: Physiologic replacement: 4-5 mg/m2/day
Adults: 5-60 mg/day in divided doses 1-4 times/day
Dosage Forms: U.S. Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Concentrate, Oral:
PredniSONE Intensol: 5 mg/mL (30 mL) [contains alcohol, usp; unflavored flavor]
Solution, Oral:
Generic: 5 mg/5 mL (5 mL, 120 mL, 500 mL)
Tablet, Oral:
Generic: 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, 50 mg
Tablet Delayed Release, Oral:
Rayos: 1 mg, 2 mg, 5 mg
Generic Equivalent Available: U.S. May be product dependent

Administration Oral: Administer after meals or with food or milk to decrease GI upset
Use Management of adrenocortical insufficiency; used for its anti-inflammatory or immunosuppressant effects
Medication Safety Issues
Sound-alike/look-alike issues:
PredniSONE may be confused with methylPREDNISolone, Pramosone, prazosin, prednisoLONE, PriLOSEC, primidone, promethazine
Adverse Reactions
Cardiovascular: Congestive heart failure (in susceptible patients), hypertension
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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, Cushings 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 increased, 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, Kaposis sarcoma
Rare but important or life-threatening: Venous thrombosis (Johannesdottir, 2013)
Contraindications Hypersensitivity to any component of the formulation; systemic fungal infections; administration of live or live attenuated vaccines with
immunosuppressive doses of prednisone
Precautions Avoid using higher than recommended doses; suppression of HPA function, suppression of linear growth (ie, reduction of growth velocity), reduced
bone mineral density, hypercorticism (Cushing's syndrome), hyperglycemia, or glucosuria may occur; titrate to lowest effective dose. Reduction in growth velocity may
occur when corticosteroids are administered to pediatric patients by any route (monitor growth). Use with extreme caution in patients with respiratory tuberculosis or
untreated systemic infections. Use with caution in patients with hypertension, heart failure, or renal impairment; long-term use has been associated with fluid retention
and hypertension. Use with caution in patients with GI diseases (diverticulitis, peptic ulcer, ulcerative colitis) due to risk of GI bleeding and perforation. High-dose
corticosteroids should not be used for management of head injury; increased mortality was observed in patients receiving high-dose I.V. methylprednisolone. Use with
caution in patients with myasthenia gravis; exacerbation of symptoms has occurred, especially during initial treatment with corticosteroids. Use with caution in patients
with hepatic impairment, including cirrhosis; enhanced pharmacologic effect due to decreased metabolism and long-term use has been associated with fluid retention.
Use with caution following acute MI; corticosteroids have been associated with myocardial rupture; hypertrophic cardiomyopathy has been reported in premature
neonates.
Use with caution in patients with diabetes; corticosteroids may alter glucose regulation, leading to hyperglycemia. Use with caution in patients with cataracts and/or
glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use; consider routine eye exams in chronic users. Use with
caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis. Use with caution in patients with thyroid dysfunction; changes in
thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid patients.
Prolonged treatment with corticosteroids has been associated with the development of Kaposi's sarcoma (case reports); if noted, discontinuation of therapy should be
considered. Use with caution in patients with thromboembolic tendencies or thrombophlebitis.
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Warnings Hypothalamic-pituitary-adrenal (HPA) suppression may occur, particularly in younger children or in patients receiving high doses for prolonged periods;
acute adrenal insufficiency (adrenal crisis) may occur with abrupt withdrawal after long-term therapy or with stress; withdrawal and discontinuation of corticosteroids
should be tapered slowly and carefully; patients with HPA axis suppression may require doses of systemic glucocorticosteroids prior to, during, and after unusual stress
(eg, surgery).
Immunosuppression may occur; patients may be more susceptible to infections; prolonged use of corticosteroids may also increase the incidence of secondary infection,
mask acute infection (including fungal infections), prolong or exacerbate viral or fungal infections, activate latent opportunistic infections, or limit response to vaccines.
Exposure to chickenpox should be avoided; corticosteroids should not be used to treat ocular herpes simplex; use caution in patients with a history of 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).
May cause osteoporosis (at any age) or inhibition of bone growth in pediatric patients. Use with caution in patients with osteoporosis. In a population-based study of
children, risk of fracture was shown to be increased with >4 courses of corticosteroids; underlying clinical condition may also impact bone health and osteoporotic effect
of corticosteroids (Leonard, 2007).
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. Acute myopathy may occur with high doses, usually in patients with neuromuscular transmission disorders;
myopathy may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed. Increased IOP may occur, especially with prolonged use; in
children, increased IOP has been shown to be dose-dependent and produce a greater IOP in children <6 years than older children (Lam, 2005). Rare cases of
anaphylactoid reactions have been reported with corticosteroids.
Oral solution contains sodium benzoate; benzoic acid (benzoate) is a metabolite of benzyl alcohol; large amounts of benzyl alcohol (99 mg/kg/day) have been
associated with a potentially fatal toxicity (gasping syndrome) in neonates; the gasping syndrome consists of metabolic acidosis, respiratory distress, gasping
respirations, CNS dysfunction (including convulsions, intracranial hemorrhage), hypotension and cardiovascular collapse; use prednisone products containing sodium
benzoate with caution in neonates; in vitro and animal studies have shown that benzoate displaces bilirubin from protein binding sites. Concentrated oral solution
(Intensol) contains propylene glycol; toxicities have been reported with use of products containing propylene glycol, including hyperosmolality, lactic acidosis, seizures,
and respiratory depression; in neonates large amounts of propylene glycol delivered orally, intravenously (eg, >3000 mg/day), or topically have been associated with
potentially fatal toxicities which can include metabolic acidosis, seizures, renal failure, and CNS depression; use oral solutions containing propylene glycol with caution
(AAP, 1997; Shehab, 2009).
Metabolism/Transport Effects Substrate of CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction
potential; Induces CYP2C19 (weak/moderate), CYP3A4 (weak/moderate)
Drug Interactions
(For additional information: Launch Lexi-Interact Drug
Interactions Program)
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may
occur. Risk C: Monitor therapy
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Aldesleukin: Corticosteroids may diminish the antineoplastic effect of Aldesleukin. Risk X: Avoid combination
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
Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Risk C: Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Management: Consider separating doses by 2 or more hours. Budesonide enteric coated tablets
could dissolve prematurely if given with drugs that lower gastric acid, with unknown impact on budesonide therapeutic effects. 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
Aprepitant: May increase the serum concentration of Corticosteroids (Systemic). Risk D: Consider therapy modification
ARIPiprazole: CYP3A4 Inducers may decrease the serum concentration of ARIPiprazole. Management: Double the oral aripiprazole dose and closely monitor clinical
response. Reduce the oral aripiprazole dose to 10-15 mg/day if the inducer is discontinued. Avoid use of CYP3A4 inducers for more than 14 days with extendedrelease injectable aripiprazole. Risk D: Consider therapy modification
Axitinib: CYP3A4 Inducers (Weakly to Moderately Effective) may decrease the serum concentration of Axitinib. Risk X: Avoid combination
Barbiturates: May decrease the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
BCG: Immunosuppressants may diminish the therapeutic effect of BCG. Risk X: Avoid combination
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Boceprevir: May increase the serum concentration of PredniSONE. Risk C: Monitor therapy
Calcitriol: Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol. Risk C: Monitor therapy
Ceritinib: Corticosteroids may enhance the hyperglycemic effect of Ceritinib. Risk C: Monitor therapy
Coccidioidin Skin Test: Immunosuppressants may diminish the diagnostic effect of Coccidioidin Skin Test. 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 (Systemic): May increase serum concentrations of the active metabolite(s) of PredniSONE. PredniSONE may decrease the serum concentration of
CycloSPORINE (Systemic). PredniSONE may increase the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
CYP3A4 Inhibitors (Strong): May increase the serum concentration of PredniSONE. Risk C: Monitor therapy
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Deferasirox: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be
increased. Risk C: Monitor therapy
Deferasirox: Corticosteroids may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk
C: Monitor therapy
Denosumab: May enhance the adverse/toxic effect of Immunosuppressants. Specifically, the risk for serious infections may be increased. 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 increase the serum concentration of PredniSONE. 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
Fosphenytoin: May decrease serum concentrations of the active metabolite(s) of PredniSONE. Risk C: Monitor therapy
Hyaluronidase: Corticosteroids may diminish the therapeutic effect of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may
not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Risk D: Consider therapy
modification
Hydrocodone: CYP3A4 Inducers (Weakly to Moderately Effective) may decrease the serum concentration of Hydrocodone. Risk C: Monitor therapy
Ibrutinib: CYP3A4 Inducers (Weakly to Moderately Effective) may decrease the serum concentration of Ibrutinib. Risk D: Consider therapy modification
Indacaterol: May enhance the hypokalemic effect of Corticosteroids (Systemic). Risk C: Monitor therapy
Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Risk X: Avoid combination
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Leflunomide: Immunosuppressants may enhance the adverse/toxic effect of Leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia,
agranulocytosis, and/or thrombocytopenia may be increased. Management: Consider not using a leflunomide loading dose in patients receiving other
immunosuppressants. Patients receiving both leflunomide and another immunosuppressant should be monitored for bone marrow suppression at least monthly. Risk
D: Consider therapy modification
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Mifepristone: May diminish the therapeutic effect of Corticosteroids (Systemic). Mifepristone may increase the serum concentration of Corticosteroids (Systemic).
Management: Avoid mifepristone in patients who require long-term corticosteroid treatment of serious illnesses or conditions (e.g., for immunosuppression following
transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Risk X: Avoid combination
Mitotane: May decrease the serum concentration of Corticosteroids (Systemic). Risk D: Consider therapy modification
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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 neuromuscular 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
Phenytoin: May decrease serum concentrations of the active metabolite(s) of PredniSONE. Risk C: Monitor therapy
Pimecrolimus: May enhance the adverse/toxic effect of Immunosuppressants. Risk X: Avoid combination
Primidone: May decrease the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Quinolone Antibiotics: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolone Antibiotics. Specifically, the risk of tendonitis and tendon rupture
may be increased. Risk C: Monitor therapy
Rifamycin Derivatives: May increase the metabolism of Corticosteroids (Systemic). Risk C: Monitor therapy
Ritonavir: May increase the serum concentration of PredniSONE. Risk C: Monitor therapy
Roflumilast: May enhance the immunosuppressive effect of Immunosuppressants. Risk D: Consider therapy modification
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
Saxagliptin: CYP3A4 Inducers may decrease the serum concentration of Saxagliptin. Risk C: Monitor therapy
Simeprevir: CYP3A4 Inducers (Weakly to Moderately Effective) may decrease the serum concentration of Simeprevir. Risk X: Avoid combination
Sipuleucel-T: Immunosuppressants may diminish the therapeutic effect of Sipuleucel-T. 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
Tacrolimus (Topical): May enhance the adverse/toxic effect of Immunosuppressants. Risk X: Avoid combination
Telaprevir: Corticosteroids (Systemic) may decrease the serum concentration of Telaprevir. Telaprevir may increase the serum concentration of Corticosteroids
(Systemic). Management: Concurrent use of telaprevir and systemic corticosteroids is not recommended. When possible, consider alternatives. If used together,
employ extra caution and monitor closely for excessive corticosteroid effects and diminished telaprevir effects. Risk D: Consider therapy modification
Telaprevir: May increase the serum concentration of Corticosteroids. Corticosteroids may decrease the serum concentration of Telaprevir. Management: Concurrent use
of telaprevir and systemic corticosteroids is not recommended. When possible, consider alternatives. If used together, employ extra caution and monitor closely for
excessive corticosteroid effects and diminished telaprevir effects. Risk D: Consider therapy modification
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Tesamorelin: May decrease serum concentrations of the active metabolite(s) of PredniSONE. Risk D: Consider therapy modification
Thiazide Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide Diuretics. Risk C: Monitor therapy
Tofacitinib: Immunosuppressants may enhance the immunosuppressive effect of Tofacitinib. Management: Concurrent use with antirheumatic doses of methotrexate or
nonbiologic disease modifying antirheumatic drugs (DMARDs) is permitted, and this warning seems particularly focused on more potent immunosuppressants. Risk
X: Avoid combination
Trastuzumab: May enhance the neutropenic effect of Immunosuppressants. Risk C: Monitor therapy
Urea Cycle Disorder Agents: Corticosteroids (Systemic) may diminish the therapeutic effect of Urea Cycle Disorder Agents. More specifically, Corticosteroids
(Systemic) may increase protein catabolism and plasma ammonia concentrations, thereby increasing the doses of Urea Cycle Disorder Agents needed to maintain
these concentrations in the target range. Risk C: Monitor therapy
Vaccines (Inactivated): Immunosuppressants may diminish the therapeutic effect of Vaccines (Inactivated). Risk C: Monitor therapy
Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Risk D: Consider therapy modification
Warfarin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Warfarin. Risk C: Monitor therapy
Pregnancy Risk Factor C (show table)

Pregnancy Implications Adverse events have been observed with corticosteroids in animal reproduction studies. Prednisone and its metabolite, 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) (Beitins, 1972). Some studies have shown an
association between first trimester systemic corticosteroid use and oral clefts (Park-Wyllie, 2000; Pradat, 2003). Systemic corticosteroids may also influence fetal
growth (decreased birth weight); however, information is conflicting (Lunghi, 2010). Hypoadrenalism may occur in newborns following maternal use of corticosteroids in
pregnancy; monitor.
When systemic corticosteroids are needed in pregnancy, it is generally recommended to use the lowest effective dose for the shortest duration of time, avoiding high
doses during the first trimester (Leachman, 2006; Lunghi, 2010; Makol, 2011; stensen, 2009). Inhaled corticosteroids are preferred for the treatment of asthma during
pregnancy. Oral corticosteroids, such as prednisone, may be used for the treatment of severe persistent asthma if needed; the lowest dose administered on alternate
days (if possible) should be used (NAEPP, 2005). Prednisone may be used to treat lupus nephritis in pregnant women who have active nephritis or substantial extrarenal
disease activity (Hahn, 2012).
Pregnant women exposed to prednisone for antirejection therapy following a transplant may contact the National Transplantation Pregnancy Registry (NTPR) at 215-9554820. 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.
Monitoring Parameters Blood pressure, weight, serum electrolytes, glucose; children's height and growth
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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.
Pharmacokinetics (Adult data unless noted) Converted rapidly in the liver to prednisolone (active)
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Prednisone - Pediatric Drug Information

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Prednisone: Pediatric drug information

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Prednisone: Pediatric drug information

Brand Names: U.S. PredniSONE Intensol; Rayos

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Generic Equivalent Available: U.S. May be product dependent

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

Pregnancy Risk Factor C (show table)

Prednisone: Pediatric drug information

Prednisone: Pediatric drug information

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