prednisone (Deltasone, Orasone, Liquid Pred, Meticortin, Rayos)
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Introduction
Systemic agent: Tradenames: Deltasone, Orasone, Liquid Pred.
Indications
- adrenal insufficiency
- inflammation associated with many disease states
- graft rejection
- acute alcoholic hepatitis associated with encephalopathy
- congenital anomalies
- cluster headache
- edema
- lung disease
- otitis externa
- inflammatory infections
- musculoskeletal inflammation
- dermatitis
- autoimmune disease
- nephrotic syndrome
- hypersensitivity
- serum sickness
- nasal polyp
- allergic rhinitis
- malignant neoplasms
Dosage
- 0.5-2 mg/kg or 5-60 mg PO QD
- 1 mg/kg may work as well as higher doses in children[8]
- physiologic replacement: 4-5 mg/m2/day
- prednisone taper
- not necessary to taper if oral dose < 60 mg/day for 10 days[7]
- taper is unnecessary when glucocorticoid therapy is < 3-4 weeks, regardless of dose[13]
- failure to taper below 5 mg/day suggests adrenal insufficiency[12]
- primary or secondary - see prednisone taper
Tabs: 1, 2.5, 5, 10, 20, 50 mg. Delayed Release tabs: (Rayos) 1 mg, 2 mg, & 5 mg[9]
Elixir: 5 mg/5 mL (120 mL, 240 mL).
Pharmacokinetics
- oral bioavailability is 80 +/- 10%
- protein binding: 75%
- metabolized in liver by cyt P450 3A4 to prednisolone
- prednisolone is inactivated by the placenta
- 3% excreted in the urine
- elimination 1/2life is 3.6 +/- 0.4 hours
- biologic 1/2life 18-36 hours[6]
elimination via liver
1/2life = 3.6 hours
protein binding = 75 %
Monitor
- blood glucose
- blood pressure
- ophthalmologic exam for long-term steroid use
Adverse effects
- common (> 10%)
- less common (1-10%)
- uncommon (< 1%)
- seizures, mood swings, headache, skin atrophy, bruising, hyperpigmentation, acne, amenorrhea, sodium & water retention, edema, Cushing's syndrome, hyperglycemia, suppression of bone growth, osteopenia, abdominal distension, ulcerative esophagitis, pancreatitis, muscle wasting, hypersensitivity reaction, delirium, hallucinations, euphoria
- other
- osteoporosis
- fractures secondary to osteoporosis are the greatest cause of morbidity in patients on long-term, low dose prednisone (50%)
- aseptic necrosis
- glaucoma
- hypertension
- weight gain
- depression
- steroid psychosis
- gastrointestinal (GI) intolerance
- accelerated atherogenesis
- opportunistic infections
- poor wound healing
- erythroderma following use of systemic glucocorticoids[6]
- too rapid a withdrawal may produce adrenal insufficiency, especially at total doses > 40 mg/day for 2 weeks[7]
- osteoporosis
- NOT teratogenic
- does NOT cause fetal pituitary-adrenal axis suppression
Mechanism of action
- intermediate-potency glucocorticoid
- some mineralocorticoid activity
- mineralocorticoid/glucocorticoid activity (1/156)[6]
More general terms
Additional terms
- cytochrome P450 3A4 (cytochrome P450 C3, nifedipine oxidase, P450-PCN1, NF-25, CYP3A4)
- prednisolone; deltahydrocortisone; metacortandralone (Pred Forte, AK-Pred, Inflamase, Pediapred, Pred Mild, Prelone, Flo-Pred, Veripred 20)
- prednisone taper; glucocorticoid taper
Component of
- gentamicin/prednisolone/prednisone
- recombinant parathyroid hormone (1-84) (Natpara)
- melphalan/prednisone/thalidomide (ThaMP)
- rituximab/cyclophosphamide/vincristine (Oncocin)/prednisone (R-CVP)
- rituximab/cyclophosphamide/doxorubicin/vincristine (Oncocin)/prednisone (R-CHOP)
- cyclophosphamide/doxorubicin/vincristine (Oncocin)/prednisone (CHOP)
- nitrogen mustard/vincristine (Oncovin)/prednisone/ procarbazine (MOPP)
- cyclophosphamide/vincristine (Oncovin)/prednisone/procarbazine (C-MOPP)
- cyclophosphamide/vincristine (Oncocin)/prednisone (CVP, COP)
References
- ↑ The Pharmacological Basis of Therapeutics, 9th ed. Gilman et al, eds. Permagon Press/McGraw Hill, 1996
- ↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 792
- ↑ Drug Information & Medication Formulary, Veterans Affairs, Central California Health Care System, 1st ed., Ravnan et al eds, 1998
- ↑ Kaiser Permanente Northern California Regional Drug Formulary, 1998
- ↑ The Pharmacological Basis of Therapeutics, 9th ed. Gilman et al, eds. Permagon Press/McGraw Hill, 1996
- ↑ 6.0 6.1 6.2 6.3 Medical Knowledge Self Assessment Program (MKSAP) 11, 17, 18. American College of Physicians, Philadelphia 1998, 2015, 2018.
- ↑ 7.0 7.1 7.2 Prescriber's Letter 10(12):68 2003
- ↑ 8.0 8.1 Prescriber's Letter 11(2):9 2004
- ↑ 9.0 9.1 Prescriber's Letter 19(12): 2012 Rayos (Prednisone) Delayed-Release Tablets Detail-Document#: http://prescribersletter.com/(5bhgn1a4ni4cyp2tvybwfh55)/pl/ArticleDD.aspx?li=1&st=1&cs=&s=PRL&pt=3&fpt=25&dd=281207&pb=PRL (subscription needed) http://www.prescribersletter.com
- ↑ 10.0 10.1 Deprecated Reference
- ↑ 11.0 11.1 NEJM Knowledge+ Psychiatry
- ↑ 12.0 12.1 NEJM Knowledge+ Complex Medical Care
- ↑ 13.0 13.1 Beuschlein F, Else T, Bancos I et a; European Society of Endocrinology and Endocrine Society Joint Clinical Guideline: Diagnosis and Therapy of Glucocorticoid-induced Adrenal Insufficiency. J Clin Endocrinol Metab. 2024 Jun 17;109(7):1657-1683. PMID: https://www.ncbi.nlm.nih.gov/pubmed/38724043 PMCID: PMC11180513 Free PMC article.
Database
- PubChem: http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5865
- PubChem: http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=4900
- PubChem: http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5282382
- PubChem: http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5289127
- PubChem: http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=637260