prednisone
Summary
Prednisone is a synthetic corticosteroid prodrug converted by the liver to prednisolone, its active form. It has potent anti-inflammatory and immunosuppressive effects, used to treat autoimmune diseases, inflammatory conditions, allergic reactions, and certain malignancies. Long-term use carries significant metabolic and immunologic side effects.
Detail
Mechanism: Prednisone binds intracellular glucocorticoid receptors, which translocate to the nucleus and modulate gene transcription—upregulating anti-inflammatory proteins (e.g., lipocortin-1, which inhibits phospholipase A2 and thus reduces arachidonic acid metabolites like prostaglandins and leukotrienes) and downregulating pro-inflammatory cytokines (IL-1, IL-2, IL-6, TNF-alpha) via inhibition of NF-kB. It also decreases neutrophil margination (causing neutrophilia), inhibits lymphocyte proliferation and induces lymphocyte apoptosis, and reduces eosinophil and monocyte activity.
Pharmacokinetics: Requires hepatic conversion (11-beta-hydroxysteroid dehydrogenase) to prednisolone; therefore, patients with severe liver disease may be given prednisolone directly.
Clinical uses: Autoimmune diseases (lupus, rheumatoid arthritis, vasculitis), inflammatory bowel disease, asthma/COPD exacerbations, allergic reactions, transplant rejection prophylaxis, certain lymphomas/leukemias (part of chemotherapy regimens like R-CHOP), nephrotic syndrome (minimal change disease), adrenal insufficiency replacement, and autoimmune hemolytic anemia/ITP.
Adverse effects (high-yield for boards): Cushingoid features (moon facies, buffalo hump, central obesity, striae), hyperglycemia/steroid-induced diabetes, hypertension, osteoporosis/avascular necrosis (especially femoral head), muscle wasting/proximal myopathy, skin thinning and easy bruising, cataracts and glaucoma, mood changes/psychosis, peptic ulcer risk (especially with NSAIDs), immunosuppression increasing infection risk (including reactivation of latent TB, strongyloides hyperinfection), adrenal suppression with abrupt withdrawal (must taper after prolonged use to avoid adrenal crisis), and growth suppression in children.
Key testable concepts: HPA axis suppression with chronic use requiring tapering; use of stress-dose steroids in acute illness for patients on chronic steroids; monitoring for opportunistic infections; and the classic side effect profile as a mnemonic (e.g., 'CUSHINGOID').
Sources
- First Aid for the USMLE Step 1
- Katzung's Basic and Clinical Pharmacology
- Goodman & Gilman's The Pharmacological Basis of Therapeutics
- UpToDate: Glucocorticoid Pharmacology
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