methylprednisolone
Summary
Methylprednisolone is an intermediate-acting synthetic glucocorticoid used for its potent anti-inflammatory and immunosuppressive effects. It is commonly used in acute exacerbations of autoimmune and inflammatory conditions (e.g., MS flares, severe asthma/COPD exacerbations, spinal cord injury, transplant rejection). It has minimal mineralocorticoid activity compared to hydrocortisone.
Detail
Methylprednisolone is a synthetic corticosteroid that binds cytosolic glucocorticoid receptors, translocates to the nucleus, and modulates gene transcription—upregulating anti-inflammatory proteins (e.g., lipocortin-1/annexin A1, which inhibits phospholipase A2 and thus reduces arachidonic acid metabolite production) and downregulating pro-inflammatory cytokines (IL-1, IL-2, IL-6, TNF-alpha), COX-2, and adhesion molecules. This results in decreased leukocyte migration, reduced capillary permeability, and suppressed cell-mediated immunity.
Clinically, methylprednisolone is used for: acute MS relapses (IV pulse therapy), severe asthma/COPD exacerbations, anaphylaxis (adjunct), acute spinal cord injury (historically, now controversial), organ transplant rejection prophylaxis/treatment, autoimmune diseases (lupus, vasculitis), and various inflammatory conditions. It is available in oral, IV, IM, and intra-articular formulations, and is often given as a Medrol dose pack for short tapering courses.
Pharmacokinetics: intermediate duration of action (12-36 hr biologic half-life), metabolized hepatically. It has minimal mineralocorticoid activity relative to hydrocortisone, making it useful when sodium/water retention is undesirable.
Adverse effects (class effects of glucocorticoids): hyperglycemia, immunosuppression/increased infection risk, osteoporosis, avascular necrosis (especially femoral head), adrenal suppression with abrupt withdrawal (requires tapering), Cushingoid features, peptic ulcers, mood changes/psychosis, cataracts, glaucoma, growth suppression in children, and myopathy. Long-term use requires monitoring glucose, bone density, and consideration of PPI/bisphosphonate prophylaxis.
Key boards points: distinguish glucocorticoid vs mineralocorticoid potency among steroids (dexamethasone > methylprednisolone > prednisone > hydrocortisone for glucocorticoid potency; fludrocortisone for mineralocorticoid). Remember HPA axis suppression with chronic use and the need for stress-dose steroids during illness/surgery. Understand mechanism via genomic (delayed) and non-genomic (rapid) pathways.
Sources
- Katzung's Basic and Clinical Pharmacology
- First Aid for the USMLE Step 1
- Goodman & Gilman's The Pharmacological Basis of Therapeutics
Reviewed by AnkiBoss editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.