Info
🌱 來自: Huppert’s Notes
Anti-Inflammatory Agents🚧 施工中
Anti-Inflammatory Agents
NSAIDS
• Mechanism: Decreased prostaglandin production and thus reduced prostaglandin-mediated capillary leakage and inflammatory cell recruitment. Most NSAIDs are non-selective inhibitors of both cyclooxygenase isoforms (COX1 and COX2).
• Clinical use: Analgesic only in most rheumatologic diseases
• Side effects: GI bleed, hypertension, hyperkalemia, AKI (ATN from inappropriate afferent arteriole constriction or tubulointerstitial nephritis)
Glucocorticoids
• Mechanism: Suppress antibody production by B cells; promote T cell apoptosis; inhibit inflammatory chemokine/cytokine production and antigen presentation by myeloid cells
• Clinical use: Rapid suppression of acute disease activity in RA, SLE, gout/pseudogout, inflammatory myopathies, PMR, etc. (1 mg/kg = common initial dose for organ-threatening rheumatologic disease)
- PJP prophylaxis should be provided for all patients on ≥20 mg prednisone daily for ≥3 weeks
- Prevention and treatment of glucocorticoid-induced osteoporosis:
• All patients on ≥2.5 mg prednisone ≥3 months should take oral calcium and vitamin D supplementation
• For patients >40 yr old on ≥2.5 mg prednisone ≥3 months: Check DEXA. If DEXA indicates moderate to high risk for fracture based on FRAX score, consider bisphosphonate therapy
• Side effects: Immunosuppression, osteoporosis, skin thinning, glaucoma, cataracts, weight gain, DM2, hypertension, mania/altered mental status, avascular necrosis, HPA axis suppression
Colchicine
• Mechanism: Impairs microtubule polymerization, and thus impairs neutrophil function
• Clinical use: Gout, pseudogout, familial Mediterranean fever, hypersensitivity vasculitis
• Side effects: Diarrhea, neuromuscular toxicity especially when co-administered with statins. Dose reduction needed for CKD