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  • 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)


  • 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


  • 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


  • Definition: DMARDs comprise a group of otherwise unrelated medications that are used to treat rheumatoid arthritis and other rheumatic conditions. The term is used in contrast to NSAIDs and steroids.

  • Medications: See Table 9.16


  • Definition: DMARDs that work by targeting immune system pathways

  • General principles of use:

    • - Screen for chronic infections prior to starting biologic DMARD therapy: Tuberculosis (PPD or IGRA), HepB, HepC, HIV

    • - Biologic DMARD administration: Subcutaneous medications can be self-administered; IV medications are administered at an infusion center

    • - Lab monitoring: Check CBC/CMP q2–3 months to evaluate for cytopenias and check renal/hepatic function

    • - Do not administer live vaccines while on biologics, including live influenza vaccine, Zostavax (→ use Shingrix instead), yellow fever vaccine

    • - Nomenclature: See Table 9.15 for structure-suffix relationships for therapeutic antibodies

  • Medications: See Table 9.17

TABLE 9.15*Structure-Suffix Relationship of Therapeutic Antibodies

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