Addison’s Disease

Addison’s Disease is a primary adrenal insufficiency.

  • Results from the destruction of the adrenal cortex from idiopathic etiology (unknown cause)
  • Half of addison’s patients have multiple endocrine related disorders (ex. Ovary, thyroid, pancreas, parathyroid gland)
    • Addison’s patients are deficient in cortisol, aldosterone, & various other androgens that may be produced by these endocrine organs
  • Can be caused by meds that inhibit cortisol synthesis or accelerate cortisol metabolism
  • S/S:  weakness, pigmentation of skin, weight loss, anorexia, n/v, hypotension & membrane pigmentation are the most common
    • Other S/S:  abdominal pain, salt craving, diarrhea, constipation, syncope, vitiligo
  • ACTH levels:         primary insufficiency = 400-2000 pg/mL              secondary insufficiency = 0-50 pg/mL
  • Goals in the treatment of Addison’s disease:  pt ed. (trxt complications, expected outcomes, what to do about missed doses, SE), want to give the lowest effective replacement dose, mimic normal diurnal adrenal rhythm
  • Treatment:
    • HCT 15 mg/day
    • cortisone 20 mg/day
    • prednisone 2.5 mg/day   (give 2/3 of daily dose in the AM, 1/3 of daily dose in the PM);  monitor symptoms every 6-8 weeks
    • Fludrocortisone acetate 0.05-0.2 mg daily is used to replace mineralocorticoid loss (minimize hypokalemia)
  • SE of corticosteroids:  GI effects, edema, HTN, hypokalemia, insomnia, excitability, diabetes, EKG changes, cushings
  • Average adult production of cortisol:  10-30 mg/day  (usually peak concentrations occur around 8 AM)
    • If ACTH or serum cortisol > 20 mcg/dL  you don’t need daily steroids
    • AM cortisol < 3 mcg/dL, continue steroid therapy
  • Taper steroids over time
    • Use shorter acting formulations at the lowest possible dose, if using possible once daily dosing, then give it in the morning to mimic normal cortisol patterns

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