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Source: Smith SM, Gums JG. Adrenal Gland Disorders. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 8th ed. http://accesspharmacy.com/content.aspx?aid=7992321. Accessed May 27, 2012.

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  • Addison’s disease

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  • Hypofunction of adrenal gland caused by primary (Addison’s disease) or secondary adrenal insufficiency

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  • Autoimmune dysfunction (e.g., Graves’ disease)
  • Autoimmune polyendocrine syndrome
  • Tuberculosis
  • Bilateral adrenalectomy
  • Medications (ketoconazole, phenytoin, rifampin, phenobarbital)

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  • Occurs when adrenal glands do not produce enough cortisol and, in some cases, aldosterone.
  • Primary adrenal insufficiency (Addison’s disease) usually causes:
    • destruction of all regions of adrenal cortex
    • deficiencies of cortisol, aldosterone, and androgens
    • compensatory increases in corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH)
  • Autoimmune dysfunction causes 80–90% of cases in developed countries; tuberculosis is leading cause in developing countries.
  • Medications that inhibit cortisol synthesis (e.g., ketoconazole) or accelerate cortisol metabolism (e.g., phenytoin, rifampin, phenobarbital) can also cause primary adrenal insufficiency.
  • Secondary adrenal insufficiency usually results from exogenous corticosteroid use, leading to suppression of hypothalamic-pituitary-adrenal axis and decreased ACTH release, resulting in impaired androgen and cortisol production.

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  • Incidence approximately 1 in 100,000
  • Can affect persons of any age, gender, or ethnicity but typically presents in adults between ages 30–50 years.

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Signs and Symptoms

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  • Weight loss, dehydration, hyponatremia, hyperkalemia, and elevated blood urea nitrogen
  • Hyperpigmentation may involve exposed and nonexposed body parts.

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Laboratory Tests

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  • Using the short cosyntropin stimulation test, an increase in cortisol level to 18 mcg/dL (500 nmol/L) or more rules out adrenal insufficiency.
  • Patients with Addison’s disease have an abnormal response to the short cosyntropin stimulation test. Plasma ACTH levels are usually 400–2000 pg/mL in primary insufficiency and normal to low (5–50 pg/mL) in secondary insufficiency.
  • A normal cosyntropin-stimulation test does not rule out secondary adrenal insufficiency.
  • Insulin hypoglycemia test, metyrapone test, and CRH stimulation test are sometimes performed.

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  • Limit morbidity and mortality.
  • Return patient to normal function.
  • Prevent episodes of acute adrenal insufficiency.

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  • Inform patients of expected outcome, treatment complications, proper medication use and adherence, and potential side effects.

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  • Corticosteroids (Table 1)
    • Use hydrocortisone, cortisone, or prednisone at the lowest effective dose twice daily to mimic normal diurnal adrenal rhythm of cortisol production.
    • Starting total daily doses: hydrocortisone 15–25 mg, cortisone acetate 25–37.5 mg, or prednisone 2.5 mg. Give 2/3 of dose in the morning and 1/3 of dose 6–8 hours later.
    • May use fludrocortisone acetate 0.05–0.2 mg orally once daily to replace mineralocorticoid loss and prevent hyperkalemia. If parenteral therapy is necessary, give deoxycorticosterone trimethylacetate in oil 2.5–5 mg IM every 3–4 weeks.
    • Because most adrenal crises occur after glucocorticoid dose reductions or lack of stress-related dose adjustments, patients receiving corticosteroid replacement should add 5–10 mg hydrocortisone (or equivalent) to their normal daily regimen shortly before strenuous activities, such as exercise. During severe ...

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