ADDISON'S DISEASE: ASPECTS OF EARLY DETECTION AND TREATMENT

Authors

  • Khalimova Z.Y
  • Alimоukhamedova G.A
  • Mehmanova S.U

Keywords:

Primary adrenal insufficiency, Addison's disease, ACTH, cortisol, renin, glucocorticoid, mineralocorticoid, adrenalitis

Abstract

Primary adrenal insufficiency, or Addison's disease, is a polyetiological disease, the most common of which is autoimmune adrenalitis. Autoimmune adrenalitis results from destruction of the adrenal cortex, resulting in a deficiency of glucocorticoids, mineralocorticoids, and adrenal androgens. In the United States and Western Europe, the estimated prevalence of Addison's disease is one case per 20,000 people; therefore, strong clinical suspicion is necessary to avoid misdiagnosis of life-threatening adrenal crisis (e.g., shock, arterial hypotension, and decreased blood volume). Clinical manifestations before an adrenal crisis are subtle and may include hyperpigmentation, fatigue, anorexia, orthostasis, nausea, muscle and joint pain, and salt cravings. Cortisol levels decrease and adrenocorticotropic hormone levels increase. If clinically suspected, patients should undergo a corticotropin stimulation test to confirm the diagnosis. Treatment of primary adrenal insufficiency requires replacement of glucocorticoids and mineralocorticoids. During times of stress (e.g., invasive surgery illness), increased doses of glucocorticoids are required because adrenal destruction prevents an adequate physiological response. Treatment of primary adrenal insufficiency or autoimmune adrenalitis requires caution regarding concomitant autoimmune diseases; 50% of patients will develop another autoimmune disease during their lifetime.

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Published

2024-07-04