An overview of Addison’s disease

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Authors: Delphina T, Dr. Alagarraja M., Darshan J, Dineshbabu S, Pratheesh M, Sruthi MS, Sudharshan RS
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Abstract

Addison’s disease, or primary adrenal insufficiency, is a rare but serious endocrine disorder caused by impaired secretion of glucocorticoids and mineralocorticoids due to adrenal cortex dysfunction. Autoimmune destruction of the adrenal glands is the leading etiology, while infections, adrenal hemorrhage, infiltrative diseases, and genetic disorders also contribute. The disease typically presents with insidious and nonspecific symptoms such as chronic fatigue, hypotension, gastrointestinal disturbances, weight loss, salt craving, and hyperpigmentation, often resulting in delayed diagnosis. Pathophysiologically, cortisol and aldosterone deficiency disrupt metabolic regulation, electrolyte balance, and the physiological stress response, while compensatory elevation of adrenocorticotropic hormone leads to characteristic pigmentation changes. Diagnosis is based on clinical suspicion supported by biochemical evaluation, including serum cortisol and ACTH levels, ACTH stimulation testing, and relevant imaging studies. Addisonian crisis represents a life-threatening emergency requiring immediate intervention. Management involves prompt correction of hypovolemia and hypoglycemia during acute crisis, followed by lifelong glucocorticoid and mineralocorticoid replacement with appropriate stress-dose adjustments. Early diagnosis, patient education, and continuous monitoring are essential to prevent complications and improve long-term outcomes. This review summarizes the etiology, pathophysiology, clinical features, diagnostic strategies, differential diagnosis, and current management approaches for Addison’s disease.

Fields of Study & Subjects

Adrenal Hormones and Disorders Hormonal Regulation and Hypertension Stress Responses and Cortisol

Publication details

Journal / source
International Journal of Pharmacology and Clinical Research
Volume
8
Issue
3
Pages
36–41
Publication date
1 March 2026
Language
EN