Endocrine Abstracts

Background: Addison’s disease affects 100–220 people per million in Western Europe and the United States. Diagnosing Addison’s disease in the acute setting is challenging, as symptoms are often non-specific and cortisol levels may be equivocal during acute illness.

Case: A 36-year-old woman with hypothyroidism presented with a 10-day history of diarrhoea, vomiting and fatigue after a recent upper respiratory tract infection. She was tachycardic and normotensive, with dry mucous membranes and reduced skin turgor. There was no evidence of hyperpigmentation, involving buccal mucosa or palmar creases. Bloods revealed severe hyponatraemia (109 mmol/l), hyperkalaemia (6.7 mmol/l) and normoglycaemia. Treatment with IV hydrocortisone and fluid resuscitation with 0.9% NaCl was recommended with close monitoring of sodium due to high risk of overcorrection. However, she has been commenced on 1.8% hypertonic saline (1.8% NaCl) that led to a rise in sodium from 109 mmol/l to 122 mmol/l within 24 hours, requiring dextrose infusion to counteract the rapid correction. Blunted cortisol response on SST, elevated ACTH (575 ng/l), elevated renin (119.5 mu/l), borderline low aldosterone (103 pmol/l), and positive adrenal cortex antibodies confirmed autoimmune adrenalitis. Following transition to oral hydrocortisone (10 mg twice daily), fludrocortisone (50 mg/day) was initiated. Over six weeks, patient fully recovered, resumed work, and had normalised electrolytes, ACTH, and renin levels. As an active runner, she received personalized education on adjusting steroid doses during training, emergency hydrocortisone use, support resources like the Addison’s Disease Self-Help Group, and advice to carry medical alert documentation.

Discussion: This case illustrates the diagnostic difficulty of adrenal insufficiency during systemic stress, where cortisol levels can be misleading. Impaired water clearance despite hypotonicity reflects persistent antidiuretic hormone (ADH) secretion secondary to glucocorticoid deficiency—a subtle but key feature. Initiation of steroids suppresses ADH, potentially causing rapid aquaresis and sodium overcorrection, highlighting the need for careful fluid and electrolyte management in such cases to prevent osmotic demyelination. Fludrocortisone dosing is best guided by renin to optimise sodium and volume status. Hydrocortisone replacement should be personalised based on clinical and biochemical responses to avoid under- or overtreatment.