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CASE REPORT
Infectious causes of Addison’s disease: 1 organ—2 organisms!
  1. Hafis Muhammed1,
  2. Ram V Nampoothiri1,
  3. Balan Louis Gaspar2,
  4. Sanjay Jain1
  1. 1Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India
  2. 2Department of Histopathology, PGIMER, Chandigarh, India
  1. Correspondence to Professor Sanjay Jain, pgimerinternalmedicine{at}gmail.com

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Background

Infectious aetiologies are the most common causes of primary adrenal failure (Addison’s disease) in low/middle-income countries while in the western world autoimmune causes predominate. The infections attributed to cause Addison’s include disseminated gonococcal infection, tuberculosis, histoplasmosis, cryptococcosis and cytomegalovirus (CMV) infection. Here, we describe two classical cases of Addison’s due to infections of the adrenal gland.

Case presentation

Case 1

A 55-year-old woman from North India was admitted with history of multiple episodes of vomiting. She had history of severe loss of appetite and loss of weight. There was also history of increased body pigmentation for the last 6 months. At admission, she was drowsy with tachycardia of 116 beats per minute and her blood pressure was 80/50 mm Hg in supine position associated with a significant postural drop. There was hyperpigmentation of fingers, face, oral mucosa and flexures. The rest of the system examination did not reveal any significant clinical finding. Initial biochemical parameters showed serum sodium of 116 meq/L and serum potassium of 6.1meq/L. Arterial blood gas analysis showed pH 7.2 and bicarbonate 14.9 mEq/L. A diagnosis of acute adrenal insufficiency was made, and after drawing blood sample for cortisol and adrenocorticotrpic hormone (ACTH), she was given a 100  mg bolus dose of intravenous hydrocortisone and 2 L of 0.9% saline. Investigations showed serum cortisol of 39.02 nmol/L (171–536) and elevated ACTH of 818.8 pg/mL (5–60) confirming diagnosis of primary adrenal insufficiency. With initial management, her blood pressure improved and steroids were tapered to oral hydrocortisone (25 mg/day) with oral fludrocortisone 0.1 mg once a day. Contrast-enhanced CT (CECT) of the abdomen revealed bilateral symmetrical enlarged adrenals with preservation of contour without any calcifications (figure 1A). The rest of her hormone profiles were within normal limits ruling out a polyendocrinopathy syndrome. Antinuclear antibody immunofluorescence (ANA-IF) and retroviral serology were negative. CT-guided biopsy from enlarged adrenal glands was performed which revealed dense lymphoplasmacytic cell infiltrates with collection of epithelioid cells …

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