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A Case of Addison’s Disease Nearly Mistaken for Anorexia Nervosa

Photographs demonstrating clinical signs of Addison’s disease. (A) longstanding weight loss and hyperpigmentation in the following sites: (B) periorbital and buccal, (C) extensor surface elbow joint, (D) old scar sites on forearm, (E) extensor surface of proximal interphalangeal joints.

A 22-year-old woman presented to her primary care physician because of an unintentional weight loss of 30 pounds (Figure A) associated with nausea, vomiting, anorexia, and generalized abdominal pain. She also described symptoms of anxiety and low mood that coincided with the breakdown of a relationship. Although she did not report body image distortion or fear of weight gain, anorexia nervosa and depressive disorder were both strongly suspected, and she underwent a trial of antidepressant therapy that was eventually stopped because her symptoms worsened. One year later, she was diagnosed with primary hypothyroidism and levothyroxine replacement was commenced.

Shortly after starting levothyroxine, she presented to the emergency department with syncope, weakness, and marked symptoms of postural hypotension that prevented her from standing up. On examination, she was cachectic, weighing only 77 pounds and measuring 5 feet 1 inch in height (body mass index, 14.5 kg/m2). She was in hemodynamic shock, with a blood pressure of 70/50 mm Hg and a pulse of 115 beats per minute. There was evidence of skin hyperpigmentation at multiple sites (Figure B–E). Biochemical investigations demonstrated a normal sodium of 136 mmol/L (reference range, 133-146 mmol/L) and a normal potassium of 4.8 mmol/L (reference range, 3.5-5.3 mmol/L), and a random cortisol was low at 48 nmol/L (1.7 μg/dL). A diagnosis of adrenal insufficiency was made, and she was successfully resuscitated with intravenous fluids and intramuscular hydrocortisone treatment.

Prior to discharge, she underwent a short Synacthen test that confirmed primary adrenal insufficiency with a low basal cortisol of 34 nmol/L (1.2 μg/dL), 30-minute stimulated cortisol of 35 nmol/L (1.3 μg/dL), and markedly elevated adrenocorticotrophic hormone of 1992 ng/L (reference range, 0-47 ng/L). Adrenal antibodies (21-hydroxylase) were positive, which confirmed a diagnosis of Addison’s disease. She was discharged on oral hydrocortisone in combination with mineralocorticoid replacement. Six weeks later, her original symptoms had resolved and she had gained 13 pounds in weight (body mass index, 16.8 kg/m2). Six months later, her weight had returned to her baseline of 107 pounds.

Addison’s disease is an autoimmune adrenalitis that causes deficiencies in cortisol, aldosterone, and adrenal androgens. Patients commonly present with fatigue, anorexia, weight loss, and gastrointestinal disturbance. Coexisting autoimmune conditions such as primary hypothyroidism, type 1 diabetes, and pernicious anemia should increase suspicion for Addison’s disease, especially in recently diagnosed hypothyroidism, as thyroxine replacement may precipitate an adrenal crisis, as it did in our patient.1

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-Claire Feeney, MBBS, PhD, MRCPKevin Buell, MBBS

This article originally appeared in the November issue of The American Journal of Medicine.

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