Poster Presentation The Joint Annual Scientific Meetings of the Endocrine Society of Australia and the Society for Reproductive Biology 2017

Addison's disease presenting with hypercalcaemia  (#252)

Kyaw Thura 1 , Richard Arenson 2 3
  1. Department of Endocrinology and Diabetes, Royal Perth Hospital , Perth , WA , Australia
  2. Department of Geriatric Medicine , Royal Perth Hospital , Perth , WA , Australia
  3. Endocrinology and Diabetes , Wexford Centre, St John of God (Murdoch) Hospital , Perth , WA , Australia

Background

Adrenal insufficiency is a rare but important cause of hypercalcaemia1. Hypercalcaemia can occur in both primary and secondary adrenal insufficiency2,3. The prevalence ranges from 6%1 to 21% in one study at the time of diagnosis of Addison's disease3.

Case Report

A 57 years old lady presented with unintentional weight loss of 4 kilograms, intermittent vomiting, polydipsia and nocturia over a few months. She denied significant lethargy or any other systemic symptoms.

On examination, she was very thin at 46 kilograms, had tanned skin. Her blood pressure was 100/60mmHg with no significant postural drop. There were no clinical signs of endocrinopathy. Systemic examination was unremarkable.

Her laboratory investigations revealed Sodium 134 mmol/L, Potassium 4.2 mmol/L, Bicarbonate 24 mmol/L, Urea 8.7 mmol/L, Creatinine 112 umol/L, eGFR 47 ml/min/1.73m2, Adjusted Calcium 2.64 mmol/L, Parathyroid Hormone (PTH) <0.3 pmol/L. Normal serum protein electrophoresis. CT Thorax, Abdomen and Pelvis revealed non-specific apical pleuro-parenchymal thickening.

Additional testing revealed repeat adjusted Calcium 2.62 mmol/L, Ionised Calcium 1.39 mmol/L, PTH 0.5 pmol/L, Urine Calcium excretion 24 umol/L, Urine N-Telopeptide/Creat Ratio 92 nmol BCE/mmol creat, Vitamin D 82 nmol/L, serum Angiotensin Converting Enzyme 64 U/L, IGF-1 92 ug/L, Thyroid stimulating hormone 0.7 mU/L, ACTH 315 pmol/L and morning Cortisol 37 nmol/L.

Based on the high ACTH and low morning cortisol, the diagnosis of primary adrenal failure was made. Treatment was initiated immediately with cortisone acetate 25 mg in the morning, 12.5 mg in the afternoon, and Fludrocortisone 100mcg. The patient’s vomiting resolved with restoration of appetite and normal energy. Her biochemistry normalised with adjusted Calcium 2.36 mmol/L, ionised Calcium 1.24 mmol/L and PTH 8.9 pmol/L.

Discussion

This case highlights the importance of rarer causes of hypercalcaemia. We suggest further assessment of adrenocortical axis in patients with PTH independent hypercalcaemia after excluding hyperthyroidism, Vitamin D intoxication, immobility and acromegaly.

  1. Nerup J 1974 Addison's disease: clinical studies, A report of 108 cases. Acta Endocrinologica 76 127–141.
  2. Wong RK 2000 A case of isolated ACTH deficiency presenting with hypercalcaemia. International Journal of Clinical Practice 54 623–624.
  3. Soule, S 1999 Addison's disease in Africa: a teaching hospital experience. Clinical endocrinology 50 115-20.