Endocrine Abstracts (2017) 49 EP85 | DOI: 10.1530/endoabs.49.EP85

'Record-breaking hyponatraemia' with Addison's disease

Irfan Khan & Elizabeth Cheyne

Southmead Hospital, Bristol, UK.

Addisons disease is a rare but potentially life threatening endocrine disorder. It is well-known for disguising as a variety of presentations before diagnosis. Here we present a case report of Addison’s disease presenting with very severe hyponatraemia. A 35 year old lady was admitted with lethargy, low mood, weight loss and feeling generally unwell for the last 3 months. Six weeks prior to her admission, her GP arranged some routine investigations including U&E which were normal with a Na of 137. He later prescribed her Mirtazapine for her low mood and anxiety which she took for 4 days. This made her feel more unwell and triggered the hospital admission. She looked tanned but there was no buccal or palmar pigmentation. She was alert with normal cognition.

Admission blood results showed a plasma Sodium of 94 mmol/l, K 5.7 and normal urea/creatinine. Further investigations showed: Serum Osmolality 252, Urine osmolality 192, Urine Na 27, TSH 3.2 and random cortisol 290. She was monitored on ITU and was given normal saline and IV Hydrocortisone for a presumed diagnosis of Addison’s disease. Her Sodium level slowly came up to 114 and then to 118 over the next few days. The short synacthen test showed a flat response with the following Cortisol values: 0 min 240, 30 min 242 and 60 min 260. She denied taking exogenous steroids in any form. Later her ACTH came back very high (>2000) with positive anti-adrenal antibodies confirming primary adrenal insufficiency. The Renin/Aldosterone results are still awaited. She transiently developed behavioral disturbance with strange affect raising the suspicion of osmotic demyelination. Fortunately this resolved with reducing the dose of Hydrocortisone suggesting ’steroid psychosis’ as cause of the behavioral symptoms. The sodium level stabilized in the low 120’s but increased further slowly with addition of Fludrocortisone.

This case demonstrates the unusual presentation of Addisons disease with very severe hyponatraemia with surprisingly few neurological signs or symptoms. It also highlights theproblem of antidepressants potentially exacerbating hyponatraemia in these patients.

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