Manchester United induced addisonian crisisBMJ 2011; 343 doi: http://dx.doi.org/10.1136/bmj.d7732 (Published 15 December 2011) Cite this as: BMJ 2011;343:d7732
- Akbar Choudhry, foundation year 2 doctor1,
- Clive Marchi, general practitioner2,
- William Stephens, consultant physician3
- 1Trafford General Hospital, Urmston, Manchester M41 5BG, UK
- 2Conway Road Health Centre, Sale, Manchester, UK
- 3Department of Medicine, Trafford General Hospital, Manchester, UK
- Correspondence to: A Choudhry
Towards the end of 2010 a 58 year old woman reported a significant deterioration in her exercise tolerance. Previously she had enjoyed excellent health and participated in high intensity training for extended periods. Within three months even leisurely walks on flat terrain resulted in severe fatigue and intermittent chest discomfort. She was referred for cardiological assessment, which included dobutamine stress echocardiography and coronary angiography. Reversible ischaemia in the territory of the left anterior descending artery was managed medically but with poor symptomatic response.
A multitude of new symptoms, including poor concentration, poor quality of sleep, visual blurring, and progressing fatigue, together with a persistent hyponatraemia (serum sodium level 120-125 mmol/L, normal range 135-145 mmol/L) led to endocrinology referral.
A diagnosis of autoimmune mediated Addison’s disease was established on the basis of an absent serum cortisol response to synacthen stimulation, increased plasma adrenocorticotrophic hormone level (509 ng/L, normal range 0-46 ng/L), undetectable plasma aldosterone with increased plasma …
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