Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2015) 37 EP33 | DOI: 10.1530/endoabs.37.EP33

ECE2015 Eposter Presentations Adrenal cortex (94 abstracts)

A case of Addison's disease: high clinical suspicion should guide diagnosis and caution should be used when reviewing initial laboratory investigations

Mark Sutton-Smith , Maria Ravelo , David Lipscomb & Naik Haya


East Sussex Healthcare NHS Trust, The Bending and Sheppard Centre for Diabetes and Endocrinology, Kings Drive, Eastbourne, East Sussex BN21 2UD, UK.


A 69-year-old lady with a history of autoimmune diabetes mellitus and primary autoimmune hypothyroidism presented to the Specialist Diabetes Clinic with a significant inexplicable variation in her capillary blood glucose. She had been undergoing investigations with the gastroenterologists for nausea, vomiting, and weight loss. Despite extensive investigations including: oesophageal–gastro-duodenoscopy, CT–thorax, abdomen, pelvis scanning, and gastric emptying studies no cause for her symptoms had been found. Her drug therapy included ranitidine, omeprazole, metformin, levothyroxine, folic acid, simvastatin, lantus, and novorapid. Given her clinical presentation and autoimmune diagnoses, metformin was stopped and she was investigated for adrenal insufficiency. Her basal serum cortisol was 410 nmol/l (normal range >400 nmol/l). Her short Synacthen test results were 421 nmol/l at 30 min and 433 nmol/l at 60 min. Basal ACTH 1100 ng/l (normal range 5–46), plasma renin 28 nmol/l per h (normal range 0.5–3.1), and plasma aldosterone 110 pmol/l (normal range 100–800). Anti-adrenal antibody titre was positive at 1:10 dilution.

Discussion: Baseline serum cortisol level was perceived to be adequate; however response to ACTH was stunted. The ACTH, aldosterone, and renin levels together with positive anti-adrenal antibody titre are consistent with a diagnosis of primary autoimmune adrenal insufficiency (Addison’s disease). She was immediately started on hydrocortisone replacement with explanation about steroid sick day rules, mineralocorticoid was added and she was reviewed in clinic 3 weeks later. Her glycaemic profile improved, hypoglycaemic episodes were abolished and gastroenterological symptoms completely resolved. This case highlights the importance of retaining a high degree of clinical of suspicion in diagnosing adrenal insufficiency despite a ‘normal’ basal cortisol and how ACTH, aldosterone, renin, and anti-adrenal antibody testing may aid diagnosis in such cases.

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