A29-year-old woman was admitted under the care of the general surgeons with a 3-week history of increasing colicky epigastric and retrosternal pain with severe nausea, profuse bile-stained vomiting, constipation and weight loss of 1.5 stone. In contrast, for the preceding 6 months she had been suffering from weight gain, ‘indigestion’, malaise, lethargy and syncopal attacks. There was no previous history of note and she had had two uneventful deliveries 3 and 5 years previously. On examination, she looked unwell, was severely dehydrated and apyrexial. Her skin was pale with a yellow tinge. Mucous membranes were pink and sclera were not pigmented. Her pulse was 92 beats per minute and her blood pressure was 93/51 mmHg. Abdominal examination revealed epigastric tenderness with guarding, but no rebound tenderness. There was no abdominal distension or succussion splash. She had marked abdominal striae which were pigmented. Laboratory results were as follows: haemoglobin 15.9 g/dl (normal range (NR) 11.0−16.5 g/dl), white cell count 10.8×109/litre (NR 3.5−11.0×109/litre), neutrophils 5.7×109/litre (NR 1.5−7.5×109/litre), haematocrit 0.478 (NR 0.36−0.45), sodium 133 mmol/litre (NR 135−146 mmol/litre), potassium 4.1 mmol/litre (NR 3.6−5 mmol/litre), urea 5.9 mmol/litre (NR 2.6−6 mmol/litre), creatinine 153 mmol/litre (NR 62−124 mmol/litre), amylase 70 U/litre (NR <300 U/litre), aspartate transaminase 35 IU/litre (NR 0−40 IU/litre), alkaline phosphatase 43 IU/litre (NR 40−105 IU/litre), bilirubin 21 mmol/litre (NR 0−17mmol/litre), calcium 2.53 mmol/litre (NR 2.12−2.62mmol/litre), albumin 41g/litre (NR 32−45g/litre), urine dipstick negative for blood and protein, and pregnancy test negative. Abdominal and chest X-rays were unremarkable. An ultrasound scan of the biliary tract revealed a solitary gall stone with a normal calibre common bile duct. Surgical differential diagnoses included biliary colic or peptic ulceration but because of the low sodium in the presence of clinical and biochemical/haematological dehydration a diagnosis of adrenocortical failure was considered. A random cortisol was performed at presentation with a value of 40 nmol/litre. A short synacthen test revealed a basal cortisol of 41 nmol/litre and virtually no response to adrenocorticotrophic hormone (ACTH) with cortisol values of 43 nmol/litre at 30 minutes and 51nmol/litre at 60 minutes confirming adrenocortical failure. A simultaneous serum ACTH was grossly elevated at 834 ng/litre (NR 0−50 ng/litre), showing this to be primary adrenocortical failure and thus Addison's disease. Subsequent investigations showed her to be hypothyroid with a thyroid-stimulating hormone level of 74 mU/litre (NR 0.35−5.5 mU/litre) and free thyroxine (T4) of 5 pmol/litre (NR 10−22 pmol/litre) and to have circulating antithyroid microsomal and adrenal antibodies.
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