Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 25 P94


1Department of Diabetes and Endocrinology, University Hospitals of Leicester NHS Trust, Leicester, UK; 2Department of Neurology, University Hospitals of Leicester NHS Trust, Leicester, UK.

A 52-year-old man was referred in June 2009 with weakness, unsteadiness, diarrhoea and weight loss of 14 kg in the last 4 months. His past medical history included hypertension, ischaemic heart disease and chronic obstructive pulmonary disease. He was a heavy smoker and admitted to drinking heavily for the past 9 months. His serum sodium was 126 mmol/l, serum potassium 2.0 mmol/l, serum bicarbonate 31 mmol/l. His chest X-ray was normal. He had had persistent hypokalaemia for 4 months which had been attributed to his diarrhoea. His serum potassium was normal in December 2008. A 24 h urinary free cortisol was very high at 1491 (normal range 28–221 nmol/24 h). However, he had no stigmata of Cushing’s disease. In view of his weight loss, smoking history and hypokalaemia ectopic ACTH syndrome was considered. He did not suppress fully after a 48 h high dose dexamethasone suppression test. ACTH was 6 ng/l. A CT thorax/abdomen/pelvis showed no evidence of a neoplasm and no adrenal mass. MRI of the pituitary gland was unhelpful as he was unable to keep still. A 24 h urine collection for 5-HIAA to exclude carcinoid syndrome was normal. Corticotrophin-releasing hormone stimulation test did not support a pituitary source of ACTH. He was readmitted a month later with recurrent hypokalaemia and muscle weakness. Serum sodium was 114 mmol/l, serum potassium 2.2 mmol/l. Over the next few days he became confused and agitated. A CT head scan excluded a subdural haematoma. CSF culture was negative. An EEG showed mild diffuse slowing. MRI of the brain showed features compatible with central pontine myelinolysis. We concluded that our patient’s cortisol abnormalities was due to pseudo-Cushing’s syndrome caused by his excessive alcohol consumption which also accounted for his hyponatraemia and hypokalaemia. Some patients have no physical evidence of glucocorticoid excess like in our patient.

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