ECE2018 Poster Presentations: Adrenal and Neuroendocrine Tumours Adrenal cortex (to include Cushing's) (70 abstracts)
Department of Endocrinology & Diabetes, Northwick Park Hospital, London, UK.
A 49-year-old female was admitted to medical HDU with diabetes ketoacidosis (DKA) and newly diagnosed diabetes. Six months previously she was diagnosed with malignant hypertension. She had poorly controlled blood pressure despite treatment with four anti-hypertensives, which were her only regular medication. She had never used any medications or creams containing glucocorticoids. She had no history of hypokalaemia and reported no use of liquorice. She recently attended an outpatient appointment with a cardiologist and investigations including MRA of renal arteries and echocardiogram were all reported as normal. She complained of a 6-month history of lethargy, severe weight gain, and a two-month history of easy bruising, lower-limb weakness, and increasing polyuria and polydipsia. There was no history of headache, palpitations, flushing, or diaphoresis. On examination, she had a BMI of 41 kg/m2, she had multiple bruises, off-color abdominal striaes, and proximal myopathy evident on lower limbs. She had no signs of androgen excess. Upon transfer to a general medical ward she was under the care of the endocrinology team. IFCC-HbA1C checked on admission was 102 mmol/mol, showing a large increment when compared to 30 mmol/mol measured 6 months previously. Anti-glutamic acid decarboxylase and anti-islet cell antibodies were both negative. Cortisol level post overnight-dexamethasone suppression was high at 163 nmol/l (RR <50 nmol/l). Total urine cortisol was 472 nmol in 24hours, confirming hypercortisolaemia. Tests were done when renal function was normal. Adrenal CT revealed a 2.6 cm right-adrenal adenoma (absolute washout=69%). 24-h urine metanephrines (×2) and aldosterone-renin-ratio were all within normal range. ACTH level was 15.9 ng/l (RR: 046). Adrenal androgen measurements are still being processed. In view of her inconclusive ACTH results, an MRI of the pituitary has also been requested and it is still pending. She was discharged on basal-bolus insulin and regular anti-hypertensives with a plan for urgent follow up in endocrinology clinic and discussion of results on adrenal MDT. This is a case of rapidly developing Cushings syndrome leading to life-threatening presentation with malignant hypertension and DKA. Glucose intolerance associated with Cushings syndrome is usually only mild to moderate in severity. Marked hyperglycaemia, glycosuria, and polyuria are uncommon, and ketosis is rare. Appropriate management could potentially lead to total remission of diabetes and hypertension.