Endocrine Abstracts

A 63-year old woman presented with a 3 weeks history of sweating, panic attacks and vomiting. Urine dipstick on admission was positive for glucose (3+) and ketones (2+) and lab glucose was elevated at 26 mmol/l. Based on the findings she was treated as diabetic ketoacidosis and commenced on insulin. Further investigations showed an elevated urinary catecholamines and marked hypercalcaemia (adjusted calcium 3.10 mmol/l) with unsuppressed PTH at 71 pg/ml (normal 12–72 pg/ml). TFT was normal. CT abdomen showed a 7.7×6.1 cm right adrenal mass and bone densitometry showed evidence of osteoporosis. The diagnosis of pheochromocytoma and primary hyperparathyroidism was made and she had a right adrenalectomy for which histology was of a benign pheochromocytoma.

Interestingly, her daughter was diagnosed with prolactinoma at the time and the possibility of Multiple Endocrine Neoplasia was raised. She subsequently underwent a total thyroidectomy and subtotal parathyroidectomy. Histology showed no evidence of C cell hyperplasia of thyroid. Genetic testing for MEN1 and MEN 2 were negative.

She was then lost to follow-up and reappeared 5 years later in the diabetic clinic being only on a minimal dose of insulin. Her HbA1c was 5.9% with no hypoglycaemia. In view of the good glycaemic control, her insulin was stopped. She was allowed a normal carbohydrate diet and asked to monitor her blood glucose and ketones. An OGTT performed 6 weeks later showed a fasting glucose of 5.8 mmol/l and 2 h glucose 8.2 mmol/l.

This case highlights the importance of considering ‘non-diabetic hyperglycaemia’ in endocrine conditions involving glucose regulatory hormones. Glucose counter-regulatory hormones are released in events of hypoglycaemia to increase hepatic glycogenolysis and gluconeogenesis. Endocrine conditions involving these hormones will therefore also result in a change of glycaemic status. In this patient, her initial marked hyperglycaemia was likely due to the pheochromocytoma that resolved after her adrenalectomy.