The glucagon stimulation test (GST) is used as a provocative test of the hypothalamic pituitary adrenal axis (HPAA) but the response to this test is variable and the mechanism of action remains unclear. The GST has never been studied in diabetic patients with autonomic neuropathy (AN). We illustrate the assessment of cortisol response in two diabetic patients with AN who were suspected of having adrenocortical deficiency. Case one: A 40 year old type 1 diabetic suffers from diabetic gastroparesis, diabetic diarrhoea, bladder atony, retinopathy, nephropathy and postural hypotension. She was diagnosed in 1996 with a craniopharyngioma and had it resected surgically. In 1998 she had an insulin stress test (IST) which showed a peak cortisol of 921nmol/l. Her MRI showed no recurrence. Her main symptoms were tiredness and anorexia, which gradually got worse. In 2001 she had a GST which revealed a peak cortisol of 360nmol/l at 120minutes but a 250microgram short synacthen test (SST) revealed a cortisol of 770nmol/l at 60 minutes with a baseline of 310nmol/l. Case two: A 47 year old type 2 diabetic on oral hypoglycemics had recurrent hypoglycaemic attacks and significant postural hypotension. Pituitary insufficiency was suspected and she went on to have a GST. The peak cortisol response to GST was 212 nmol/l and the rest of the pituitary function was normal. MRI revealed a 3mm pituitary cyst. We were surprised that the rest of the pituitary function was normal and therefore performed a SST to reconfirm the diagnosis of cortisol deficiency. This revealed a cortisol of 1245nmol/l at 60 minutes with a baseline of 203nmol/l. These cases suggest that the autonomic nervous system is an integral part of the HPAA response to glucagon and that caution should be used in interpreting the test in this situation.
08 - 11 Apr 2002
British Endocrine Societies