A 31-year-old male presented to A&E with confusion, lethargy, polyuria and blurred vision. The previous month he had been diagnosed with diabetes and started on metformin by his GP. On examination he was cachectic (BMI 17 kg/m2), dehydrated and hypotensive (88/56). Baseline investigations revealed a metabolic acidosis (pH 7.30), with capillary glucose 20 mmol/l and moderate ketonuria. Treatment for diabetic ketoacidosis was commenced. Further results revealed he was hyponatraemic (sodium 111 mmol/l).
Over the next 48 h, his condition improved significantly with insulin sliding scale (converted to basal bolus regime after 24 h) and i.v. fluids, however his sodium did not fully correct and reached a plateau of 127 mmol/l by day 4 post admission.
Further investigations revealed a 0900 h cortisol of 521 nmol/l, however his ACTH was markedly elevated at 329 ng/l. The diagnosis of Addisons was confirmed on a short synacthen test (time 0 min cortisol 386 nmol/l, 30 min 397 nmol/l and 60 min 378 nmol/l). He was started on hydrocortisone and fludrocortisone after which his sodium corrected to normal.
Co-presentation of type 1 diabetes and adrenal insufficiency is uncommon but suggests an underlying diagnosis of type 2 polyglandular autoimmune syndrome. Further tests revealed he was positive for islet cell and anti-GAD antibodies, but not adrenal cortex antibodies. Thyroid and gonadal function was normal, as were his vitamin B12 levels. The hyponatraemia was likely contributed to by hyperglycaemia, an appropriate ADH response to hypotension and hypocortisolaemia.
Conclusions: Though the prevalence of type 2 diabetes is on the increase, practitioners should be alert to the possibility of late-onset autoimmune type 1 diabetes, particularly in those of a lean phenotype.
Hyponatraemia can be multifactorial in origin, and an incompletely corrected level should prompt further investigation. A normal cortisol in the context of acute illness may be misleading and an ACTH is of value in this setting.