We describe two similar but distinct cases of newly presenting coexistent adrenocortical insufficiency and type 1 diabetes.
Case 1; an 18 yr old woman presented with a two week history of polydipsia, polyuria and accelerated weight loss. Random glucose 20.2 mmol/L but no evidence of ketoacidosis. She was thin, pigmented, hypotensive and dehydrated and confirmed one years weight loss, lethargy, abdominal pain and occasional vomiting. Short synacthen test confirmed adrenocortical insufficiency (cortisol: 15 nmol/L at 0 min, 16 nmol/L at 30 mins, ACTH 239.6 pmol/L at 0 min).Glucagon stimulated C-terminal peptide test confirmed type 1 diabetes.
Case 2; a 20 yr old male presented in extremis with hypotension (59/34 mmHg), hypothermia and barely responsive. Investigations showed Na 120, K 8.1, Urea 22.5, Creat 299, random glucose 1.5. He was resuscitated and in ITU. History revealed weight loss, anorexia and intermittent abdominal pain over six months. Short synacthen test (cortisol: <26 nmol/L at 0 min, <26 nmol/L at 30 min) confirmed adrenal insufficiency and he was commenced on replacement hydrocortisone. Surprisingly HbA1c at this time was 6.2%. Within 1 week of commencing steroids he represented with weight loss, polydipsia and polyuria and a random blood glucose 35 mmol/L.
These two cases highlight the intrinsic role corticosteroids have in glucose control within the body and how the co-deficiency of cortisol and insulin can mask the typical presentation of either diabetes or Addisons disease. In case one, a typical presentation of diabetes was masked by cortisol deficiency curtailing the ketogenic effects of insulin deficiency. In case two, the development of diabetes was masked by cortisol deficiency which was then revealed after glucocorticoid replacement was commenced.
Type 1 diabetes and Addisons disease are known to be associated and we would, in light of these two cases, stress the importance of considering dual presentation of disease in the atypical presentation.