A 59-year-old gentleman with poorly controlled type 1 diabetes mellitus managed on a Lantus-based basal bolus regimen, presented with severe recurrent hypoglycaemic episodes requiring rapid and significant reduction of his total daily insulin from 50units to 34units per day over a period of 2 weeks.
His diabetes complications include ischaemic heart disease, cerebrovascular disease, peripheral vascular disease, diabetic foot ulceration, proliferative diabetic retinopathy, painful peripheral neuropathy and autonomic neuropathy. His other comorbidities include COAD, chronic back pain and peptic ulcer disease.
Medications included fludrocortisone 100mcg bd, perindopril 4mg daily, aspirin 100mg daily, pantoprazole 40mg daily, atorvastatin 40mg nocte, paracetamol 1g BD, pregabalin 150mg mane/75mg nocte, paracetomol 500mg/codeine 30mg BD, Spiriva and Ventolin inhalers.
A short Synacthen test was as follows:
|
Time |
Cortisol (nmol/L) |
|
0minutes |
52 |
|
90minutes |
267 |
|
120minutes |
348 |
Other relevant investigations were:
|
Test |
Result |
|
ACTH |
<1.2pmol/L |
|
Renin |
<0.10ug/L/hr |
|
LH |
20.1IU/L |
|
Testosterone |
11.8nmol/L |
|
TSH |
0.543mU/L |
|
T4 |
15.9pmol/L |
|
Prolactin |
252mIU/L |
|
IGF-1 |
6.4nmol/L |
MRI pituitary showed partial agenesis of the corpus callosum with absence of splenium and posterior body. The pituitary gland is of normal size. An incidental CT abdomen and pelvis done 3 weeks later for symptoms suggestive of bowel obstruction revealed no pathology in the adrenals.
This may be a case of idiopathic adrenocorticotropin deficiency. Patients were typically over 40 years, hypogonadism may be present and there is absence of structural pituitary defects except for an empty sella1. It can also be associated with a transient growth hormone deficiency6. The partial agenesis of the corpus callosum is likely to be an incidental finding.
Some studies have shown increased biochemical adrenal insufficiency and prevalence of adrenal antibodies in patients with type 1 diabetes2,3whereas others did not show significant increase in prevalence compared with control subjects4,5. Testing for anti-adrenal antibodies would be necessary to completely rule out coexisting primary adrenal insufficiency.