Endocrine Abstracts

The Case: We are presenting a 51-year-old Caucasian lady with known type 1 diabetes who was diagnosed with Autoimmune Addison’s Disease (AAD) during investigation of persistent hyponatremia. She was admitted with DKA back in November 2022 that was believed to be due to gastroenteritis. Usually, her diabetes control has been reasonable over the years with no severe chronic complications or diabetes-related hospital admissions. In the hospital, she suffered from ongoing hyponatremia that was thought be be due hypovolemia and excessive Dextrose 5% used with IV insulin. On discharge, Sodium and potassium were 126 and 4.9 mmol/l respectively. GP got back to us two weeks after discharge since sodium failed to improve and hence hyponatremia work up was initiated. This revealed low morning cortisol that remained stationary after Synacthen stimulation. The ACTH came back strikingly high and adrenal antibodies came back positive. Clinically, the patient was completely asymptomatic with no manifestations of hypoadrenalism. BP was 120/70 with no orthostasis. She neither had GI symptoms or hyperpigmentation.

The rest of routine biochemistry was normal*Cut off level to diagnose adrenal insufficiency is 450 nmol/l

Treatment: Despite being asymptomatic, we decided to treat with hydrocortisone and fludrocortisone and monitor clinical and biochemical follow up

Conclusion and points for discussion: • AAD has a long latency before presentation in most patients. • Adrenal steroidogenic function is on a steep downward trajectory at the time of diagnosis and that declines irrespective of the steroid replacement treatment and changes to ACTH levels. • This looks like the opposite of honeymoon period in T1DM where there’s slight improvement of B-cell function following insulin therapy. • A minor subset of patients with AAD like this lady, have residual low-level adrenal steroidogenesis. Whether these patients represent a distinct cohort either in terms of their etiopathogenesis, requirement for steroid replacement or resilience to adrenal crisis and other complications remains unknown. • This somehow resembles mild C-peptide positivity in some patients with milder forms of T1DM.• This observation is important, because it likely indicates preservation of adrenal capsular stem cells despite the autoimmune attack. This may open new therapeutic window in the future to ameliorate this chronic condition.