Z012

 

Bilateral adrenal incidentalomas, unilateral Conn’s and subclinical Cushing’s syndromes

 

T Glyn, N Thorogood, University Hospital Bristol NHS Foundation Trust

 

Abstract: We present the case of a 60-year-old woman with bilateral adrenal incidentalomas and no stigmata of endocrinopathy. Biochemical investigations were consistent with autonomous cortisol secretion: ODST 593nmol/L; ACTH 1ng/L; two 24hr UFC collections 414 and 518nmol/24hrs (<120nmol/24hrs). Cortisol after LDDST was 587nmol/L. Final cortisol following Yanovski test was 377nmol/L (<38nmol/L). Two urinary collections for catecholamines were normal, as was initial ARR. CT abdomen showed two lesions on the left (2.6cm and 1.9cm) and one on the right (1.9 cm), unchanged from 2012. Her co-morbidities included HTN requiring three agents and T2DM. Her BMI was 23 kg/m2. Her DEXA was normal.

 

She was referred for AVS and metomidate PET scan for lateralisation of excess cortisol production. An active nodule with increased uptake of C-metomidate in the upper part of the isthmus of the left adrenal gland was seen. There was no gradient for cortisol production, but a clear aldosterone gradient from the left adrenal gland (8,000 mmol/L) compared to the right (194 mmol/L) was observed. Genetic testing for ACTH independent macronodular adrenal hyperplasia was negative. Metyrapone was commenced, normalising her cortisol secretion.

 

Left adrenalectomy was performed in June 2019. Histology revealed three adrenocortical adenomas with Weiss score 2. Postoperative morning cortisol was 507nmol/L. ODST one month later revealed unsuppressed cortisol at 547nmol/L. Her postoperative plasma renin activity was normal. Her BP was 138/86 on lisinopril, amlodipine and doxazosin and HBA1c 52mmol/mol on sitagliptin.

 

This case highlights the diagnostic challenges arising in a patient with functional bilateral adrenal nodules. It demonstrates the current difficulties in lateralising excess cortisol secretion, and how, whilst attempting to do this, co-existing hyperaldosteronism was picked up.

 

The post-operative results suggest that although the primary hyperaldosteronism has been cured by the left adrenalectomy, autonomous cortisol secretion continues. Despite not being clinically Cushingoid, she has co-morbidities, which may well be a consequence of this. She is now faced with the decision of whether to have a right adrenalectomy, rendering her hypoadrenal, or life-long medical management of hypercortisolaemia.