Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2013) 31 P74 | DOI: 10.1530/endoabs.31.P74

SFEBES2013 Poster Presentations Clinical practice/governance and case reports (79 abstracts)

Spironolactone interference in the immunoassay of androstenedione in a patient with a cortisol-secreting adrenal adenoma

Deirdre Broderick 1 , Rachel K Crowley 1 , Triona O’Shea 1 , Gerard Boran 2 , Kevin Conlon 3 , Vincent Maher 4 , James Gibney 1 & Mark Sherlock 1


1Department of Endocrinology, Tallaght Hospital, Dublin 24, Ireland; 2Department of Chemical Pathology, Tallaght Hospital, Dublin 24, Ireland; 3Department of Surgery, Tallaght Hospital, Dublin 24, Ireland; 4Department of Cardiology, Tallaght Hospital, Dublin 24, Ireland.


A 48-year-old man was referred for investigation of uncontrolled hypertension on four agents (olmesartan, felodipine, hydrochlorothiazide and spironolactone) and a 3 cm right-sided adrenal adenoma (pre-contrast Hounsfield units 25). Endocrine investigation for the hypertension and adrenal mass included: androstenedione 19.9 nmol/l 2.8–10.5) (elevated on two occasions on a Siemens Coat-A-Count assay), DHEA 0.7 μmol/l (2.1–15.2), 1 mg overnight dexamethasone suppression test 0900 h cortisol 159 nmol/l and 48 h low dose dexamethasone suppression test 0900 h cortisol 153 nmol/l. ACTH levels were <5 pmol/l. Thus, there was evidence of hormone hypersecretion from two zones of the adrenal gland, and a lipid-poor lesion on imaging; both characteristics would be suspicious for adrenocortical carcinoma.

Spironolactone, diuretics and olmesartan were discontinued to assess his renin-angiotensin-aldosterone system and 6 weeks later a plasma renin activity and aldosterone were performed (3.0 ng/ml per h and 708 pmol/l respectively) and androstenedione was now normal at 3.7 nmol/l (2.8–10.5).

The diagnosis of a cortisol-producing adrenal adenoma was made and the patient underwent laparoscopic adrenalectomy. He was commenced on glucocorticoid cover post-operatively and his 6 week post operative synacthen test revealed glucocorticoid deficiency in keeping with the diagnosis (cortisol 0 min 279 nmol/l, 30 min 366 nmol/l). Histology showed an adrenal adenoma with 0/9 Weiss criteria.

Spironolactone has only recently been described as interfering with the androstenedione assay using the Siemens Coat-A-Count method in three patients with polycystic ovary syndrome. This is the first report of this interference in a patient undergoing endocrine evaluation of an adrenal mass. It is important to recognise spironolactone assay interference; the increased levels of androstenedione as well as cortisol would raise the possibility of adrenal malignancy and influence decision-making when planning the extent of surgical resection.

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