Abstract

Aims and objectivesAdrenal adenomas are usually non-functioning, but can secrete aldosterone or cortisol. It has recently been suggested that many more adenomas than previously thought secrete more than one hormone. This has important implications for their clinical management. Our aim was to determine the frequency of cortisol co-secretion in primary hyperaldosteronism at our institution and investigate the difference in metabolic profiles and clinical outcomes between co-secreting and non-co-secreting patients.Design and patientsA retrospective study of 25 patients with primary hyperaldosteronism who also underwent formal dexamethasone suppression tests to determine cortisol co-secretion.MeasurementsPost-dexamethasone suppression test cortisol, serum ALT, total cholesterol, HDL-cholesterol, LDL-cholesterol, HbA1C (were recorded) and mean arterial pressure are reported in this cohort of patients with primary hyperaldosteronism.ResultsFour out of 25 patients with primary hyperaldosteronism failed dexamethasone suppression tests. This suggests a frequency of co-secretion ranging between 4 and 16%. No significant difference was found in serum ALT, total cholesterol, serum HDL-cholesterol, LDL-cholesterol and mean arterial blood pressure at presentation between co-secretors and non-co-secretors.ConclusionA frequency range of 4–16% suggests that a significant proportion of patients with primary hyperaldosteronism co-secrete cortisol. Co-secretors did not have a worse metabolic profile than non-secretors. The impact of co-secretion on metabolic profile and surgical management remains unclear and warrants further study.

Highlights

  • Primary hyperaldosteronism (PA) is an important, yet underdiagnosed cause of secondary hypertension, accounting for an estimated 10% of all cases of elevated blood pressure [1]

  • This was a retrospective analysis of all patients undergoing adrenal vein sampling (AVS) for pre-surgical work-up of biochemically confirmed primary hyperaldosteronism (PA) between 2011 and 2017 at Imperial College London NHS Trust

  • We identified those patients who underwent formal dexamethasone suppression tests

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Summary

Introduction

Primary hyperaldosteronism (PA) is an important, yet underdiagnosed cause of secondary hypertension, accounting for an estimated 10% of all cases of elevated blood pressure [1]. Adrenal corticosteroid autonomy (Cushing’s syndrome) is a rarer cause of hypertension, accounting for approximately 1% of cases, but associated with numerous other metabolic complications including weight gain and diabetes [2]. Aldosterone and cortisol co-secretion is a topic of debate, with recent studies demonstrating that it is possibly more common than previously understood. This is important, since removal of an undiagnosed cortisolsecreting adenoma (i.e. one that was thought to be aldosterone-producing only) could result in lifethreatening cortisol deficiency postoperatively. Even less is known about the clinical significance of this [5], and adrenal crisis after resecting a PA adenoma is very rarely reported

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