Diagnosis and Treatment > Investigation > Fludrocortisone suppression

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Rémi Goupil Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Ipswich Road, Woolloongabba, Brisbane, Queensland, 4102, Australia
Hôpital du Sacré-Coeur de Montréal, University of Montreal, Montreal, Quebec, H4J 1C5, Canada

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Martin Wolley Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Ipswich Road, Woolloongabba, Brisbane, Queensland, 4102, Australia

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Jacobus Ungerer Department of Chemical Pathology, Pathology Queensland, Brisbane, Queensland, 4001, Australia

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Brett McWhinney Department of Chemical Pathology, Pathology Queensland, Brisbane, Queensland, 4001, Australia

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Kuniaki Mukai Department of Biochemistry, Medical Education Center, Keio University School of Medicine, Shinjuku-ku, Tokyo, Japan

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Mitsuhide Naruse Department of Endocrinology, Metabolism and Hypertension, National Hospital Organization Kyoto Medical Center, Kyoto, Japan

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Richard D Gordon Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Ipswich Road, Woolloongabba, Brisbane, Queensland, 4102, Australia

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Michael Stowasser Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Ipswich Road, Woolloongabba, Brisbane, Queensland, 4102, Australia

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Summary

In patients with primary aldosteronism (PA) undergoing adrenal venous sampling (AVS), cortisol levels are measured to assess lateralization of aldosterone overproduction. Concomitant adrenal autonomous cortisol and aldosterone secretion therefore have the potential to confound AVS results. We describe a case where metanephrine was measured during AVS to successfully circumvent this problem. A 55-year-old hypertensive male had raised plasma aldosterone/renin ratios and PA confirmed by fludrocortisone suppression testing. Failure of plasma cortisol to suppress overnight following dexamethasone and persistently suppressed corticotrophin were consistent with adrenal hypercortisolism. On AVS, comparison of adrenal and peripheral A/F ratios (left 5.7 vs peripheral 1.0; right 1.7 vs peripheral 1.1) suggested bilateral aldosterone production, with the left gland dominant but without contralateral suppression. However, using aldosterone/metanephrine ratios (left 9.7 vs peripheral 2.4; right 1.3 vs peripheral 2.5), aldosterone production lateralized to the left with good contralateral suppression. The patient underwent left laparoscopic adrenalectomy with peri-operative glucocorticoid supplementation to prevent adrenal insufficiency. Pathological examination revealed adrenal cortical adenomas producing both cortisol and aldosterone within a background of aldosterone-producing cell clusters. Hypertension improved and cured of PA and hypercortisolism were confirmed by negative post-operative fludrocortisone suppression and overnight 1 mg dexamethasone suppression testing. Routine dexamethasone suppression testing in patients with PA permits detection of concurrent hypercortisolism which can confound AVS results and cause unilateral PA to be misdiagnosed as bilateral with patients thereby denied potentially curative surgical treatment. In such patients, measurement of plasma metanephrine during AVS may overcome this issue.

Learning points

  • Simultaneous autonomous overproduction of cortisol and aldosterone is increasingly recognised although still apparently uncommon.

  • Because cortisol levels are used during AVS to correct for differences in dilution of adrenal with non-adrenal venous blood when assessing for lateralisation, unilateral cortisol overproduction with contralateral suppression could confound the interpretation of AVS results

  • Measuring plasma metanephrine during AVS to calculate lateralisation ratios may circumvent this problem.

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