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Endocrine Abstracts (2024) 100 WD3.1 | DOI: 10.1530/endoabs.100.WD3.1

SFEEU2024 Society for Endocrinology Clinical Update 2024 Workshop D: Disorders of the adrenal gland (20 abstracts)

Primary aldosteronism in a young man with a family history of hypertension and stroke

Kiran Issuree


University Hospitals Birmingham NHS Trust, Birmingham, United Kingdom


A 25 year old Afro-Caribbean man was referred for adrenal vein sampling for suspected Conn’s syndrome and the finding of a right adrenal nodule. He initially presented to his local hospital with vomiting. He had hypokalaemia, which persisted even after the vomiting had resolved. He required oral potassium supplementation to maintain a normal serum potassium level. He gave a history of fatigue and occasional muscle cramps during the last 3 years. Intermittent spontaneous hypokalaemia was apparent on checking his historical blood tests during the same time. His GP had started him on amlodipine 10 mg once daily about 6 weeks earlier but his BP was above the recommended target of 140/90, despite compliance with the medication. He was otherwise fit and well. He is a non-smoker, rarely drinks alcohol, and does not use illicit drugs. His father died of a stroke and uncontrolled hypertension at the age of 45. His paternal grandfather also died of a stroke. His younger brother aged 18, was healthy with no known hypertension. On examination, he was normotensive on eplerenone 50 mg twice daily and amlodipine 10 mg once daily. His BMI was normal. He did not have any Cushingoid features. Biochemical testing, when he was potassium replete and not on eplerenone, showed a suppressed renin (2.0 mU/l), high aldosterone (827 pmol/l), ARR 413.9 (<91) and failure of aldosterone to suppress on saline infusion (819 from 1320 pmol/l). A biochemical diagnosis of primary hyperaldosteronism was therefore confirmed. The 1 mg overnight dexamethasone suppression test showed an appropriately suppressed cortisol of 33 nmol/l, thereby excluding Connshing syndrome. Cross-sectional imaging confirmed a right adrenal adenoma (a 15 mm nodule with unenhanced attenuation of 0 HU on CT and a homogeneous lipid-rich nodule on MRI) Metanephrines were not required since the unenhanced attenuation of the adrenal nodule was less than 10 HU. Adrenal vein sampling was not deemed necessary since he was younger than 35, had marked hyperaldosteronism, spontaneous hypokalaemia and a solitary adrenal adenoma. Genetic testing for CYP11B1/CYP11B2 chimeric gene and germline KCNJ5 mutations were negative. Following the reassuring genetic test results, he was referred directly for laparoscopic right adrenalectomy for the 15 mm aldosterone-producing right adrenal adenoma.

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