{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,4,27]],"date-time":"2025-04-27T20:40:09Z","timestamp":1745786409687,"version":"3.40.4"},"reference-count":24,"publisher":"BMJ","content-domain":{"domain":["bmj.com"],"crossmark-restriction":true},"short-container-title":["BMJ Case Reports"],"accepted":{"date-parts":[[2017,12,7]]},"abstract":"<jats:p>A middle-aged woman with obesity, hyperlipidaemia and diet-controlled diabetes was referred for resistant hypertension. Her blood pressure (BP) was uncontrolled on five medications, including a diuretic. Physical exam revealed a systolic ejection murmur, and ECHO demonstrated moderate hypertrophy. Laboratory examination revealed elevated aldosterone level (20.7\u2009ng\/dL) and elevated aldosterone:renin ratio (41.4 (ng\/dL)\/(ng\/mL\/h)), meeting criteria for primary aldosteronism (PA), and confirmed by saline infusion testing. CT scan of the adrenals was non-localising. Adrenal venous sampling confirmed bilateral idiopathic adrenal hyperplasia. Concurrent primary hyperparathyroidism was demonstrated by elevated calcium and parathyroid hormone levels and localised by sestamibi scan. Idiopathic adrenal hyperplasia was treated medically with spironolactone. Her BP remained elevated until postparathyroidectomy. Evidence shows that a hyperfunctioning parathyroid gland may contribute to maintaining hyperaldosteronism in PA making this bidirectional link unique. The significance of this case is in the potential for further understanding of the pathophysiology of common causes of secondary hypertension.<\/jats:p>","DOI":"10.1136\/bcr-2017-221530","type":"journal-article","created":{"date-parts":[[2017,12,23]],"date-time":"2017-12-23T05:49:58Z","timestamp":1514008198000},"page":"bcr-2017-221530","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":2,"title":["Double hit! 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