A 51-year-old lady was referred to our clinic because of severe hypertension; blood pressure 214/119 mm Hg despite treatment with an angiotensin receptor antagonist and a calcium channel blocker. Her initial laboratory results showed hypokalaemic alkalosis with normal urea and creatinine levels. Her 24-h urinary sodium excretion was markedly elevated at 244 mmol (equivalent to a daily intake of approximately 16 g of salt). Hyperaldosteronism was suspected but her plasma aldosterone level was subsequently found to be normal. On further questioning, the patient admitted to eating considerable amounts of salted liquorice and a diagnosis of acquired apparent mineralocorticoid excess was made. Liquorice has a well-known mineralocorticoid activity as it inhibits the action of 11β-hydroxysteroid dehydrogenase 2 and can induce mineralocorticoid hypertension. After stopping eating the salted liquorice, the patient's blood pressure quickly normalised and all her antihypertensive medications were stopped.