A n 84-year-old man presented to the emergency department with a hypertensive emergency. He reported a 1-week history of persistently elevated measurements, taken at home, of systolic blood pressure (between 180 and 210 mm Hg), along with symptoms of headache, photophobia, chest pain and fatigue. On presentation to the emergency department, his blood pressure was 196/66 mm Hg. He had signs of volume overload on physical examination, including pulmonary crackles on auscultation and pitting edema of the lower extremities up to the knees. Chest radiography was consistent with mild pulmonary edema.The patient's initial laboratory results in the emergency department showed a low potassium level of 2.5 (reference range 3.5-5.0) mmol/L, an elevated bicarbonate level of 31 (reference range 23-29) mmol/L and an increased troponin level of 0.14 (upper limit of normal 0.04) µg/L, with no signs of myocardial ischemia on the electrocardiogram.The patient had long-standing hypertension. A blood pressure measurement taken 4 months earlier showed adequate control (125/60 mm Hg). He also had a history of coronary artery disease, type 2 diabetes and dyslipidemia. His medications included irbesartan, hydrochlorothiazide, acetylsalicylic acid, metformin, empagliflozin, insulin, ezetimibe and atorvastatin. He took furosemide on alternating days for mild venous insufficiency causing pitting edema of the feet.On admission, the patient was started on a combination of amlodipine, metoprolol and hydralazine. Irbesartan was initially held to avoid altering tests of endocrine biochemistry and later resumed. Hydrochlorothiazide was held until the end of his hospital stay to avoid aggravating the hypokalemia. The patient's presenting symptoms resolved over the next 24 hours, except for orthopnea and paroxysmal nocturnal dyspnea, which improved after several days of diuresis with intravenous furosemide.On further questioning, the patient volunteered that he had been ingesting 1 to 2 glasses of homemade licorice root extract called "erk sous" daily for the 2 weeks leading up to his presentation. Although he knew of the potential association between licorice consumption and high blood pressure, he did not think of it when he noticed his blood pressure starting to rise.Screening for pheochromocytoma and Cushing syndrome was negative. Plasma renin activity (0.01 ng/L/s; reference range 0.45-2.06 ng/L/s) and serum aldosterone (71 pmol/L; reference range 111-860 pmol/L) were both suppressed, confirming a state of pseudohyperaldosteronism. We diagnosed licorice-induced pseudohyperaldosteronism.With complete abstinence from licorice extract while he was in hospital, the patient's blood pressure gradually improved and was 140/80 mm Hg on discharge from the hospital 13 days after presentation. He was sent home on amlodipine, metoprolol, irbesartan, hydrochlorothiazide and a taper of furosemide, along with the remainder of his usual medications.The patient was seen in clinic 3 weeks later; his blood pressure was 110/57 mm Hg and he felt well. He had not ...