Abstract
Compound glycyrrhizin tablets, derived from licorice root, are widely used for their anti-inflammatory and hepatoprotective properties. However, their active metabolite, glycyrrhetinic acid, can induce acquired apparent mineralocorticoid excess (AME) - a clinical syndrome where cortisol abnormally activates mineralocorticoid receptors due to the inhibition of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), mimicking primary aldosteronism. We report a case of a 57-year-old male who developed severe hypertension and hypokalemia after 30 days of treatment with compound glycyrrhizin (150 mg, t.i.d.). Laboratory investigations revealed profound hypokalemia (2.03 mmol/L) and metabolic alkalosis. Critically, both plasma renin activity (< 0.5 μIU/mL) and aldosterone levels (2.4 - 2.7 ng/dL) were significantly suppressed, effectively ruling out primary and secondary hyperaldosteronism. A diagnosis of acquired AME was established based on the temporal relationship with glycyrrhizin intake, the "double-low" hormonal profile, and the exclusion of Cushing's syndrome. Following treatment with amlodipine and potassium supplementation, the patient's symptoms resolved. At the 2-week post-discharge follow-up, after discontinuing all medications, his blood pressure remained stable (< 140/90 mmHg) and serum potassium normalized to 4.55 mmol/L, confirming the reversible nature of acquired AME.