A case of pseudoaldosteronism induced by glycyrrhizin

• Published in: Nihon Jinzo Gakkai shi Vol. 34; no. 1; pp. 99 - 102
• Main Author: KAGEYAMA, YO
• Format: Journal Article
• Language: English
• Published: Japan Japanese Society of Nephrology 1992
• Subjects: Aldosterone - blood; Anti-Inflammatory Agents, Non-Steroidal - adverse effects; Chronic Disease; Glycyrrhetinic Acid - adverse effects; Glycyrrhetinic Acid - analogs & derivatives; Glycyrrhizic Acid; Hepatitis - drug therapy; Humans; Hyperaldosteronism - blood; Hyperaldosteronism - chemically induced; Male; Middle Aged; mineralocorticoid, cortisol, cortisone, li-beta-hydroxysteroid dehydrogenase, glycyrrhizin; Renin - blood
• ISSN: 0385-2385; 1884-0728
• DOI: 10.14842/jpnjnephrol1959.34.99

A 55-year-old man was referred to us for evaluation of hypertension and hypokalemia. He had been administered glycyrrhizin from one year before admission for the treatment of chronic hepatitis. On admission, his blood pressure was 230/105 mmHg; serum potassium, 2.4mEq/l; the plasma aldosterone concentration (PAC) and plasma renin activity (PRA) were undetectable. His blood pressure, potassium, PRA and PAC returned to normal within about 4 weeks after discontinuation of the glycyrrhizin. Re-administration of glycyrrhizin caused increases in PRA and PAC. His urinary cortisol excretion was increased and urinary cortisone excretion decreased, while his serum cortisol level remained unchanged. Supplementation of dexamethasone led to a decrease in blood pressure, and increased levels of serum potassium, PRA, and PAC. These results suggest that increased renal cortisol as a result of decreased conversion to cortisone might play an important role in the development of pseudoaldosteronism as well as in its own mineralocorticoid activity.