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Licorice-induced pseudoaldosteronism is a common adverse effect in traditional Japanese Kampo medicine, and 3-monoglucuronyl glycyrrhetinic acid (3MGA) was considered as a causative agent of it. Previously, we found 22 α -hydroxy-18 β -glycyrrhetyl-3- O -sulfate-30-glucuronide ( 1 ), one of the metabolites of glycyrrhizin (GL) in the urine of Eisai hyperbilirubinuria rats (EHBRs) treated with glycyrrhetinic acid (GA), and suggested that it is also a possible causative agent of pseudoaldosteronism. The discovery of  1  also suggested that there might be other metabolites of GA as causal candidates. In this study, we found 22 α -hydroxy-18 β -glycyrrhetyl-3- O -sulfate ( 2 ) and 18 β -glycyrrhetyl-3- O -sulfate ( 3 ) in EHBRs’ urine.  2  and  3  more strongly inhibited rat type 2 11 β -hydroxysteroid dehydrogenase than  1  did  in vitro . When EHBRs were orally treated with GA, GA and  1 – 3  in plasma and  1 – 3  in urine were detected; the levels of 3MGA were quite low.  2  and  3  were shown to be the substrates of organic anion transporter (OAT) 1 and OAT3. In the plasma of a patient suffering from pseudoaldosteronism with rhabdomyolysis due to licorice, we found 8.6 µM of  3 , 1.3 µM of GA, and 87 nM of  2 , but  1 , GL, and 3MGA were not detected. These findings suggest that 18 β -glycyrrhetyl-3- O -sulfate ( 3 ) is an alternative causative agent of pseudoaldosteronism, rather than 3MGA and  1 .

18β-glycyrrhetyl-3-O-sulfate would be a causative agent of licorice-induced pseudoaldosteronism