Most herbal medicines contain licorice, which may inhibit 11-beta-hydroxysteroid dehydrogenase type 2 (11βHSD2). When licorice inhibits 11βHSD2, accumulated cortisol binds excessively to the mineralocorticoid receptor (MR) instead of aldosterone, promoting sodium absorption and potassium excretion. This condition has been called pseudoaldosteronism due to its clinical manifestations resembling those of primary aldosteronism, producing excessive aldosterone. Primary aldosteronism and pseudoaldosteronism usually present with increased urine potassium excretion in the face of hypokalemia due to excessive MR activation by aldosterone and cortisol, respectively, the so-called renal potassium loss. Here, we report an atypical case of licorice-induced pseudoaldosteronism, which unexpectedly presented with decreased urine potassium excretion in the presence of severe hypokalemia in an elderly patient. A spot potassium-to-creatinine ratio was decreased to 4.5 mmol/g creatinine. A 24-hour urine collection also revealed decreased urine potassium excretion of 7.5 mmol/day in the presence of severe hypokalemia. These results on urine potassium were atypical for pseudoaldosteronism. Urine sodium excretion was also significantly reduced to 27.5 mmol/day, suggesting low sodium intake due to anorexia. Low sodium intake followed by low sodium delivery to the collecting duct was the crucial cause of decreased urine potassium excretion in pseudoaldosteronism. Clinicians need to understand the side effects of licorice and assess the risks and benefits associated with the use of licorice-containing drugs, especially in patients with risk factors for pseudoaldosteronism, such as advanced age or low body weight. Careful follow-up of blood pressure or serum potassium concentration is required to prevent the development of pseudoaldosteronism.