Severe asymptomatic hypokalemia associated with prolonged licorice ingestion: A case report

Excessive ingestion of licorice can cause pseudohyperaldosteronism. A few case reports in the available literature have described significant hypokalemia secondary to licorice consumption with clinical manifestations of muscle weakness, paralysis, or severe hypertension. To our knowledge, no report has discussed severe asymptomatic hypokalemia associated with licorice consumption.

A 79-year-old man presented to the urology clinic with a several-month history of urinary frequency and a weak stream. Routine laboratory investigations revealed serum potassium (K) level of 1.8 mmol/L, and he was immediately admitted to the nephrology department.

He was in a good state of health, and systemic and neurological examinations were unremarkable. However, laboratory investigations revealed severe hypokalemia and metabolic alkalosis accompanied with renal K wasting and hypertension, suggesting a state of mineralocorticoid excess. Hormonal studies revealed low serum renin and aldosterone but normal serum cortisol levels. Detailed history taking revealed that he had used licorice tea daily during the preceding 18 months.

The patient's serum K returned to normal levels after vigorous K replacement and discontinuation of licorice intake. He was also diagnosed with benign prostatic hyperplasia during hospitalization and was treated.

Chronic licorice ingestion can precipitate severe hypokalemia, although patients may remain asymptomatic. This case report indicates that the severity of a patient's clinical presentation depends on individual susceptibility, as well as the dose and duration of licorice intake.