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[Licorice--not just candy].

Kristian Heldal1, Karsten Midtvedt

  • 1Nyreseksjonen Medisinsk avdeling Rikshospitalet 0027 Oslo. kristian.heldal@tss.telemax.no

Tidsskrift for Den Norske Laegeforening : Tidsskrift for Praktisk Medicin, Ny Raekke
|July 3, 2002
PubMed
Summary

Excessive liquorice consumption can cause severe hypertension, hypokalaemia, and metabolic alkalosis due to glycyrrhetinic acid inhibiting 11-beta-hydroxysteroid dehydrogenase. Symptoms resolve after stopping liquorice intake, demonstrating its potent mineralocorticoid activity.

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Area of Science:

  • Endocrinology
  • Pharmacology

Background:

  • Liquorice (Glycyrrhiza glabra) is a common flavoring agent and herbal remedy.
  • Its consumption is associated with potential adverse effects, including hypertension, hypokalemia, and metabolic alkalosis.

Observation:

  • A case of a 19-year-old female presenting with severe hypertension, hypokalemia, and metabolic alkalosis.
  • Urine analysis revealed inhibition of 11-beta-hydroxysteroid dehydrogenase.

Findings:

  • The patient's symptoms were directly linked to excessive liquorice ingestion.
  • Glycyrrhetinic acid, the active component in liquorice, inhibits 11-beta-hydroxysteroid dehydrogenase.
  • This enzyme inhibition leads to cortisol acting as a mineralocorticoid, causing hypertension and electrolyte imbalances.

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Implications:

  • This case highlights the significant mineralocorticoid activity of liquorice and the risk of intoxication.
  • Understanding the mechanism of 11-beta-hydroxysteroid dehydrogenase inhibition is crucial for managing liquorice-induced side effects.
  • Clinicians should consider liquorice consumption in patients presenting with unexplained hypertension and electrolyte disturbances.