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Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique

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[Severe hypokalemia after holidays return].

A Brasseur¹, J Ducobu

¹Service de Médecine Interne, C.H.U. Tivoli, La Louvière. albrasse@ulb.ac.be

Revue Medicale De Bruxelles

|December 6, 2008

Summary

This case highlights how licorice consumption can mimic primary aldosteronism, causing severe hypokalemia and hypertension. Careful patient history is crucial for diagnosing this reversible condition.

Area of Science:

Endocrinology
Nephrology
Internal Medicine

Background:

Primary aldosteronism is a condition characterized by excessive aldosterone secretion.
It can lead to hypertension, hypokalemia, and metabolic alkalosis.
Distinguishing primary aldosteronism from pseudohyperaldosteronism is critical for appropriate management.

Observation:

A 52-year-old man presented with severe hypertension, hypokalemia, metabolic alkalosis, rhabdomyolysis, and ECG changes.
Diagnostic workup revealed inappropriate potassium excretion with suppressed plasma renin and aldosterone levels.
The patient reported daily consumption of a licorice-based aperitif.

Findings:

The clinical presentation and laboratory findings were consistent with pseudohyperaldosteronism.

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Glycyrrhetinic acid, found in licorice, inhibits the enzyme 11-beta-hydroxysteroid dehydrogenase type 2, mimicking aldosterone's effects.

Discontinuation of licorice consumption led to resolution of symptoms.

Implications:

This case underscores the importance of thorough patient history, including dietary habits, in diagnosing endocrine disorders.
Pseudohyperaldosteronism due to licorice ingestion is a reversible cause of severe electrolyte abnormalities and hypertension.
Awareness of glycyrrhetinic acid's effects is essential for clinicians managing patients with hypertension and hypokalemia.