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Liquorice 11-Beta-HSD2 Inhibition AME — ESENeph MCQ

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HardTubular DisordersLiquorice 11-Beta-HSD2 Inhibition AMEESENeph

A 52-year-old woman presents with progressive muscle weakness, polyuria, and constipation. Bloods: K+ 2.2 mmol/L, Na+ 146 mmol/L, bicarbonate 32 mmol/L. BP is 168/102 mmHg. Renin is suppressed, aldosterone is suppressed. 24-hour urine cortisol is normal. She takes large quantities of liquorice for digestive symptoms. What is the mechanism of her electrolyte abnormality?

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Correct answer: A — Liquorice inhibits 11-beta-hydroxysteroid dehydrogenase type 2, allowing cortisol to activate mineralocorticoid receptors

Glycyrrhizinic acid in liquorice inhibits 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in the distal nephron. This enzyme normally converts cortisol to cortisone (which does not activate the mineralocorticoid receptor). When inhibited, cortisol — which circulates at much higher concentrations than aldosterone — activates mineralocorticoid receptors, causing sodium retention, potassium wasting, metabolic alkalosis, and hypertension. This is the syndrome of apparent mineralocorticoid excess (AME). Both renin and aldosterone are suppressed because cortisol-mediated sodium retention expands volume, suppressing the RAAS. The picture mimics Liddle syndrome clinically but the mechanism is different.

Reference: https://guidelines.ukkidney.org