Endocrine Abstracts

A 59-year-old lady with headaches and malaise was found to be hypertensive with a blood pressure (BP) 210/105. An MRI brain revealed a haemorrhagic lesion in the right temporal lobe. There were no other signs of end organ damage. Her medications included atenolol 25 mg OD, ramipril 10 mg OD and bendroflumethiazide 2.5 mg OD. It transpired that she has been drinking 5 cups of liquorice tea per day over the last 18 months. Following a vomiting illness she stopped liquorice tea consumption. Her BP normalised and antihypertensive medications were weaned off.

Biochemically, her potassium (K⁺) was 5.2 mmol/l, sodium (Na⁺) 139 mmol/l and creatinine 113 μmol/l. Retrospectively, she had low/normal K⁺ (3.6–4.1 mmol/l) and Na⁺ at the upper limit of normal (142–145 mmol/l). Renin and aldosterone were not measured. However, given her history and biochemistry, the cause of hypertension is likely secondary to liquorice ingestion.

Liquorice consumption is an unusual but well-reported cause of secondary hypertension. Excessive consumption of liquorice can cause hypertension and hypokalaemia, which may lead to cardiac arrhythmias and myopathy. The pathogenesis involves the action of glycyrrhetinic acid (GA), the active metabolite of liquorice, on the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). GA inhibits the action of 11β-HSD2 resulting in a mineralocorticoid excess state causing hypertension hypokalaemia, alkalosis, sodium and water retention, and suppression of renin–aldosterone system.

The lowest observed dose resulting in adverse effects is 100 mg of GA daily. Hence, using a safety factor of 10, a daily intake of 10 mg GA per person is regarded as an acceptable safe dose. This means no more than 10–30 mg liquorice, i.e. no more than half a cup of liquorice tea per day.

This case demonstrates a rare cause of hypertension and highlights the importance of taking a detailed history to avoid unnecessary investigations and treatment.