Endocrine Abstracts

A 31-year-old German lady attended A&E with a 1 week history of bilateral leg swelling. The leg swelling had been gradual in onset and was not associated with shortness of breath, chest pain or haemoptysis. She had no history of renal or cardiac disease. Her only past medical history was of mild indigestion. She did not have any regular medication use. On examination she was systemically well but had bilateral pitting lower limb oedema. Blood pressure was 120/80 mmHg (compared to her normal of 90/60 mmHg). There was no evidence of cardiac failure or chronic liver disease. Urinalysis was negative for blood and protein. Plasma concentration of sodium was 143 mmol/l, potassium 2.6 mmol/l and creatinine 60 micromol/l. Liver function tests, electrocardiogram and chest radiograph were all normal. A pregnancy test was negative. She was admitted to hospital overnight. The history was revisited. She had ingested large amounts of liquorice recently for her indigestion. A working diagnosis of liquorice-induced hypokalaemia was made and she was advised to discontinue the liquorice. Her potassium reverted to normal within 48 h and she was discharged home. Subsequent out-patient investigations showed a suppressed plasma renin activity (PRA) and no evidence of renal potassium wasting. Her symptoms completely resolved off the liquorice and her blood pressure reverted to its normal level. In summary, we present a case of acquired apparent mineralocorticoid excess (AME) due to liquorice ingestion. The case highlights the importance of taking a thorough dietary history. Liquorice, a potent competitive inhibitor of distal convoluted tubule cytoplasmic 11 beta-hydroxysteroid dehydrogenase type 2 (11 β-HSD2), can allow unmetabolised cortisol to bind to the nuclear renal mineralocorticoid receptor inducing sodium retention, hypokalaemia, suppression of PRA and hypertension.