SFEBES2013 Poster Presentations Clinical biochemistry (22 abstracts)
Wirral University Teaching Hospital NHS Foundation Trust, Wirral, UK.
Long-term liquorice ingestion is a well-known cause of secondary hypertension and hypokalemia. However, its initial presentation with a very severe hypokalemia and rhabdomyolysis is exceedingly rare. We report a 46-year-old gentleman who presented with acute onset bilateral leg weakness. Medication included allopurinol, aminophylline, fluoxetine, gabapentin, omeprazole, and inhalers. He had a 40 pack year smoking history and drank alcohol heavily in the past.
On examination he had power of 2/5 in his legs and 5/5 in upper limbs. Severe hypokalemia of 2.6 mmol/l and raised creatinine kinase of 42 660 IU/l was noted. He had raised urinary potassium excretion at 104 mmol/24 h, suppressed aldosterone (61 pmol/l) and renin (0.3 pmol/ml per h)concentration and normal levels of cortisol and thyroid function.
Muscular weakness resolved with potassium replacement. Renal potassium excretion and hypokalemia normalised after several weeks. He represented with very similar symptoms and with potassium of 1.7 mmol/l. A detailed dietary history revealed that he consumed 1 bag (140 g) of liquorice daily for many years. He was diagnosed as suffering from Liquorice induced hypokalemia. 24 h urinary steroid chromatography profile was consistent with 11β-hydroxysteroid dehydrogenase two deficiency. He was discharged home with advice that he should stop consuming liquorice.
Liquorice induced hypokalemia and rhabdomyolysis is very rare. Liquorices active ingredient, glycyrrhizic acid inhibits 11β-hydroxysteroid dehydrogenase, the renal enzyme which is responsible for conversion of cortisol to cortisone. As a result, renal mineralocorticoid receptors are activated by excessive cortisol, which causes sodium and water retention and hypokalemia. In this patient a clear history of excessive liquorices ingestion, elevated renal potassium excretion, suppressed aldosterone and renin and biochemical confirmation of suppressed 11β-hydroxysteroid dehydrogenase deficiency confirmed the diagnosis. This emphasizes the importance of a detailed dietary history in unexplained hypokalaemia.