The Poison Review

Cocktail Paralysis. Hammond K et al.  Amer J Med. 2009;122:907-908.

No abstract available on-line

This interesting case report, from the University of Saskatchewan, describes a 44-year-old woman who was transferred to the neurology service after developing severe muscle weakness (able to lift head but not any extremity against gravity) and hypokalemia (K = 1.6 mmol/L).  Workup revealed that she was excreting large amount of potassium in her urine, and had apparent mineralocorticoid excess syndrome.  In this syndrome, the key word is “apparent” — it actually results from an excess of the glucocorticoid cortisol, not an excess of mineralocorticoid.  A toxin-indcued deficiency of renal 11-Β-hydroxysteroid dehdrogenase (11-BHD) activity increases the level of cortisol, which at large concentrations has significant mineralocorticoid activity. Detailed history revealed that this patient denied any licorice ingestion, but had been consuming large amounts of the licorice-flavored liqueur Sambuca, which contains glycyrrhizinic acid, a steroid that inibhits 11-BHD.

With potassium replacement (IV and PO) the patient’s muscular strength returned to normal by hospital day 3.  A Sambuca re-challenge test was not attempted.