Licorice-related rhabdomyolysis: a big price for a sweet tooth

Abstract

A 50-year-old lady on hydrochlorothiazide (HCTZ) presented to the hospital after 4 days of generalized muscle aches and dark urine. She admitted to consuming one and a half bags of black licorice bites containing 2% natural licorice during the past 3 weeks. Examination showed high blood pressure, while labs revealed elevated creatine kinase, hypokalemia, hypocalcemia and hypophosphatemia with low aldosterone and plasma renin levels and high intact PTH. The active component of licorice is glycyrrhizic acid, which inhibits an enzyme required to convert cortisol to a less active metabolite, cortisone. This causes excess cortisol, simulating syndrome of apparent mineralocorticoid excess (AME), thus resulting in hypertension, hypokalemia and metabolic alkalosis. In our patient, licorice induced hypokalemia resulted in rhabdomyolysis. The rhabdomyolysis along with the effect of licorice led to secondary hypocalcaemia, which in turn triggered secondary hyperparathyroidism. This might have had a phosphaturic effect that caused hypophosphatemia, further worsening rhabdomyolysis. This case illustrates the complex relationship of various electrolytes, which can lead to self perpetuation of the disease, hence demanding more vigilance.