Case Presentation: A 67-year-old male with history of alcohol abuse and chronic hyponatremia related to beer potomania presented to hospital with nosebleed and coincidently found to have hyponatremia of 118 meq/L and hypokalemia of 3.3 meq/L. He was treated with fluid restriction, Lasix 20 mg and sodium chloride 2 gm daily. Upon outpatient follow up his sodium improved to 133meq/L but he was noticed to have a drop-in potassium to 2.4 mEq/L. Therefore, he was started on potassium supplements 20 mEq twice daily. Subsequent bloodwork did not reveal any improvement of Potassium despite being on supplements. Patient was advised to be admitted to hospital for closer monitoring and effective intravenous potassium replacement. Upon arrival patient was completely asymptomatic, denied any fever, dyspnea, nausea, vomiting, diarrhea, muscle weakness, dizziness or any other systemic symptoms. Physical examination showed blood pressure of 185/89 mmHg, heart rate 83 bpm, chest auscultation revealed regular heart sounds with no murmur, normal abdominal and neurological examination. Electrocardiogram showed sinus rhythm and mildly prolonged QT interval 510 milliseconds. The initial laboratory data showed severe hypokalemia of 2.5 mEq/L, Na of 131 meq/L, Mg of 2 mg/dl. Over the next 48 hours’ patient received high doses of intravenous and oral potassium, total of 460 mEq with very slow progressive correction. During the hospitalization, he was witnessed consuming large amount of black licorice candy which was stopped. The clinical course was favorable and patient was discharged home with correction of potassium of 4.3meq/L.
Discussion: This case illustrates the development of severe hypokalemia due to excessive ingestion of Licorice. Our patient consumed 1 pack of candy, which constitutes 22gm of Licorice for almost 1 week, which was enough for inducing hypokalemia and rise in blood pressure. Licorice contains a steroid, glycyrrhetinic acid that inhibits both competitively, and by reducing gene expression of 11-beta-hydroxysteroid dehydrogenase type2, that converts cortisol to inactive cortisone, prevents cortisol from binding to the mineralocorticoid receptor(MR). This leads to markedly increase net mineralocorticoid activity in patients who are chronically or excessively ingesting licorice. As in our case, the diagnosis is typically based upon biochemical abnormalities and elicited history of licorice ingestion. Urine analysis, urinary free cortisol and cortisol levels may help may diagnosis ,but it is not necessary if a history of licorice ingestion is evident.
Conclusions: In conclusion, whenever you see severe hypokalemia with normal magnesium level and aggressive potassium correction yielding slow progressive improvement always keep in mind licorice abuse.