Abstract | November 17, 2023

Refractory Hypertension and Hypokalemia in the Setting of Licorice Consumption

Laura Harrison, MD, Internal Medicine/Pediatrics, PGY-3, The University of Tennessee Health Science Center, Memphis, TN

M. Colleen Hastings, MD, Professor, Nephrology, The University of Tennessee Health Science Center, Memphis, TN; Michelle McAmis, MD, Assistant Professor, Medicine, The University of Tennessee Health Science Center, Memphis, TN

Learning Objectives

  1. Recognize the clinical signs of hyperaldosteronism.
  2. Interpret plasma renin activity and aldosterone levels.
  3. Recognize the syndrome of apparent mineralocorticoid excess, which is associated with severe hypertension, hypokalemia, and suppressed aldosterone levels.

Introduction: Secondary hypertension affects 5-10% of the hypertensive population, with hyperaldosteronism as the most common cause. Excessive aldosterone activity results in sodium reabsorption and potassium excretion, resulting in hypertension, hypokalemia, and suppressed renin.

Case Presentation: A 46-year-old hypertensive male was evaluated at his primary care clinic for dizziness and worsening hypertension. Blood pressure had been previously well controlled on lisinopril 10 mg daily. He was hypertensive (191/97) and bradycardic to 40 beats per minute. Physical exam was unremarkable except for bradycardia. EKG demonstrated sinus bradycardia with borderline QTc prolongation at 457. Serum potassium was 2.6 mmol/L. Amlodipine 10 mg daily and potassium chloride 40 mEq daily were added. One week later, he remained hypertensive and repeat labs revealed persistent hypokalemia (2.9 mmol/L). Lisinopril was increased to 40 mg daily and potassium chloride to 40 mEq twice daily. Repeated lab work demonstrated continued hypokalemia despite supplementation. Renal ultrasound, echocardiogram, stress test, serum creatinine, and urine microalbumin/creatinine ratio were normal. He was referred to Nephrology for evaluation. In the Nephrology clinic, aldosterone was <3.0 ng/dL and renin was 3.2 ng/mL/hr. At primary care follow-up, the patient revealed that he had been eating a 6-oz box of sugar-coated black licorice candy (Good & Plenty) daily for the past several months.

Working diagnosis: Glycyrrhizin, a compound found in licorice that inhibits cortisol deactivation in the kidneys causing excessive build-up of cortisol and stimulation of the renal mineralocorticoid receptors, may cause a syndrome of apparent mineralocorticoid excess, which is characterized by clinical findings of hypertension, hypokalemia, and suppressed aldosterone.

Outcome/Follow-up: Licorice consumption and potassium supplementation were discontinued. One week later, hypokalemia had resolved. At subsequent visits, antihypertensive agents were de-escalated due to improved blood pressure. This case adds to the growing body of literature illustrating the association between licorice consumption and hypertension and serves as a salient reminder to review dietary practices as part of a thorough clinical history.

References and Resources

  1. Hegde S, Ahmed I, Aeddula NR. Secondary Hypertension. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. Available from: https://www-ncbi-nlm-nih-gov.ezproxy.uthsc.edu/books/NBK544305/
  2. Smedegaard SB, Svart MV. Licorice induced pseudohyperaldosteronism, severe hypertension, and long QT. Endocrinol Diabetes Metab Case Rep. 2019 Dec 12;2019:19-0109. doi: 10.1530/EDM-19-0109. Epub ahead of print. PMID: 31829973; PMCID: PMC6935715.
Posted in: Medicine & Medical Specialties74
Back to Abstracts