Licorice Poisoning Workup

  • Author: Seth Schonwald; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Apr 4, 2011
 

Laboratory Studies

  • Diagnosis is generally confirmed by combination of hypokalemia, increased urinary free cortisol, elevated cortisol-cortisone metabolite ratio, and low or absent urinary aldosterone.
  • Low serum potassium level is the most helpful screening result for establishing mineralocorticoid excess in patients with hypertension.
  • Elevated urinary potassium level may be present.
  • Dilutional anemia may be present, and hematocrit may be depressed.
  • Licorice poisoning can cause hypokalemic rhabdomyolysis with resultant myoglobinuria and elevated serum creatine kinase level.[20, 21] Elevated creatine phosphokinase level can cause acute tubular necrosis.
  • In so-called pseudo-primary hyperaldosteronism, plasma and urinary aldosterone levels are not elevated.
Next

Imaging Studies

  • Chest radiography: Assess for pulmonary edema if clinically indicated.
  • Abdominal CT or MRI: If urine aldosterone levels are high in a patient with evidence of hypermineralocorticoidism (eg, hypertension, hypokalemia, suppression of renin-angiotensin system), causative tumors are more likely than chronic licorice toxicity, and imaging may be warranted.
Previous
Next

Other Tests

  • Electrocardiography: Evaluate for hypokalemic changes and evidence of arrhythmia, including torsades des pointes.
  • Pulse oximetry and arterial blood gas (ABG) measurement: Evaluate for pulmonary edema and respiratory muscle weakness.
  • Many tests are expensive and time-consuming. Consultation with an endocrinologist and toxicologist may be helpful for determining initial workup. Measure serum GRA and GZA levels with enzyme-linked immunoabsorbent assay (ELISA) and high-performance liquid chromatography (HPLC). Measure urinary GRA level with gas chromatography-mass spectrometry (GC-MS). Ascertaining plasma renin activity and urine aldosterone level (24 h collections) may be helpful (both are typically low). Determining urine cortisol levels (often elevated) and cortisol-cortisone metabolite ratios (often elevated) may be helpful.
Previous
Proceed to Treatment & Management
 
 
Contributor Information and Disclosures
Author

Seth Schonwald  MD, FACEP, Consulting Staff, Director of Toxicology, Department of Urgent Care, East Boston Neighborhood Health Center

Seth Schonwald is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, Massachusetts Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

B Zane Horowitz, MD, FACMT  Professor, Department of Emergency Medicine, Oregon Health and Sciences University; Medical Director, Oregon Poison Center; Medical Director, Alaska Poison Control System

B Zane Horowitz, MD, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Medical Toxicology

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Michael Hodgman, MD  Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare

Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References

  1. Isbrucker RA, Burdock GA. Risk and safety assessment on the consumption of Licorice root (Glycyrrhiza sp.), its extract and powder as a food ingredient, with emphasis on the pharmacology and toxicology of glycyrrhizin. Regul Toxicol Pharmacol. Dec 2006;46(3):167-92. [Medline].

  2. Carmines EL, Lemus R, Gaworski CL. Toxicologic evaluation of licorice extract as a cigarette ingredient. Food Chem Toxicol. Sep 2005;43(9):1303-22. [Medline].

  3. Davis EA, Morris DJ. Medicinal uses of licorice through the millennia: the good and plenty of it. Mol Cell Endocrinol. Jun 1991;78(1-2):1-6. [Medline].

  4. Anderson DM, Smith WG. The antitussive activity of glycyrrhetinic acid and its derivatives. J Pharm Pharmacol. Jul 1961;13:396-404. [Medline].

  5. Krausse R, Bielenberg J, Blaschek W, Ullmann U. In vitro anti-Helicobacter pylori activity of Extractum liquiritiae, glycyrrhizin and its metabolites. J Antimicrob Chemother. Jul 2004;54(1):243-6. [Medline].

  6. Cooper H, Bhattacharya B, Verma V, McCulloch AJ, Smellie WS, Heald AH. Liquorice and soy sauce, a life-saving concoction in a patient with Addison's disease. Ann Clin Biochem. Jul 2007;44(Pt 4):397-9. [Medline].

  7. Ross EJ. Liquorice and Addison's disease. Br Med J. Jun 20 1970;2(5711):733. [Medline].

  8. Dhiman RK, Chawla YK. Herbal medicines for liver diseases. Dig Dis Sci. Oct 2005;50(10):1807-12. [Medline].

  9. Kim YW, Kang HE, Lee MG, Hwang SJ, Kim SC, Lee CH, et al. Liquiritigenin, a flavonoid aglycone from licorice, has a choleretic effect and the ability to induce hepatic transporters and phase-II enzymes. Am J Physiol Gastrointest Liver Physiol. Feb 2009;296(2):G372-81. [Medline].

  10. Farese RV Jr, Biglieri EG, Shackleton CH, Irony I, Gomez-Fontes R. Licorice-induced hypermineralocorticoidism. N Engl J Med. Oct 24 1991;325(17):1223-7. [Medline].

  11. Walker BR, Edwards CR. Licorice-induced hypertension and syndromes of apparent mineralocorticoid excess. Endocrinol Metab Clin North Am. Jun 1994;23(2):359-77. [Medline].

  12. van Uum SH. Liquorice and hypertension. Neth J Med. Apr 2005;63(4):119-20. [Medline].

  13. Palermo M, Quinkler M, Stewart PM. Apparent mineralocorticoid excess syndrome: an overview. Arq Bras Endocrinol Metabol. Oct 2004;48(5):687-96. [Medline].

  14. Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. Mar-Apr 2006;19 Suppl 9:S86-96. [Medline].

  15. Armanini D, Bonanni G, Palermo M. Reduction of serum testosterone in men by licorice. N Engl J Med. Oct 7 1999;341(15):1158. [Medline].

  16. Armanini D, Mattarello MJ, Fiore C, Bonanni G, Scaroni C, Sartorato P. Licorice reduces serum testosterone in healthy women. Steroids. Oct-Nov 2004;69(11-12):763-6. [Medline].

  17. Biglieri EG. Spectrum of mineralocorticoid hypertension. Hypertension. Feb 1991;17(2):251-61. [Medline].

  18. Elinav E, Chajek-Shaul T. Licorice consumption causing severe hypokalemic paralysis. Mayo Clin Proc. Jun 2003;78(6):767-8. [Medline].

  19. Barrella M, Lauria G, Quatrale R, Paolino E. Hypokaliemic rhabdomyolysis associated with liquorice ingestion: report of an atypical case. Ital J Neurol Sci. Aug 1997;18(4):217-20. [Medline].

  20. van den Bosch AE, van der Klooster JM, Zuidgeest DM, Ouwendijk RJ, Dees A. Severe hypokalaemic paralysis and rhabdomyolysis due to ingestion of liquorice. Neth J Med. Apr 2005;63(4):146-8. [Medline].

  21. Zenone T, Blanc Q. [Rhabdomyolysis with major hypokalemia secondary to chronic glycyrrhizic acid ingestion]. Rev Med Interne. Jan 2009;30(1):78-80. [Medline].

  22. Epstein MT, Espiner EA, Donald RA, Hughes H. Liquorice toxicity and the renin-angiotensin-aldosterone axis in man. Br Med J. Jan 22 1977;1(6055):209-10. [Medline].

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.