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Plant Poisoning, Licorice: Differential Diagnoses & Workup

Author: Seth Schonwald, MD, FACEP, FACMT, Consulting Staff, Director of Toxicology, Department of Urgent Care, East Boston Neighborhood Health Center
Contributor Information and Disclosures

Updated: Jul 6, 2009

Differential Diagnoses

Acute Respiratory Distress Syndrome
Pediatrics, Respiratory Distress Syndrome
Congestive Heart Failure and Pulmonary Edema
Plant Poisoning, Herbs
Encephalitis
Respiratory Distress Syndrome, Adult
Hypernatremia
Rhabdomyolysis
Hypertensive Emergencies
Hypokalemia
Myopathies

Other Problems to Be Considered

Other causes of hypokalemia

Aminoglycosides
Barium poisoning
Beta-adrenergic agonists
Diarrhea
Diuretics
Enemas or laxative use
Hyperaldosteronism
Ileal loop
Insulin
Leukemia
Magnesium depletion
Metabolic syndrome
Periodic hypokalemic paralysis
Renal tubular necrosis
Steroids
Theophylline 

Other causes of hyperaldosteronism

Adrenal adenoma
Bartter syndrome (ie, hyperaldosteronism, hyperreninism, hypokalemic acidosis)
Bilateral adrenal hyperplasia
Ectopic adrenocorticotropic hormone (ACTH) syndrome (eg, Wilms tumor) 
Hypertensive urgencies
Mineralocorticoid excess syndrome (eg, congenital adrenal hyperplasias)

Workup

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.

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.

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. 

More on Plant Poisoning, Licorice

Overview: Plant Poisoning, Licorice
Differential Diagnoses & Workup: Plant Poisoning, Licorice
Treatment & Medication: Plant Poisoning, Licorice
Follow-up: Plant Poisoning, Licorice
References
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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].

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  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].

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Further Reading

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Keywords

licorice toxicity, natural licorice, liquorice, licorice extract, licorice root, chronic licorice ingestion, glycyrrhizic acid, GZA toxicology, Glycyrrhiza glabra, 18-beta-glycyrrhetinic acid, GRA, hypermineralocorticoid syndrome, hypermineralocorticoidism, glycyrrhizin

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Contributor Information and Disclosures

Author

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

Medical Editor

B Zane Horowitz, MD, FACMT, Professor, Fellowship Director, 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.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & 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.

Managing Editor

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.

CME Editor

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, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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