eMedicine Specialties > Emergency Medicine > Toxicology
Plant Poisoning, Licorice: Treatment & Medication
Updated: Jul 6, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Prehospital Care
Provide supportive treatment, including airway, breathing, and circulatory support (ABCs), as clinically indicated. Provide cardiac monitoring if clinically indicated.
Emergency Department Care
- Monitor electrolytes, especially potassium.
- Supplement potassium, as indicated.
- Consider potassium-sparing diuretics, as needed.
- Treat rhabdomyolysis, if present (eg, hydration, alkalinization of urine, mannitol).
- Monitor for and treat electrolyte-induced dysrhythmias.
- Monitor for and treat pulmonary edema and respiratory muscle weakness.
Consultations
Consultations with an endocrinologist and a toxicologist may be helpful.
Medication
The goals of pharmacotherapy are to reduce morbidity and to prevent complications.
Diuretics, potassium-sparing
These agents may be used to correct potassium deficiency or fluid/electrolyte imbalance.
Spironolactone (Aldactone)
Competes with aldosterone for receptor sites in distal renal tubules by increasing water excretion while retaining potassium and hydrogen ions.
Adult
50-100 mg/d PO initial; typical dose is 100 mg/d, adjusted frequently as licorice toxicity resolves
Pediatric
0.5-1.5 mg/kg PO bid; not to exceed 200 mg/d
May decrease effect of anticoagulants; potassium and potassium-sparing diuretics may increase toxicity of spironolactone; lithium generally should not be given with diuretics because they reduce lithium's renal clearance and add a high risk of lithium toxicity; administer NSAIDs with caution (monitor serum potassium frequently); may attenuate positive inotropic effect of digoxin; may block tubular secretion of digoxin, reducing clearance and increasing levels; coadministration with ACE inhibitors may lead to hyperkalemia
Documented hypersensitivity; anuria, renal failure, or hyperkalemia
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in renal and hepatic impairment; adverse effects include nausea, vomiting, gastric ulcers, life-threatening hyperkalemia, metabolic acidosis (in patients with cirrhosis), gynecomastia, and impotence
Triamterene (Dyrenium)
Potassium-sparing diuretic with relatively weak natriuretic properties. Exerts diuretic effect on distal renal tubule to inhibit reabsorption of sodium in exchange for potassium and hydrogen. Increases sodium excretion and reduces excessive loss of potassium and hydrogen associated with hydrochlorothiazide. Not a competitive antagonist of mineralocorticoids; potassium-conserving effect is observed in patients with Addison disease (ie, without aldosterone).
Adult
50-100 mg PO bid; adjust frequently as licorice toxicity resolves
Pediatric
1-2 mg/kg PO bid
Coadministration with other potassium-conserving agents, such as spironolactone, amiloride HCl, or other formulations containing triamterene, may significantly increase serum potassium levels; lithium generally should not be given with diuretics because they reduce lithium's renal clearance and add a high risk of lithium toxicity; acute renal failure reported in patients receiving indomethacin and formulations containing triamterene; administer NSAIDs with caution (monitor serum potassium level frequently); may interfere with measurement of quinidine; may attenuate positive inotropic effect of digoxin; may block tubular secretion of digoxin, reducing clearance and increasing levels; coadministration with ACE inhibitors may lead to hyperkalemia
Documented hypersensitivity; elevated serum potassium levels (>5.5 mEq/L); impaired renal function (anuria, acute renal insufficiency, chronic renal insufficiency, significant renal impairment); diabetes
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in severe hepatic encephalopathy, diabetes, renal dysfunction, renal stones, and history of renal stones; adverse effects include hyperuricemia, renal stones, interstitial nephritis, photosensitization, glucose intolerance, and life-threatening hyperkalemia
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 |
| « Previous Page | Next Page » |
References
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].
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].
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].
Anderson DM, Smith WG. The antitussive activity of glycyrrhetinic acid and its derivatives. J Pharm Pharmacol. Jul 1961;13:396-404. [Medline].
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].
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].
Ross EJ. Liquorice and Addison's disease. Br Med J. Jun 20 1970;2(5711):733. [Medline].
Dhiman RK, Chawla YK. Herbal medicines for liver diseases. Dig Dis Sci. Oct 2005;50(10):1807-12. [Medline].
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].
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].
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].
van Uum SH. Liquorice and hypertension. Neth J Med. Apr 2005;63(4):119-20. [Medline].
Palermo M, Quinkler M, Stewart PM. Apparent mineralocorticoid excess syndrome: an overview. Arq Bras Endocrinol Metabol. Oct 2004;48(5):687-96. [Medline].
Khanna A, Kurtzman NA. Metabolic alkalosis. J Nephrol. Mar-Apr 2006;19 Suppl 9:S86-96. [Medline].
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].
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].
Biglieri EG. Spectrum of mineralocorticoid hypertension. Hypertension. Feb 1991;17(2):251-61. [Medline].
Elinav E, Chajek-Shaul T. Licorice consumption causing severe hypokalemic paralysis. Mayo Clin Proc. Jun 2003;78(6):767-8. [Medline].
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].
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].
Zenone T, Blanc Q. [Rhabdomyolysis with major hypokalemia secondary to chronic glycyrrhizic acid ingestion]. Rev Med Interne. Jan 2009;30(1):78-80. [Medline].
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].
Further Reading
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
