Acetazolamide and Licorice: Interaction Details
AI-assisted, pharmacist-reviewed · Source data updated Jul 10, 2026 · Sources: FDA labeling, DDInter 2.0, cited literature
Acetazolamide
Licorice
No brand names on record
How we grade severity & evidence
Severity levels
- Contraindicated: These should generally not be used together.
- Major: Potentially serious — often needs a change or close monitoring.
- Moderate: Can be significant — usually manageable with monitoring.
- Minor: Usually limited clinical impact.
Evidence grades
- Established: Well documented — supported by controlled studies or strong clinical data.
- Probable: Good supporting evidence, though not definitively proven.
- Suspected: Some evidence suggests this interaction, but it is not well established.
- Possible: Limited or conflicting evidence; the interaction may occur.
- Theoretical: Predicted from the drugs' pharmacology; not yet confirmed in people.
Ratings come from the documented interaction literature and are reviewed by a pharmacist. They describe the documented risk of the combination, not what will necessarily happen to you — your dose, timing, and health picture all matter.
What happens
Increased risk of hypokalemia and/or reduced effectiveness of the diuretic
Interaction Deep Dive
Cases have been reported in which patients experienced hypokalemia and hypertension with concomitant use of licorice and diuretics1786. Symptoms of congestive heart failure and hypokalemia occurred in a patient taking licorice, furosemide, and digoxin 1. Hypokalemic paralysis has resulted from licorice use; concomitant diuretic use increased the risk 910211. Licorice alone has been reported to be the likely cause of hypokalemia, hypertension, and cardiac arrhythmia 31213141516. The glycyrrhetinic acid component of licorice is metabolized to 3-monoglucuronyl-glycyrrhetinic acid (3MGA), which inhibits 11-beta-hydroxysteroid dehydrogenase and reduces cortisol breakdown, resulting in a hypermineralocorticoid effect 1718.
Why it happens (mechanism)
Pseudoaldosteronism from licorice ingestion resulting in hypokalemia
Literature reports
7 reports — tap to read
a) An 84-year-old male developed hypokalemia and symptoms of congestive heart failure after 7 days of concurrent use of a licorice-containing Chinese herbal laxative with digoxin and furosemide. The patient complained of fatigue, appetite loss, and lower extremity edema. Pulse rate was 30 beats per minute, potassium was 2.9 milliequivalents/Liter (mEq/L), and digoxin level 2.9 nanograms/milliliter (ng/mL). Chest radiograph revealed an enlarged cardiac silhouette and lung congestion. Partial arterial oxygen pressure and saturation was low, carbon dioxide pressure was high. Plasma renin activity was 0.3 ng/mL/hour (normal 0.3 to 2.9 ng/mL/hour) and aldosterone was 3.8 nanograms/deciliter (ng/dL) (normal 3.6 to 24 ng/dL). Digoxin and the herbal laxative were stopped; after 18 days, the patient's pulse increased to 60 beats per minute and symptoms of congestive heart failure were relieved. Potassium increased to 4.3 mEq/L, renin activity was 1 ng/mL/hour, aldosterone was 12 ng/dL, and digoxin level was 0.6 ng/mL 1.
b) Fifty-nine cases of glycyrrhizin-induced hypokalemic myopathy (GIHM) were reviewed. The combined use of licorice and hypotensive diuretic agents increased the risk of GIHM in the majority of cases. Of 56 cases which were reported, serum potassium was 1.98 milliequivalents/liter (mEq/L). Average blood aldosterone in 30 patients was normal, though 15 of those patients had below-normal values. Plasma renin activity averaged 0.17 nanograms/milliliter/hour (ng/mL/hour) (normal: 0.8-4.4 ng/mL/hour) in 27 patients. Complete cure was attained in 57 of the 59 cases of GIHM when licorice ingestion was discontinued and potassium supplementation given 2.
c) A 49-year-old female presented with persistent hypertension and hypokalemia (2.6 mmol/L; normal 3.3 to 4.8 mmol/L) following consumption of licorice. Blood pressure was found to be volume-sensitive and plasma renin activity and plasma aldosterone were low. The patient's hypokalemia was unresponsive to amiloride but normalized with spironolactone. Prior to discontinuing her regular licorice intake, her blood pressure control was unsatisfactory on a combination of furosemide 120 mg daily, felodipine 2.5 mg daily, monoxidine 0.2 mg daily, spironolactone 75 mg daily, and doxazosin 4 mg daily. The patient then admitted to consuming 30 to 40 Pontefract cakes, a licorice-based sweet, per week (approximately 0.25 kilograms). After discontinuing the Pontefract cakes, blood pressure fell steadily allowing progressive withdrawal of antihypertensive treatment 3.
d) A 21-year-old female developed headache and hypertension (190/120 mmHg), associated with licorice consumption (100 grams daily) along with an oral contraceptive. She was advised to discontinue eating licorice. Blood pressure remained elevated with treatment combining atenolol, lisinopril, hydrochlorothiazide, and amlodipine. Drug treatment was discontinued, and 2 weeks later blood pressure was 180/110 mmHg, potassium 2.6 mmol/L (normal 3.8 to 5.0 mmol/L), bicarbonate 35.9 mmol/L (normal 23 to 29 mmol/L). Plasma aldosterone was 160 picomoles/liter (pmol/L) (normal 320 to 2000 pmol/L). The patient then admitted to replacing her licorice intake with two packets of Stimerolol Sugar Free(R) chewing gum per day. This chewing gum contains 585 mg licorice in each 15 gram packet, which equals 8% to 12% glycyrrhizinic acid. Her glycyrrhizinic acid intake was calculated to be 120 mg daily. Within 3 weeks of discontinuing the gum, her blood pressure and potassium level normalized 4.
e) A 35-year-old woman taking an oral contraceptive and chlorothiazide experienced hypokalemia (2.2 mmol/L). Her blood pressure was 140/80 mmHg. Chlorothiazide was stopped and potassium chloride 600 mg three times daily was started. After one week, potassium remained abnormal at 2.0 mmol/L, after 2 weeks it decreased further to 1.5 mmol/L. Intravenous potassium supplementation was started. Although she denied licorice use, it was discovered that she used BenBits Cool Mint(R) chewing gum (Leaf, United Kingdom), 3 packets daily. This product contained 160 mg licorice in each 16 gram packet, of which 10% was glycyrrhizinic acid. After 2 days of intravenous potassium and 15 days of oral potassium, and within 3 weeks of discontinuing the chewing gum, edema disappeared, blood pressure decreased to 110/80 mmHg and potassium increased to 4.2 mmol/L. The authors attributed the hypokalemia to the licorice intake 4.
f) A 38-year-old male was hospitalized with respiratory and kidney failure due to complications of somnolence, flaccid paralysis of the extremities, arterial hypertension, edema and severe hypokalemia. He had been ingesting 200 grams of licorice daily for 10 weeks together with a thiazide diuretic for 2 weeks 5.
g) A 70-year-old male developed hypokalemia (1.9 millimoles/Liter (mmol/L)) and rhabdomyolysis while treated with a thiazide diuretic. Blood pressure and potassium were normalized following treatment with spironolactone, potassium chloride, and verapamil. It was discovered that he had been eating 60 to 100 grams of licorice candies daily for 4 to 5 years, containing 0.3% glycyrrhizic acid. Licorice ingestion was discontinued, then spironolactone and potassium were discontinued. Rechallenge with licorice (300 mg glycyrrhetinic acid) per day resulted in subnormal potassium (3.4 mmol/L), blood pressure 154/72 mmHg, and increased body weight by 4.9 kg. Licorice caused plasma renin activity to fall from 2.4 nanograms/Liter/second (ng/L/second) (normal 0.14 to 1.8 mg/L/second) to 0.2 mg/L/second after the week of licorice. Following the study, verapamil was continued while the patient abstained from licorice. Blood pressure and potassium remained normal 6.
Common questions
Can I take Acetazolamide and Licorice together?
Increased risk of hypokalemia and/or reduced effectiveness of the diuretic Always confirm with your pharmacist or prescriber before making any change.
How serious is the Acetazolamide and Licorice interaction?
It is rated moderate. Can be significant — usually manageable with monitoring.
How quickly could this interaction happen?
The documented onset is "delayed". Effects tend to build up gradually over days to weeks.
How strong is the evidence for this interaction?
The evidence is graded "probable". Good supporting evidence, though not definitively proven.
From our Q&A
Real reader questions about these medications, each personally answered by our pharmacist:
Questions for your pharmacist
- Does my dose of Acetazolamide or Licorice need adjusting while I take them together?
- What symptoms should prompt me to call you or my prescriber right away?
- Does the timing of my doses matter for this combination?
- Is there anything you'd monitor while I'm on both?
References (18)
- Harada T, Ohtaki E, Misu K, et al: Congestive heart failure caused by digitalis toxicity in an elderly man taking a licorice-containing Chinese herbal laxative. Cardiology 2002; 98(4):218. PubMed
- Shintani S, Murase H, Tsukagoshi H, et al: Glycyrrhizin (Licorice)-induced hypokalemic myopathy. Eur Neurol 1992; 32(1):44-51. DOI
- Dellow EL, Unwin RJ, & Honour JW: Pontefract cakes can be bad for you: refractory hypertension and liquorice excess. Nephrol Dial Transplant 1999; 14:218-220. DOI
- deKlerk G, Neiuwenhuis M, & Beutler J: Hypokalemia and hypertension associated with use of liquorice flavoured chewing gum. Br Med J 1997; 314(7082):731-32.
- Folkersen L, Knudsen NA, & Teglbjaerg PS: Licorice. A basis for precautions one more time!. Ugeskr Laeger 1996; 158(51):7420-7421.
- Farese RV, Biglieri EG, Shackleton CHL, et al: Licorice-induced hypermineralocorticoidism. N Eng J Med 1991; 325(17):1223-1227. PubMed
- deKlerk G, Neiuwenhuis M, & Beutler J: Hypokalemia and hypertension associated with use of liquorice flavoured chewing gum. Br Med J 1997; 314(7082):731-732.
- Folkerson L, Knudsen NA, & Teglbjaerg PS: Licorice. A basis for precautions one more time!. Ugeskr Laeger 1996; 158(51):7420-7421.
- Hussain RM: The sweet cake that reaches parts other cakes can't!. Postgrad Med J 2003; 79:115-116. PubMed
- Lin SH, Yang SS, Chau T, et al: An unusual cause of hypokalemic paralysis: chronic licorice ingestion. Am J Med Sci 2003; 325(3):153-156. DOI
- Corsi FM, Galgani S, Gasparini C, et al: Acute hypokalemic myopathy due to chronic licorice ingestion: report of a case. Ital J Neurol Sci 1983; 4(4):493-497. DOI
- Eriksson JW, Carlberg B, & Hillorn V: Life-threatening ventricular tachycardia due to liquorice-induced hypokalemia. J Int Med 1999; 245(3):307-310.
- Kageyama K, Watanobe H, Nishie M, et al: A case of pseudoaldosteronism induced by a mouth refresher containing licorice. Endocr J 1997; 44(4):631-632. PubMed
- Bernardi M, D'Intino PE, Trevisani F, et al: Effects of prolonged ingestion of graded doses of licorice by healthy volunteers. Life Sci 1994; 55(11):863-872. PubMed
- Blachley JD & Knochel JP: Tobacco chewer's hypokalemia: licorice revisited. N Engl J Med 1980; 302(14):784-785. DOI
- Wash LK & Bernard JD: Licorice-induced pseudoaldosteronism. Am J Hosp Pharm 1975; 32(1):73-74. DOI
- Kato H, Kanaoka M, Yano S, et al: 3-Monoglucuronyl-glycyrrhetinic acid is a major metabolite that causes licorice-induced pseudoaldosteronism. J Clin Endocrinol Metab 1995; 80(6):1929-1933. PubMed
- Walker BR & Edwards CRW: Licorice-induced hypertension and syndromes of apparent mineralocorticoid excess. Endocrinol Metab Clin North Am 1994; 23:359-377. DOI
Keep reading about Acetazolamide
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