ArticleCureus2023
A Licorice-Flavored Edema: A Case Report of Glycyrrhizic Acid Toxicity From Chronic Licorice Root Consumption.
Article in Cureus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Molecular Mechanism of Compound Glycyrrhizin in Kainic Acid-Induced Epilepsy in Rat Model.Molecular biotechnology · 2026Article
- Licorice in nephropathy treatment: phytochemical compositions and pharmacological mechanisms.Frontiers in pharmacology · 2025Review
- Licorice-induced severe hypokalemic rhabdomyolysis.Archives of medical science : AMS · 2024Article
- Liquorice Toxicity: A Comprehensive Narrative Review.Nutrients · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This article presents a case study of a 49-year-old patient who was admitted to the emergency department with hypertension, edema, and intense fatigue caused by excessive consumption for three weeks of licorice herbal teas purchased on the internet. The patient was only taking antiaging hormonal treatment. The examination revealed bilateral edema of the face and lower limbs, and blood tests showed discrete hypokalemia (3.1 mmol/L) and low aldosterone levels. The patient revealed that she had been consuming large amounts of licorice herbal teas to compensate for the lack of sweetness in her low-sugar diet. This case study highlights that although licorice is widely used for its sweet taste and has medicinal properties, it can also have a mineralocorticoid-like activity that can lead to apparent mineralocorticoid excess (AME) when consumed in excess. The main component of licorice responsible for these symptoms is glycyrrhizic acid, which increases the availability of cortisol by decreasing its catabolism and has a mineralocorticoid effect through the inhibition of the enzyme 11-β-hydroxysteroid dehydrogenase (11-β-HSD) type 2. The case also discusses the clinical effects of licorice consumption, such as sodium retention and potassium excretion, leading to potential cardiovascular complications, as well as a differential diagnosis of similar clinical presentations mainly based on laboratory findings including aldosterone level and plasma renin activity (PRA). The potential dangers of consuming excessive amounts of licorice are well established, and we advocate stricter regulations and increased awareness and education for both the general public and the medical profession about these negative side effects and suggest that physicians should consider licorice consumption in their approach to patients' lifestyles and diets.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.