[Prinzmetal angina after licorice consumption]. / Prinzmetal-Angina nach Lakritz-Konsum.

Medical history | We report on a 44-year-old patient with recurrent thoracic pain occurring 4 months apart. The patient complained about intense thoracic pain and acute dyspnoea in the morning. In the course of the second presentation the anamnesis revealed that the previous day the patient had consumed an entire bag of licorice (200 g). Investigations | The blood pressure was 90/65 mmHg, heart rate 68 beats / min. Neither the performed ECG nor the transthoracic echocardiography showed abnormalities. The blood tests revealed elevated troponin levels only. No coronary artery stenosis was evident on left heart catheterization. After 4 months- the symptoms reappeared- the blood pressure was 110/50 mmHg. An ECG showed infarct-typical ST elevations. The performed coronary angiography showed no stenosis or embolism. Intracoronary nitro administration resulted in significant vasodilatation. After 6 hours in the control- ECG the ST elevations were missing. We diagnosed a Prinzmetal angina. Treatment and course | The patient was given advice not to consume licorice in the future. Her medication was adjusted to 2.5 mg amlodipine per day. There has been no further presentation with similar symptoms since then. Conclusion | Case reports provide evidence of unknown potential side- effects concerning well-known medical plants or substances. It is already known that the ingredients of licorice may induce hypertension. Potential spastic reactions, such as a Prinzmetal angina, due to the possible cardiac effects caused by glycyrrhizin and glycyrrhetinic acid are rare side effects of licorice ingestion.

Apparent mineralcorticoid excess syndrome, an often forgotten or unrecognized cause of hypokalemia and hypertension: case report and appraisal of the pathophysiology.

The glicyrrhizic acid, contained in licorice, has a mineralcorticoid-like effect. Chronic excess intake of licorice induces the rare syndrome of "apparent mineralcorticoid excess", due to the inhibitory effect of glicyrrhizic acid on 11 ß-hydroxysteroid dehydrogenase type 2 determining clinical/biochemical manifestations as resistant hypertension, metabolic alkalosis and severe hypokalemia. We report a typical clinical case of licorice abuse to emphasize the importance of a detailed anamnesis, which is essential for the diagnosis, avoid unnecessary and expensive investigations, and reduce the duration of hospitalization. We also provide an appraisal of the pathophysiology of "apparent mineralcorticoid excess" syndrome, still an often forgotten or unrecognized cause of hypokalemia and hypertension.

Licorice induced hypokalemia, edema, and thrombocytopenia.

Licorice originates from the root of Glycyrrhiza glabra, which has a herbal ingredient, glycyrrhizic acid, and has a mineralocorticoid-like effect. Chronic intake of licorice induces a syndrome similar to that found in primary hyperaldosteronism. Excessive intake of licorice may cause a hypermineralocorticoidism-like syndrome characterized by sodium and water retention, hypertension, hypokalemia, metabolic alkalosis, low-renin activity, and hypoaldosteronism. In this case report, an association of hypokalemia, edema, and thrombocytopenia that is developed due to the excessive intake of licorice is presented. There are case reports in the literature, which suggest that toxicity findings may emerge with hyperaldosteronism-like manifestations such as hypokalemia, edema, and hypertension. However, any knowledge of thrombocytopenia as a resultant was not encountered among these reported toxic effects. Our case is important because it shows that the excessive intake of licorice may cause a toxic effect in the form of thrombocytopenia. This report is the first presented case to show thrombocytopenia due to licorice syrup consumption.

Brugada syndrome with aborted sudden cardiac death related to liquorice-induced hypokalemia.

OBJECTIVE: It was the aim of this study to report an aborted cardiac arrest due to ventricular fibrillation and electrocardiographic changes consistent with Brugada syndrome due to liquorice-induced hypokalemia. CLINICAL PRESENTATION AND INTERVENTION: Ventricular fibrillation was witnessed in a 50-year-old woman who was admitted to our emergency department with a history of liquorice ingestion, a herbal product. After stopping liquorice ingestion, the Brugada-like electrocardiographic pattern changed progressively with potassium replacement. A diagnosis of Brugada syndrome was made after the ajmaline challenge test. The patient was discharged with an implantable cardioverter defibrillator and had an uneventful follow-up. CONCLUSION: This report illustrates the importance of the investigation for herbal medications in the detailed history of a patient in the cases of electrolyte disturbances and the potential role of hypokalemia in the induction of malignant arrhythmia in Brugada syndrome.

Glycyrrhizic acid toxicity caused by consumption of licorice candy cigars.

A 49-year-old female physician presented with peripheral edema, weight gain and relative hypertension caused by the consumption of licorice candy cigars containing glycyrrhizic acid (GZA) found in natural licorice extract. Although the patient's response to GZA resolved spontaneously, emergency physician awareness of the toxic effects of natural licorice extract may avert symptom progression in early-identified cases. The benefits of natural licorice extract as a flavour enhancer and herbal medicine are recognized worldwide. The Canadian public is likely not generally aware of the toxic potential of GZA, or that it may be present in the following commonly consumed products: black licorice, chewing gum, herbal teas, soft drinks, tobaccos and herbal remedies for cough, stomach ailments and constipation. Emergency physicians should inquire about the consumption of products that may contain natural licorice extract when patients present with unexplained hypertension, hypokalemia, edema, rhabdomyolysis or myoglobinuria.

Licorice-induced hypokalemia as a treatable cause of dropped head syndrome.

Isolated weakness of the extensor muscles of the neck is a relatively rare condition, known as "dropped head syndrome" (DHS). This paper reports the case of a patient with DHS whose symptoms resolved rapidly on supplementation with potassium and discontinuation of licorice consumption. To the best of our knowledge, there are no reports in the literature of DHS due to licorice-induced hypokalemia.

[Licorice--not just candy]. / Lakris--ikke bare sukkertøy.

BACKGROUND: Liquorice is widely used as a flavour and also as a medical drug. Possible side effects include hypertension, hypokalaemia and metabolic alkalosis. MATERIALS AND METHODS: We present a case history and a review on liquorice intoxication based on relevant literature found from searches on Medline. RESULTS AND INTERPRETATION: A 19-year-old girl was admitted to hospital with severe hypertension, hypokalaemia and metabolic alkalosis. Urine analysis showed inhibition of 11-beta-hydroxysteroid dehydrogenase. It turned out that she ingested a lot of liquorice; after she stopped eating it she became normotensive without any medication. Three months later there were no signs of inhibition of the enzyme. The active component of liquorice is glycyrrhetinic acid, which inhibits the enzyme 11-beta-hydroxysteroid dehydrogenase. This enzyme promotes the conversion of cortisol to cortisone and is thereby responsible for the specificity of the mineralocorticoid receptor to aldosterone in the collecting tubules. Inhibition of the enzyme allows cortisol to act as the major endogenous mineralocorticoid producing a marked elevation in mineralocorticoid activity, resulting in hypertension, hypokalaemia and metabolic alkalosis.

Hypokaliemic rhabdomyolysis associated with liquorice ingestion: report of an atypical case.

We here present an unusual case of hypokaliemic rhabdomyolysis, characterised by a sthenic deficit exclusively involving the distal muscles of the upper limbs and secondary to chronic glycyrrhizic acid intoxication, and by the absence of even ictal arterial hypertension. We discuss the etiopathogenetic bases and the risks related to the development of this secondary hypokaliemic syndrome, also in relation to other concomitant risk factors such as prolonged physical exercise and exposure to low temperatures.