Liquorice-induced hypertension--a new understanding of an old disease: case report and brief review.

The case is described of a 40-year-old female with severe hypertension and hypokalaemic metabolic alkalosis, due to prolonged liquorice ingestion. The pseudo-aldosterone-like effects of liquorice have always been attributed to glycyrrhizic acid, but its biochemical substrate has remained elusive. It is now known that glycyrrhetenic acid, the hydrolytic metabolite of glycerrhizic acid, is the active component of liquorice which causes inhibition of the peripheral metabolism of cortisol. Cortisol binds with the same affinity as aldosterone to the mineralocorticoid receptor resulting in a hypermineralocorticoid condition. Ingestion of liquorice may therefore result in retention of sodium and water, hypertension, hypokalaemia, alkalosis and suppression of the renin-aldosterone system. The literature on liquorice-induced hypertension is briefly reviewed with emphasis on the biochemical features of this mineralocorticoid excess syndrome.

[Hypertensive retinopathy and papilledema. Apropos of a case of glycyrrhizin poisoning]. / Rétinopathie hypertensive et oedème papillaire. A propos d'un cas d'intoxication par la glycyrrhizine.

We present a case report of a patient suffering of severe hypertension and grade IV hypertensive retinopathy according to the Keith-Wagener classification. Simultaneously hypertensive encephalopathy was present confirming the poor prognosis of discoedema occurring in the course of hypertension when left untreated. Hypertension was related to chronic poisoning with glycyrrhiza, and its hyperaldosteronism like effect. Pathogenesis of discoedema in malignant hypertension is discussed.

[Fatal poisoning by alcohol-free aniseed aperitif]. / Intoxication mortelle par le pastis sans alcool.

A case of chronic poisoning with alcohol-free "pastis" leading to the death of a 32 year old alcoholic patient is reported. The mean daily amount of ingested glycyrrhizinic acid was 0.35 g. "Torsades de pointes" secondary to severe hypokalemia were observed and prolonged cardiac arrest occurred. There was evidence of chronic hypokalemic myopathy and of rhabdomyolysis with acute renal failure. Furthermore, the origin of an associated cardiomyopathy is discussed.

[Pseudo-hyperaldosteronism caused by licorice. Pathogenetic considerations and presentation of a clinical case]. / Pseudo-iperaldosteronismo da liquerizia. Considerazioni patogenetiche e presentazione di un caso clinico.

A case of pseudo-hyperaldosteronism secondary to prolonged daily ingestion of liquorice is reported. Extreme severity of hypokalemia and of the ensuing neuro-muscular impairment characterized this case. The pathogenetic features leading to the glycyrrhizic acid dependent sodium retention are thoroughly discussed, on the basis of the latest literature. The authors stress the fact that public opinion is to a large extent unaware of risks due to prolonged ingestion of liquorice derivatives.

[Acute rhabdomyolysis and tetraparesis secondary to hypokalemia due to ingested licorice]. / Rabdomiólisis aguda y tetraparesia secundarias a hipocaliemia por ingesta de regaliz.

The glycirrinic acid, a common component of the natural licorice, has a potent mineralacorticoid effect (primary pseudohyperaldosteronism) which may cause severe hypokalemia and acute rhabdomyolysis. We present the case of a 36-years-old patient who, as the result of the intake of five daily licorice sticks (25 gr/day) for one month, developed analytical and clinical signs of acute rhabdomyolysis associated to the typical disorders of mineralcorticoid excess, that is, severe hypokalemia, arterial hypertension and metabolic alkalosis. The relevance of this clinical case lies on the low frequency of this finding and on the need that physicians working at emergency care centers must be aware of the onset of acute tetraparesis related to hypokalemia secondary to licorice ingesta. The early detection of this pathology is essential, since it will result in the beginning of an specific treatment, avoiding thus, as far as possible, the severe complications that might appear.

[Pseudohyperaldosteronism secondary to licorice poisoning associated with hemorrhagic gastritis]. / Pseudoiperaldosteronismo secondario ad intossicazione da liquirizia associato a gastrite emorragica.

The case is described of a 6 1/2-year-old child with pseudohyperaldosteronism due to excessive and prolonged liquorice ingestion. The authors debate its differential diagnosis, its physiopathological mechanism (glycyrrhetinic acid, the active metabolite of liquorice, inhibits the conversion of cortisol in cortisone) and its unusual association with haemorrhagic gastritis never observed in the course of liquorice intoxication.

[Pseudo-Conn's syndrome due to intoxication with nonalcoholic pastis]. / Pseudo-syndrome de Conn par intoxication au pastis sans alcool.

A case is reported in a patient who presented with hypertension and quadriparesis, both due to ingestion of a new beverage, non-alcoholic pastis (an anise-based aperitif), containing glycyrrhizinic acid. Consumers, especially if they are ex-alcoholics, diabetics or hypertensives, may develop potentially serious effects from hypermineralocorticism.

[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.

[Hypokalemia without arterial hypertension by licorice poisoning]. / Hypokaliémie sans hypertension artérielle par intoxication à la réglisse.

We report a case of chronic intoxication with glycyrrhizinic acid, at a dosage of 1000 to 1500 mg per month over a period of 11 months, in a former alcoholic. This intoxication was revealed by profound hypokalaemia and rhabdomyolysis. However, blood pressure remained constantly normal. Analysis of the literature shows that liquorice intoxication, which blocks renal 11 beta-hydroxysteroid dehydrogenase evolves more frequently as isolated hypokalaemia than as a picture of pseudo-primary hyperaldosteronism accompanied with hypertension. Hypokalaemia with urinary potassium wasting and without hypertension should therefore lead to considering liquorice intoxication, which can be confirmed by disclosing shut-off of the renin-angiotensin-aldosterone axis, and by the increase of the urinary ratio of [cortisol metabolites (5 alpha tetrahydrocortisol + 5 beta tetrahydrocortisol)]/[cortisone metabolite (5 beta tetrahydrocortisol)] together with increase of urinary free cortisol excretion.

Glycyrrhizin and glycyrrhetinic acid determination from formalin-fixed tissue.

Glycyrrhetinic acid (GA), the main metabolic product of glycyrrhizin (GLY), could be detected in formalin-fixed tissue from a man who died 6 hours after therapeutic administration of a GLY-containing agent. GA was extracted from homogenized formalin-fixed liver tissue and 3 ng GA/g could be detected by HPLC. The extraction from formalin-fixed liver tissue gave the same retention time peak as the GLY control. GA could also be detected by mass spectrometry in the blood sample. This confirms that the man had received a GLY-containing agent for therapeutic use prior to his death and that GA can be determined from formalin-fixed tissue.