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It takes all sorts--a curious case of pseudohyperaldosteronism, hypertension and liquorice tea.

Background

This case highlights a rare and interesting medical condition bought about by liquorice ingestion. While there have been many previous reports of liquorice toxicity secondary to eating confectionary, I have only found one case report of liquorice toxicity secondary to liquorice tea ingestion and the patient there had only a mild case of hypokalaemia and did not require hospital admission unlike patient X. [1]

Case presentation

Patient X is a usually fit and well 49-year-old woman who was admitted following a collapse. Prior to this collapse she had experienced a 3-week history of gradual onset, slowly worsening dull headache and a feeling of tingling in her hands which increased over this timeframe. On the day of admission, she experienced nausea. Her past medical history included migraines, for which she self-medicated with paracetamol, ibuprofen and codeine as necessary. She was also using Cerazette. She was in full time work, was a lifelong non-smoker and used alcohol very rarely. She had no family history of note.

On examination, Patient X was a slim individual who was hypertensive with a blood pressure of 170/100 mmHg. Her other observations were normal. Her general and neurological examinations were unremarkable.

While initially the medical team felt that Conn's syndrome was a likely cause of the abnormalities, this was reconsidered on a ward round where, following research on the internet into her abnormalities, patient X brought it to the attention of the team that she had been consuming between six and eight liquorice tea infusions per day for the past two months and had been consuming around three a day for a significant period time prior to this (roughly 18 months). The diagnosis was made based on her history.

Investigations

A venous gas demonstrated a metabolic alkalosis with a pH of 7.57.

Blood tests revealed hypokalaemia (K+ = 2.2 mmol/L) and hypophosphataemia (PO4 = 0.35mmol/L). No other abnormalities were detected.

More specialist assays were undertaken, and demonstrated that her plasma renin was 2.3 ng/mL/hour (normal range 0.2-3.3 ng/mL/hour). Her morning supine plasma aldosterone level was 29 pg/mL (normal range 30-160 pg/mL). Her morning plasma cortisol level was 612 nmol/L (normal range 138-635 nmol/L).

In addition, the patient also underwent a CT head and a CT renal angiogram, both of which were normal.

DIFFERENTIAL DIAGNOSIS

* Apparent mineralocorticoid excess

* Exogenous mineralocorticoid excess

* Liddle's syndrome

* Congenital adrenal hyperplasia

* Cushing syndrome

* Liquorice

Treatment

Intravenous potassium and phosphate replacement, cessation of liquorice intake and amlodipine 5mg OD.

Outcome and follow-up

The patient was discharged with a blood pressure of 132/66 mmHg on amlodipine, a potassium level of 2.9, and a phosphate level of 1.16. She was given oral potassium supplementation to be taken 3 times per day. After two weeks, the amlodipine was stopped as she became mildly hypotensive. Her blood pressure was 120/60 following cessation of amlodipine. Three months later her plasma potassium level was 4.6 without supplementation. Mrs X required no follow up although she reports an ongoing feeling of tingling in her hands.

Discussion

Liquorice is an extract of the roots of the Glycyrrhiza glabra plant and has been used as both a confectionary flavouring agent and a herbal remedy. It is also commonly used as a laxative, and as a flavouring agent in chewing gums, sweets, and food products.

The active ingredient in liquorice is glycyrrhetinic acid which inhibits the enzyme 11-0-hydroxysteroid dehydrogenase. This enzyme converts cortisol into inactive cortisone within the distal tubule of the kidney and so in liquorice toxicity there is a build-up of cortisol in distal tubular cells. [2] This results in increased mineralocorticoid like activity as there are structural similarities between cortisol and aldosterone, with increased Na+ and water retention in conjunction with increased H+ and K+ excretion. [3] Here hyperaldosteronism occurs, but with a low or low-normal plasma aldosterone and renin level. Serum glycyrrhetinic acid levels can be measured with enzyme-linked immunosorbent assay (ELISA) and high-performance liquid chromatography (HPLC). Urinary glycrrhetinic acid levels can be measured with gas chromatography-mass spectrometry (GC MS). [4]

Pseudoaldosteronism secondary to liquorice consumption is a relatively rare occurrence. Case reports demonstrate a range of clinical manifestations from an asymptomatic patient fortuitously diagnosed to those with more severe presentations such as rhabdomyolysis, hypertensive encephalopathy, asthenia, paralysis, heart failure, and cardiac arrhythmias such as polymorphic ventricular tachycardia and ventricular fibrillation secondary to hypokalaemia. For these reasons, it has been suggested that the public should be made aware of the potential dangers associated with liquorice consumption. [5-13]

The combination of alkalosis hypokalaemia and hypertension suggests increased mineralocorticoid activity leading to increased renal tubular Na+ reabsorption along with increased k+ and H+ excretion. Both primary and secondary hyperaldosteronism cause these abnormalities, the former via an appropriate response (renin release) to decreased renal perfusion pressure or decreased sodium concentration in the ultra filtrate, the latter an inappropriate release of aldosterone from the adrenal cortex, often a result of an adrenal adenoma.

Other genetic syndromes, such as Bartter's or Gitelman's, cause hypokalaemia with alkalosis but without hypertension. [14]

Features of low potassium include generalised weakness and lethargy, ascending paralysis, and rhabdomyolysis. [15] [17] Decreased intake is rarely a cause of low potassium as the western diet usually contains significantly more potassium than is needed and because the renal tubular reabsorption mechanism can be extremely effective in limiting potassium excretion. [17]

The maximum recommended dose of liquorice is 100mg/day although cases of liquorice toxicity have been reported in association with doses as low as 80mg/day. Each liquorice tea bag contains approximately 500mg of glycyrrhetic acid, of which approximately 20mg is ingested per infusion.

This is a relatively rare occurrence and it has been suggested that certain groups are more susceptible to toxicity than others --for example those with 11-[??]-hydroxysteroid dehydrogenase deficiency. [18] It is also thought that those with essential hypertension are also more at risk. [19]

LEARNING POINTS/TAKE HOME MESSAGES

* Consumption of liquorice can cause pseudoaldosteronism.

* The clinical picture is similar to that of primary aldosteronism, but is characterised by low levels of both aldosterone and renin.

* While liquorice toxicity can be asymptomatic, clinical manifestations are wide ranging and include cardiac arrhythmias, rhabdomyolysis, weakness and paralysis.

* Pseudohyperaldosteronism caused by liquorice consumption is reversible and generally resolves upon cessation of liquorice consumption. Prior to resolution, potassium supplements are usually necessary.

Acknowledgements

Dr Paul Johnston, Consultant Nephrologist, Royal Cornwall Hospital.

Competing Interests

None declared

PETER ALLAN, MBChB(hons) and M(Biol), Royal Perth Hospital, Australia. MICHAEL NEWMAN, MBChB and MSc AND BSc(Hons), Queen Alexandra Hospital, Portsmouth, Uk. TAREQ HUSEIN, MBBS, Morriston Hospital, Swansea, Uk. CORRESPONDENCE: TAREQ HUSEIN, 43 Glan Yr Afon Gardens, Swansea, SA2 9HX.

Email: tareqhusein@yahoo.co.uk

References

[1.] Emily Allcock and James Cowdery. Hypertension induced by Liquorice tea. BMJ Case Reports. 2015.

[2.] Armanini D, Fiore C, Mattarello MJ, Bielenberg J, Palermo M. History of the endocrine effects of licorice. Experimental and Clinical Endocrinology and Diabetes. 2002. p. 257-61.

[3.] Armanini D, Lewicka S, Pratesi C, Scali M, Zennaro MC, Zovato S, et al. Further studies on the mechanism of the mineralocorticoid action of licorice in humans. J Endocrinol Invest. 1996;19:624-9.

[4.] Seth Schonwald MD, FACEP. Liquorice poisoning workup. Medscape. Updated 2017.

[5.] Janse A, van Iersel M, Hoefnagels WHL, Olde Rikker MGM. The old lady who liked liquorice: hypertension due to chronic intoxication in a memory-impaired patient. The Netherlands journal of medicine. 2005. p. 149-50.

[6.] Van den Bosch AE, van der Klooster JM, Zuidgeest DMH, Ouwendijk RJT, Dees A. Severe hypokalaemic paralysis and rhabdomyolysis due to ingestion of liquorice. The Netherlands journal of medicine. 2005. p. 146-8.

[7.] Van Beers EJ, Stam J, van den Bergh WM. Licorice consumption as a cause of posterior reversible encephalopathy syndrome: a case report. Crit Care. 2011;15:R64.

[8.] Robles BJF, Sandoval a RH, Dardon JDP, Blas CA. Lethal liquorice lollies (liquorice abuse causing pseudohyperaldosteronism). BMJ Case Rep [Internet]. 2013; 2013:9-11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24051150

[9.] Famularo G, Corsi F GM. Iatrogenic worsening of hypokalemia and neuromuscular paralysis associated with the use of glucose solutions for potassium replacement in a young woman with licorice intoxication and furosemide abuse. Acad Emerg Med. 1999;6:960-3.

[10.] Harada T, Ohtaki E M k. Congestive heart failure caused by digitalis toxicity in an elderly man taking a licorice-containing chinese herbal laxative. Cardiology. 2002;98(218).

[11.] Eriksson J, Carlberg B, Hill??rn V. Life-threatening ventricular tachycardia due to liquorice-induced hypokalaemia. J Intern Med. 1999;245:307-10.

[12.] Brusselaers N, Vogelaers D, Blot S. The rising problem of antimicrobial resistance in the intensive care unit. Annals of Intensive Care. 2011. p. 47.

[13.] Omar HR, Komarova I, El-Ghonemi M, Fathy A, Rashad R, Abdelmalak HD, et al. Licorice abuse: time to send a warning message. Therapeutic Advances in Endocrinology and Metabolism. 2012. p. 125-38.

[14.] Simon DB, Lifton RP. The molecular basis of inherited hypokalemic alkalosis: Bartter's and Gitelman's syndromes. Am J Physiol. 1996;271:F961-F966.

[15.] Cumming AM, Boddy K, Brown JJ, Fraser R, Lever AF, Padfield PL, et al. Severe hypokalaemia with paralysis induced by small doses of liquorice. Postgraduate medical journal. 1980. p. 526-9.

[16.] Kishore B, Thurlow V, Kessel B. Hypokalaemic rhabdomyolysis. Annals of clinical biochemistry. 2007. p. 308-11.

[17.] Rastegar A, Soleimani M. Hypokalaemia and hyperkalaemia. Postgrad Med J. 2001;77:759-64.

[18.] Edwards C. lessons from licorice. N Engl J Med. 1991;325:1242-3.

[19.] Sigurjonsdottir HA, Manhem K, Axelson M, Wallerstedt S. Subjects with essential hypertension are more sensitive to the inhibition of 11 beta-HSD by liquorice. Journal of human hypertension. 2003 p. 125-31.
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Title Annotation:Case Report
Author:Allan, Peter; Newman, Michael; Husein, Tareq
Publication:British Journal of Medical Practitioners
Date:Mar 1, 2018
Words:1610
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