Chewing gum and hypokalaemia

Rosseel, Michael; Schoors, Danny

doi:10.1016/0140-6736(93)90036-g

Cited by 13 publications

(10 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Oestrogens may react with the mineralocorticoid receptor or inhibit 11β-hydroxysteroid dehydrogenase activity,11 which may explain why female sex and the use of oral contraceptives can increase the susceptibility to glycyrrhizinic acid 8. Interestingly, both our patients were women using oral contraceptives, but other predisposing factors may be important as the association has been described in a man 9. The inhibition of 11β-hydroxysteroid dehydrogenase lasts for two weeks after glycyrrhizinic acid is removed, but suppression of the renin-angiotensin-aldosterone axis may persist for as long as two to four months,12 as happened in case 1.…”

Section: Discussionmentioning

confidence: 68%

“…A dose-response study of glycyrrhizinic acid in healthy volunteers showed that a significant fall in plasma potassium concentration from 4.3 mmol/l to 3.5 mmol/1 occurred at a dose of 800 mg or more a day 8. To our knowledge, only two similar cases of hypermineralocorticoidism associated with the use of chewing gum have been described 9 10. Why some people are susceptible to low doses of glycyrrhizinic acid remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Lesson of the week: hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum

Klerk¹,

Nieuwenhuis²,

Beutler³

1997

BMJ

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

Lesson of the week: hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum

Klerk¹,

Nieuwenhuis²,

Beutler³

1997

BMJ

View full text Add to dashboard Cite

“…The chewing gum she used contained 24 mg of glycyrrhizin per 16 g pack. Hypokalaemic hypertension using the same chewing gum brand has been described in a patient taking two packs a day, considerably less than in patient B [18]. The continuously suppressed plasma renin activity and aldosterone concentration, despite a repeatedly negative urinary 18βGA assay, may have resulted from intermittent liquorice intake.…”

Section: Discussionmentioning

confidence: 99%

“…Hypokalaemic hypertension with a low plasma renin activity level is not pathognomonic for liquorice‐induced hypertension, because it can also be found in several other conditions such as primary aldosteronism, Liddle’s syndrome and deoxycorticosterone‐excess states, like 11β‐hydroxylase and 17α‐hydroxylase deficiency, adrenal carcinoma and Cushing’s syndrome. Furthermore, glycyrrhizin is not only a compound of liquorice, but is frequently added as a sweetener to many food products including beverages, chewing gum, smokeless tobacco and certain medications [2, 6, 16–18]. Due to this widespread use, a patient can be completely unaware of consuming any glycyrrhizin‐containing product.…”

Section: Introductionmentioning

confidence: 99%

Gas chromatographic–mass spectrometric analysis of urinary glycyrrhetinic acid: an aid in diagnosing liquorice abuse

Kerstens

Guillaume²,

Wolthers³

et al. 1999

Journal of Internal Medicine

View full text Add to dashboard Cite

Abstract. Kerstens MN, Guillaume CPF, Wolthers BG, Dullaart RPF (University Hospital Groningen, Groningen, The Netherlands). Gas chromatographic±mass spectrometric analysis of urinary glycyrrhetinic acid: an aid in diagnosing liquorice abuse. J Intern Med 1999; 246: 539±547.Objectives. Liquorice abuse can lead to severe clinical complications, caused by its active compound 18b-glycyrrhetinic acid (18bGA). 18bGA inhibits dehydrogenase activity of 11b-hydroxysteroid dehydrogenase (11bHSD). This enzyme catalyses the interconversion between cortisol and cortisone and normally protects the mineralocorticoid receptor from being activated by cortisol. Diagnosing liquorice abuse can be notoriously difficult. The aim of our study was to develop an accurate and clinically applicable 18bGA urinary assay. Design. We developed a urinary 18bGA assay based on gas chromatography and mass spectrometry (GCMS) with sufficient sensitivity to detect 18bGA at low concentrations. The assay was validated in four volunteers consuming different amounts of liquorice. We applied its use in two patients with hypokalaemic hypertension and suppressed plasma renin activity and serum aldosterone, who were suspected of liquorice abuse. Results. The detection limit for 18bGA of the GC assay was 10 mg L 21 , which was lowered to 3 mg L 21 by subsequent application of MS. In all volunteers, urinary 18bGA was detected during liquorice intake. Urinary 18bGA remained detectable until 5 days after stopping continued liquorice intake and until at least 51 h after ingestion of a single large amount. Urinary 18bGA was demonstrated in both patients, establishing a diagnosis of liquorice abuse. One patient showed changes in urinary cortisol metabolites, consistent with 11bHSD inhibition. Changes in cortisol metabolites were less pronounced in the other patient. Conclusion. Liquorice abuse can result in hypokalaemic hypertension with prolonged suppression of plasma renin activity and aldosterone concentration. This is caused by 18bGA-mediated inhibition of 11bHSD, resulting in activation of the renal mineralocorticoid receptor by cortisol. Urinary 18bGA measurement by GCMS is a useful aid in establishing liquorice abuse.

show abstract

“…5 Licorice flavoring in chewing gum (glycyrrhiza) can induce hypokalemia and hypertension. 6,7 Frequent oral cavity exposure to concentrated sugars facilitates dental caries.…”

Section: Discussionmentioning

confidence: 99%

Chewing Gum Bezoars of the Gastrointestinal Tract

Milov¹,

Andres²,

Erhart³

et al. 1998

Pediatrics

View full text Add to dashboard Cite

ABSTRACT. Children have chewed gum since the Stone Age. Black lumps of prehistoric tar with human tooth impressions have been found in Northern Europe dating from ϳ7000 BC (Middle Stone Age) to 2000 BC (Bronze Age). 1The bite impressions suggest that most chewers were between 6 and 15 years of age. The Greeks chewed resin from the mastic tree (mastic gum). North American Indians chewed spruce gum. The first manufacturing patent for chewing gum was issued in 1869 for a natural gum, chicle, derived from the Sopadilla tree, indigenous to Central America. Chewing gum sold today is a mixture of natural and synthetic gums and resins, with added color and flavor sweetened with corn syrup and sugar. Chewing gum is big business. A significant amount of the $21 billion US candy industry sales is from chewing gums, many of which appeal almost exclusively to children. Despite the history and prevalence of gum chewing, the medical literature contains very little information about the adverse effects of chewing gum. In the present report, we briefly review gum-chewing complications and describe three children who developed intestinal tract and esophageal obstruction as a consequence of swallowing gum. Pediatrics 1998;102(2). URL: http://www.pediatrics.org/cgi/content/full/102/2/e22; gum, chewing gum, constipation; fecal mass. CASE REPORTSCase 1

show abstract

Chewing gum and hypokalaemia

Cited by 13 publications

References 2 publications

Lesson of the week: hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum

Lesson of the week: hypokalaemia and hypertension associated with use of liquorice flavoured chewing gum

Gas chromatographic–mass spectrometric analysis of urinary glycyrrhetinic acid: an aid in diagnosing liquorice abuse

Chewing Gum Bezoars of the Gastrointestinal Tract

Contact Info

Product

Resources

About