PDF(Sci-hub)
Abstract：
BACKGROUND: Liquorice is found in many food products, soft drinks, and herbal medicines. Liquorice ingestion is an uncommon cause of apparent mineralocorticoid excess or pseudo-aldosteronism. The mechanism involves the inhibition of 11-beta-hydroxysteroid dehydrogenase type-2 by the active ingredient called glycyrrhizin. This leads to the uninhibited activation of mineralocorticoid receptors by cortisol. Confectionary products that contain liquorice are readily available in many countries around the world.
METHODS: We report a case of severe refractory hypokalaemia with hypertensive crisis and acute pulmonary oedema due to excessive liquorice consumption. A 79-year-old female presented to the emergency department following a road traffic accident. She described feeling weak and dizzy while driving before the collision. She attended her general practitioner (GP) several weeks earlier for fatigue and was being managed for hypokalaemia on oral potassium supplements. Investigations revealed hypertension (BP 180/69 mmHg), severe hypokalaemia (K 2.2 mmol/l), normal renal function, normal serum magnesium with metabolic alkalosis. Spot urinary potassium was 22 mmol/l. The patient denied taking medications including over-the-counter or herbal medication that can cause hypokalaemia. Hypokalaemia persisted despite aggressive intravenous (i.v.) and oral potassium replacement. She later developed a hypertensive crisis (BP 239/114 mmHg) with pulmonary oedema. She required admission to the intensive care unit and was managed with intravenous furosemide infusion and isosorbide dinitrate infusion. On further discussion, our patient admitted to struggling with nicotine cravings since quitting smoking two months earlier. She began eating an excessive amount of liquorice sweets to manage her cravings. Suppression of plasma renin and aldosterone supported the diagnosis of apparent mineralocorticoid excess secondary to excessive liquorice consumption. Her symptoms and hypokalaemia resolved after stopping liquorice intake.
CONCLUSIONS: This case highlights the life-threatening and refractory nature of hypokalaemia secondary to excessive liquorice consumption. This case also emphasizes the importance of comprehensive history taking including dietary habits. Increased awareness among the public is required regarding the potential health hazards of excessive liquorice consumption.
METHODS: We report a case of severe refractory hypokalaemia with hypertensive crisis and acute pulmonary oedema due to excessive liquorice consumption. A 79-year-old female presented to the emergency department following a road traffic accident. She described feeling weak and dizzy while driving before the collision. She attended her general practitioner (GP) several weeks earlier for fatigue and was being managed for hypokalaemia on oral potassium supplements. Investigations revealed hypertension (BP 180/69 mmHg), severe hypokalaemia (K 2.2 mmol/l), normal renal function, normal serum magnesium with metabolic alkalosis. Spot urinary potassium was 22 mmol/l. The patient denied taking medications including over-the-counter or herbal medication that can cause hypokalaemia. Hypokalaemia persisted despite aggressive intravenous (i.v.) and oral potassium replacement. She later developed a hypertensive crisis (BP 239/114 mmHg) with pulmonary oedema. She required admission to the intensive care unit and was managed with intravenous furosemide infusion and isosorbide dinitrate infusion. On further discussion, our patient admitted to struggling with nicotine cravings since quitting smoking two months earlier. She began eating an excessive amount of liquorice sweets to manage her cravings. Suppression of plasma renin and aldosterone supported the diagnosis of apparent mineralocorticoid excess secondary to excessive liquorice consumption. Her symptoms and hypokalaemia resolved after stopping liquorice intake.
CONCLUSIONS: This case highlights the life-threatening and refractory nature of hypokalaemia secondary to excessive liquorice consumption. This case also emphasizes the importance of comprehensive history taking including dietary habits. Increased awareness among the public is required regarding the potential health hazards of excessive liquorice consumption.
摘要：
背景：甘草存在于许多食品中，软饮料,和草药。甘草摄入是明显的盐皮质激素过量或假性醛固酮增多症的罕见原因。该机制涉及被称为甘草甜素的活性成分抑制11-β-羟基类固醇脱氢酶2型。这导致皮质醇对盐皮质激素受体的激活不受抑制。含有甘草的糖果产品在世界许多国家都很容易获得。
方法：我们报告一例重度难治性低钾血症伴高血压危象和因过量饮用甘草引起的急性肺水肿。一名79岁的女性在道路交通事故后出现在急诊室。她描述了撞车前开车时感到虚弱和头晕。几周前，她因疲劳而参加了全科医生（GP），并正在接受口服钾补充剂的低钾血症治疗。调查显示高血压（BP180/69mmHg），严重低钾血症（K2.2mmol/l），肾功能正常,正常血清镁与代谢性碱中毒。点尿钾为22mmol/l。患者否认服用可导致低钾血症的药物，包括非处方药或草药。尽管有积极的静脉（i.v.）和口服钾替代，但低钾血症仍然存在。她后来出现了高血压危象（BP239/114mmHg）并伴有肺水肿。她需要进入重症监护病房，并接受了呋塞米静脉输注和硝酸异山梨酯输注。关于进一步的讨论,自从两个月前戒烟以来，我们的病人承认一直在与尼古丁的渴望作斗争。她开始吃过量的甘草糖果来控制她的渴望。血浆肾素和醛固酮的抑制支持诊断出明显的盐皮质激素过量继发于甘草消耗。停止摄入甘草后，她的症状和低钾血症得以缓解。
结论：该病例突出了过量食用甘草继发的低钾血症的危及生命和难治性。这个案例还强调了包括饮食习惯在内的全面病史的重要性。需要提高公众对过量食用甘草的潜在健康危害的认识。
方法：我们报告一例重度难治性低钾血症伴高血压危象和因过量饮用甘草引起的急性肺水肿。一名79岁的女性在道路交通事故后出现在急诊室。她描述了撞车前开车时感到虚弱和头晕。几周前，她因疲劳而参加了全科医生（GP），并正在接受口服钾补充剂的低钾血症治疗。调查显示高血压（BP180/69mmHg），严重低钾血症（K2.2mmol/l），肾功能正常,正常血清镁与代谢性碱中毒。点尿钾为22mmol/l。患者否认服用可导致低钾血症的药物，包括非处方药或草药。尽管有积极的静脉（i.v.）和口服钾替代，但低钾血症仍然存在。她后来出现了高血压危象（BP239/114mmHg）并伴有肺水肿。她需要进入重症监护病房，并接受了呋塞米静脉输注和硝酸异山梨酯输注。关于进一步的讨论,自从两个月前戒烟以来，我们的病人承认一直在与尼古丁的渴望作斗争。她开始吃过量的甘草糖果来控制她的渴望。血浆肾素和醛固酮的抑制支持诊断出明显的盐皮质激素过量继发于甘草消耗。停止摄入甘草后，她的症状和低钾血症得以缓解。
结论：该病例突出了过量食用甘草继发的低钾血症的危及生命和难治性。这个案例还强调了包括饮食习惯在内的全面病史的重要性。需要提高公众对过量食用甘草的潜在健康危害的认识。
