<br>过量摄入甘草继发假性醛固酮增多症危及生命的一例,BMC Endocrine Disorders

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过量摄入甘草继发假性醛固酮增多症危及生命的一例
BMC Endocrine Disorders ( IF 2.8 ) Pub Date : 2021-08-06 , DOI: 10.1186/s12902-021-00816-4
Joseph McHugh ₁ , Ramesh Nagabathula ₂ , Ma Pyeh Kyithar ₁

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许多食品、软饮料和草药中都含有甘草。摄入甘草是导致盐皮质激素明显过量或假性醛固酮增多症的罕见原因。其机制涉及活性成分甘草甜素对 2 型 11-β-羟基类固醇脱氢酶的抑制。这导致皮质醇不受抑制地激活盐皮质激素受体。含有甘草的糖果产品在世界许多国家都很容易买到。我们报告一例因过量食用甘草而导致严重难治性低钾血症并伴有高血压危象和急性肺水肿的病例。一名 79 岁女性因道路交通事故被送往急诊室。她描述在碰撞前开车时感到虚弱和头晕。几周前，她因疲劳而去看全科医生 (GP)，并通过口服钾补充剂治疗低钾血症。检查显示高血压（BP 180/69 mmHg）、严重低钾血症（K 2.2 mmol/l）、肾功能正常、血清镁正常伴代谢性碱中毒。现场尿钾为 22 mmol/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。尽管积极静脉注射（iv）和口服钾替代疗法，低钾血症仍持续存在。她后来出现高血压危象（血压 239/114 mmHg）并伴有肺水肿。她需要住进重症监护室，并接受静脉输注呋塞米和硝酸异山梨酯输注治疗。在进一步讨论中，我们的患者承认自从两个月前戒烟以来，他一直在与尼古丁的渴望作斗争。她开始吃过量的甘草糖来控制自己的食欲。血浆肾素和醛固酮的抑制支持了因过量甘草摄入导致的明显盐皮质激素过多的诊断。停止摄入甘草后，她的症状和低钾血症得到缓解。该病例凸显了因过量甘草摄入而继发的低钾血症的危及生命和难治性的性质。该病例还强调了包括饮食习惯在内的全面病史采集的重要性。需要提高公众对过量甘草消费的潜在健康危害的认识。

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A life-threatening case of pseudo-aldosteronism secondary to excessive liquorice ingestion

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. 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. 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.

更新日期：2021-08-07

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