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Abstract: SA-PO699

Licorice-Induced Hypocalcemia: A Rare Outcome of Chronic Licorice Consumption

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Mustafa, Nabiha, Bakhtawar Amin Medical and Dental College, Multan, Pakistan
  • Khan, Mohammad Raza, Bakhtawar Amin Medical and Dental College, Multan, Pakistan
  • Qadir, Areebah, Bakhtawar Amin Medical and Dental College, Multan, Pakistan
  • Khakwani, Aemen Shams, Suburban Community Hospital, Norristown, Pennsylvania, United States
  • Ali, Sana, Allama Iqbal Medical College, Lahore, Pakistan
  • Hameed, Aamna Faisal, Shifa College of Medicine, Islamabad, Pakistan
  • Rasool, Sohaib, Bakhtawar Amin Medical and Dental College, Multan, Pakistan
  • Khan, Usman A., Oklahoma University Medical Center, Oklahoma City, Oklahoma, United States
Introduction

A syndrome mimicking mineralocorticoid excess resulting in hypokalemia, hypertension, and hypernatremia is a common occurrence after chronic licorice consumption, according to various published case reports. However, licorice induced hypocalcemia with eunatremia is rarely reported. The authors present a case of a patient diagnosed with hypocalcemia due to excessive licorice consumption.

Case Description

69 year old male presented to our department with primary complaints of oral numbness, muscle cramping, and paresthesia. On admission, he was hypertensive (160/90mmHg) with a heart rate of 84 bpm. An initial lab analysis showed hypocalcemia [Ca, 2.7 mg/dL], hypokalemia [2.7 mEq/dL], and hypomagnesemia [1.1 mg/dL]. The patient was immediately started on IV potassium and calcium replacement, and spironolactone. Dietary history revealed that the patient had been consuming licorice excessively since 2 and half months due to its presumed anti-inflammatory action. The replacement therapy was continued to day 3 and then stopped. The laboratory results were monitored till day 7. Follow-up on day 28 showed normal values as summarized in Table 1.

Discussion

Glycyrrhetic acid and Glycyrrhizic acid are two components of Licroice root extract that have been shown to mimic mineralocorticoid excess by inhibiting enzyme 11ßhydroxysteroid which converts cortisol to cortisone. This results in an increased plasma half-life of cortisol, which binds to aldosterone receptors in renal tubules and activates them. Eventually, the volume overload increases sodium, calcium, and magnesium delivery to the distal tubules. Sodium is absorbed in exchange for calcium and magnesium which induces hypocalcemia and hypomagnesemia. Low magnesium also impairs the function of the Parathyroid hormone. Licorice is quite popular among the geriatric American population because of its assumed anti-oxidant properties and this case report highlights the significance of physician’s knowledge regarding its chronic use and but life-threatening complication of hypocalcemia.

Table 1: Laboratory analysis
DayPotassium [mEq/dL]Calcium [mg/dL]
12.75.7
33.37.1
73.98.2
283.88.1