ABSTRACT
Introduction : Hypokalaemia is a common electrolyte disorder and mild imbalances are frequently found in routine outpatient blood testing. However, severe potassium deficiency (<2,5 mmol/L) is rare and could provide a diagnostic challenge for clinicians. This report describes a case of hypokalaemia due to pseudohyperaldosteronism caused by the ingestion of liquorice, and demonstrates the importance of dietary intake assessment in hypokalaemia patients. Case presentation : A 45-year-old female without a notable medical history was admitted to the hospital with severe hypokalaemia (2.3 mmol/L) on laboratory testing. Two years earlier, her serum potassium level was adequate (3.8 mmol/L). She denied diarrhea and her only complaint was fatigue. Save for oral contraceptives, she reported no use of medications. On examination, she appeared malnourished and had high blood pressures. Although dietary intake was not evaluated at the time of presentation, it was eventually discovered she consumed liquorice daily since childhood. Furthermore, she tested positive for COVID-19 and had low serum magnesium and phosphate levels as well. Urine potassium excretion was never measured. Intravenous potassium phosphate was administered in high doses, in addition to magnesium supplementation and spironolactone, with eventual correction of the hypokalaemia and resolution of hypertension. The patient was advised to refrain from further liquorice consumption. Discussion : This case of hypokalaemia is thought to be induced by excessive liquorice ingestion, which can cause pseudohyperaldosteronism by inhibiting the conversion of cortisol to cortisone, thus increasing the cortisol levels which bind the mineralocorticoid receptor similarly to aldosterone, subsequently activating the renin-angiotensin-aldosterone system (RAAS) and causing features of mineralocorticoid excess, including hypokalaemia and hypertension. This patient also presented with aggravating factors. First, a magnesium deficit, which is known to impair potassium reabsorption across the renal tubules. Therefore, magnesium should be replaced to facilitate potassium correction, especially in hypokalaemia refractory to supplementation, as was done here. Second, concomittant COVID-19 infection could have contributed to the severity of hypokalaemia in this patient, as COVID-19 is thought to downregulate ACE2 expression, consequentially increasing angiotensin II, which will augment the potassium excretion in the urine. In conclusion, dietary preferences and nutritional status should be assessed in all patients presenting with hypokalaemia, as this could provide important clues for differential diagnosis and etiology of hypokalaemia. In this patient, electrolyte imbalances caused by malnutrition, and concomitant COVID-19 infection could explain why her liquorice consumption only now proved to be problematic after years of excessive intake.