Licorice, today chiefly utilized as a flavoring additive in tea, tobacco and candy, is one of the oldest used herbs for medicinal purposes and consists of up to 300 active compounds. The main active constituent of licorice is the prodrug glycyrrhizin, which is successively converted to 3β-monoglucuronyl-18β-glycyrrhetinic acid (3MGA) and 18β-glycyrrhetinic acid (GA) in the intestines. Despite many reported health benefits, 3MGA and GA inhibit the 11-β-hydrogenase type II enzyme (11β-HSD2) oxidizing cortisol to cortisone. Through activation of mineralocorticoid receptors, high cortisol levels induce a mild form of apparent mineralocorticoid excess in the kidney and increase systemic vascular resistance. Continuous inhibition of 11β-HSD2 related to excess licorice consumption will create a state of hypernatremia, hypokalemia and increased fluid volume, which can cause serious life-threatening complications especially in patients already suffering from cardiovascular diseases. Two recent meta-analyses of 18 and 26 studies investigating the correlation between licorice intake and blood pressure revealed statistically significant increases both in systolic (5.45 mmHg) and in diastolic blood pressure (3.19/1.74 mmHg). This review summarizes and evaluates current literature about the acute and chronic effects of licorice ingestion on the cardiovascular system with special focus on blood pressure. Starting from the molecular actions of licorice (metabolites) inside the cells, it describes how licorice intake is affecting the human body and shows the boundaries between the health benefits of licorice and possible harmful effects.

Partial nephrectomy is the gold standard treatment in small renal tumours. During partial nephrectomy, the renal artery is clamped which creates transient ischemia. This can damage nephrons and may...

Previous studies have found critically ill patients with COVID-19 to have an increased risk of thromboembolic complications. In this case report of two patients admitted with symptomatic COVID-19, both patients developed pulmonary embolism within a few days after hospital discharge. Both patients received thromboprophylaxis and had an increasing fibrin D-dimer during their hospital stay. Continued thromboprophylaxis after hospital discharge may be indicated for patients with COVID-19, especially for patients at high risk of thrombosis with elevated levels of fibrin D-dimer.