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87 ��kat/L (RR: 0.83�C2.84) [7118 U/L (RR: 50�C170)] at admission and increased to 925.48 ��kat/L (55 418 U/L) few days after admission; urinary myoglobin was 930.37 nmol/L (RR: [http://en.wikipedia.org/wiki/MERTK UNC2881] remained normal during his stay. In the endocrine investigations the suppression of renin and aldosterone and the elevated urinary free cortisol are most noticeable (Table ?(Table1).1). We also noted a marked polyuria (up to 5 L/24 h in the first few days) inconsistent with the amount of intravenous fluid administration. Table 1. Endocrine findings and urinary potassium Differential diagnosis The key abnormalities of our case were an extreme hypokalaemia, accompanied by metabolic alkalosis, moderate hypertension, [http://www.selleckchem.com/products/AP24534.html AP24534 ic50] rhabdomyolysis and polyuria. Diuretic abuse was excluded through urinary sampling and our patient denied laxative abuse. Bartter and Gitelman syndrome, Liddle syndrome, congenital adrenal hyperplasia and other congenital or genetic disorders were highly unlikely in view of his age and since previous potassium levels were normal. The suppressed renin and aldosterone and normal morning cortisol suggested an apparent mineralocortoid excess-like disorder. Other endocrinopathies, such as Cushing syndrome and ectopic corticotrophin syndrome, could be excluded through laboratory findings (Table ?(Table1).1). Through a careful medication and dietary history our patient disclosed the consumption of two centimetres of liquorice root a day for the last 2 months, an equivalent of 1.5 g liquorice daily. Treatment All oral medication and liquorice ingestion was ceased. Up to 15 mmol potassium chloride per hour was needed to correct the hypokalaemia, which took about 3 days. Due to persistent hypertension an ACE-inhibitor was started. At discharge alkalosis was still present, but the kalaemia remained within the normal range without further need for substitution. One month after permanent cessation of the liquorice ingestion, all ion, metabolic and endocrine disorders returned to normal. This confirmed our diagnosis of liquorice-induced apparent mineralocorticoid excess syndrome with hypokalaemic paraparesis, rhabdomyolysis and nephrogenic diabetes insipidus. Discussion Liquorice is made from the root of Glycyrrhiza glabra, commonly known for its [http://www.selleckchem.com/products/Imatinib-Mesylate.html STI571 chemical structure] sweet flavour. Throughout history it has been used in herbal medicine and there are even reports of anti-inflammatory, antiviral, antimicrobial, antioxidative, hepatoprotective and cardioprotective properties [2]. Nevertheless liquorice is also well known for inducing hypertension and other health hazards. The active component is glycyrrhizin, which inhibits renal 11-beta?hydroxysteroid dehydrogenase type 2 (11-beta-HDS2). This enzyme converts active cortisol to the inactive cortisone. Hence cortisol escapes inactivation and this leads to the characteristics of the syndrome of apparent mineralocorticoid excess [1, 3].