Guillain-Barré syndrome (GBS) may be complicated by severe hypertension (HT) and in turns severe HT can occur with neurological damage mimicking a GBS, so that underlying causes should be investigated. We describe a case of a 62-year-old woman presented to the emergency department for hypertensive crisis with symmetric flaccid paralysis, hypotonia and hyporeflexia of both upper and lower limbs. Brain computed tomography, magnetic resonance imaging and lumbar puncture were normal. Laboratory investigations revealed severe hypokalemia, renal failure, liver impairment, rabdomyolysis, metabolic alkalosis, and low plasma renin and aldosterone levels. Continuous potassium replacement led to complete clinical resolution. A detailed history revealed chronic intake of 250 g/day black liquorice. Hypokalaemic muscle weakness may simulate a GBS. When serum potassium level falls below 2.5 mmol/l, rhabdomyolysis may occur. In this clinical case, an apparent mineralocorticoid excess syndrome was induced by chronic ingestion of liquorice. This latter contains the glycyrrhetic acid that inhibits the enzyme 11-β-hydroxysteroid dehydrogenase enzyme type-2 leading an aldosterone-like effect and causing hypertension, hypokalemia, metabolic alkalosis and low renin values. The clinical presentation is similar to that observed in the primary aldosteronism, but in this syndrome plasma aldosterone levels are low rather than elevated as in primary aldosteronism. Liquorice-induced hypertension with severe hypokalemia and rhabdomyolysis is a rare condition and the initial presentation with acute muscle paralysis is still more unusual. Before performing instrumental examinations in middle-aged peoples with hypertension crisis and neurological impairment, a detailed clinical history is mandatory.
Keywords: Glycyrrhetic acid; Guillain–Barrè syndrome; Hypokalemia; Rhabdomyolysis; Secondary hypertension.