Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic and toxic effects caused by prolonged daily ingestion of Liquorice are well known in the literature. Such acquisition doesn't seem to be known enough by practitioners and by common people. Besides active substances such as Glycyrrhizin , Liquorice contains even steroids similar to the adrenocortical ones; among these the most important is Beta-Glycyrrhetinic acid. This one, in vivo and in vitro, produces salt and water retention by means of a "DOCA-like" mineral-corticoid mechanism, and clear suppression of the Renin-Angiotensin-Aldosterone axis. A low plasmatic level of Renin and Aldosterone is a common feature. The clinical picture in many ways is similar to the primary Aldosteronism and for this reason the above mentioned syndrome is usually called "Pseudoaldosteronism". Symptoms and signs can be classified into the following main groups: symptoms linked with water and salt retention: oedemas, hypertension, cardiac involvement. Symptoms linked with serum Potassium depletion: asthenia, paralysis (due to Potassium deficiency), myopathy with myoglobinuria. The diagnosis is essential based on an accurate pharmacological dietetic history, aimed to recognise an excessive use of Liquorice (pure or more often as substitute) in the screening of hypertension with or without hypopotassemia. Finally, the more or less quick normalisation of blood pressure and biochemical signs--as an "ex juvantibus" criterion--is the most important reason for the diagnosis. After a wide survey of the literature, the clinical and biological picture in four patients with chronic Liquorice ingestion and Pseudoaldosteronism syndrome is described.
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PMID:[Pseudoaldosteronism caused by licorice. Review of the literature and description of 4 clinical cases]. 380 7

50 years old female patient, with history of diabetes mellitus and hypertension, receiving metformin (500 mg BID) and atenolol (50 mg BID), presented to the Emergency Room with asthenia and dizziness. The patient was also receiving alternative medication (Dragon Blanco) which contains no licorice. During the emergency workup she developed syncope and three episodes of ventricular fibrillation. She was electrically defibrillated and treated with amiodarone and potassium replacement. The patient was admitted to the Intensive Care Unit. Physical exam: BP: 160/90 mm Hg, RR: 15, Pulse: 83: Cardiovascular: grade II systolic murmur which irradiated to the neck. The rest of the examination was unremarkable. Labs: Na: 138 meg/dl, K: 1.6 meg/dl, Cl: 84 meg/dl, BUN: 17 mg/dl, Creat.: 1.1 mg/dl, Gluc.: 148 mg/dl, Renin: < 0.15 mcgr/ml, Aldosterone: 20.1 mcg%. Aldosterone-Renin ratio: 133. Chest X-Ray: cardiomegaly. EKG: RBBB, long QT segment and prominent broad "u" waves compatible with severe hypokalemia. A CT SCAN of the Abdomen/Pelvis showed a 3.2 cm right adrenal mass, most likely adenomatous. The patient was discharged with the diagnosis of primary aldosteronism. Due to the diagnosis of diabetes mellitus, hypertension and the three episodes of ventricular fibrillation, surgical treatment was postponed until stress tests and eventual coronary angiographic studies were performed. We found in our review of the medical literature 9 reports of fibrillation associated with hyperaldosteronism. Of those, only two were associated with primary aldosteronism, one of them with a fatal outcome. This case is highly unusual and emphasizes the importance of an adequate diagnosis of secondary hypertension.
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PMID:Ventricular fibrillation as the first manifestation of primary hyperaldosteronism. 1961 May 66