| Title | Drug-induced disorders in electrolyte and acid-base balance | |
| Authors | Thomas A. Mavracanas, Achilleas Mandalos, Stavros Kiakos, Athinodoros Valavanis, Emmanouel Restas, Charalambos Stefanidis, George Sevastos and Maria Mironidou-Tzouveleki
Department of Pharmacology, Medical School, Aristotle University of Thessaloniki, Thessaloniki, Greece |
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| Citation | Mavracanas, T.A., Mandalos, A., Kiakos, S., Valavanis, A., Restas, E. et al.: Drug-induced disorders in electrolyte and acid-base balance, Epitheorese Klin. Farmakol. Farmakokinet. 16(2): 117-124 (2002) | |
| Publication Date | Received for publication: 10 November 2001
Accepted for publication: 1 December 2001 |
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| Full Text Language | English | |
| Order – Buy | Ηλεκτρονική Μορφή: pdf (10 €) – Digital Type: pdf (10 €)
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| Keywords | Drugs-electrolyte disorders, acid base disturbances, adrenergic agonists, adrenergic antagonists, succinylcholine, cardiac glycosides, diuretics, angiotensin converting enzyme inhibitors (ACEIs), vitamin B12, folic acid, laxatives, theophylline, insulin, corticosteroids, penicillins, folic acid antagonists, amphotericin B, non-steroidal anti-inflammatory drugs (NSAIDs), salicylates, contrast media, heparin, cyclosporine, phenytoin, demeclocycline, lithium, chlorpropamide, carbamazepine, vincristine, tricyclic antidepressants, cyclophosphamide, tolbutamide, opiates, barbiturates, anesthetics. | |
| Other Terms | review article | |
| Summary | This review discusses the drug-induced major disorders in electrolyte and acid-base balance. We report the disturbances caused by each drug, as well as the main mechanism of the drug’s action on the homeostatic mechanisms that control the electrolyte and acid-base balance. For example, β-agonists and α2-antagonlsts may cause hypokalemia. Unlike β-agonists, β-blockers cause hyperkalemia. Osmotic diuretics enhance free water excretion and induce hyponatremia and hypokalemia with increased plasma osmolality. Carbonic anhydrase inhibitors cause metabolic acidosis and hypokalemia. On the contrary, potassium-sparing agents lead to hyperkalemia and loop diuretics cause hypokalemia or metabolic alkalosis. Furthermore, excessive doses of digoxin lead to hyperkalemia. The administration of angiotensin converting enzyme inhibitors (ACEIs) may also lead to hyperkalemia. Moreover, insulin enhances Na+, K1+ ATPase activity on cell membranes, increasing Κ+ influx and causing hypokalemia. Mineralocorticoids lead to hypokalemia and metabolic alkalosis as a result of iatrogenic aldosteronism. Non-steroidal anti-inflammatory drugs (NSAIDs), such as indomethacin, cause hyperkalemia via suppression of the renin-angiotensin-aldosterone axis. It is known that aspirin toxicity causes a mixed acid-base disorder characterized by respiratory alkalosis and metabolic acidosis. Finally, heparin and cyclosporine have been found to induce hyperkalemia by suppressing aldosterone production in the adrenal zona glomerulosa. | |
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