Drug-induced oedema
C. Schindler (1), S. Schellong (2)
(1) Institut für Klinische Pharmakologie, Medizinische Fakultät der TU Dresden; (2) II. Medizinische Klinik, Städtisches Krankenhaus Dresden-Friedrichstadt
Summary
Besides more classical aetiologies for oedema such as heart failure, liver cirrhosis, nephrotic syndrome and chronic venous insufficiency, in practice we increasingly observe iatrogenic or drug-induced oedema as adverse events. Many drugs have the potential to cause oedema or to worsen pre-existing oedema prior to the initiation of drug therapy. Drug-induced oedema is frequently caused by calcium-channel-blockers of the dihydropyridine-type but can also be caused by dihydralazine and minoxidil which are less frequently prescribed. Other drugs which may support the formation of oedema are diuretics, non-steroidal anti-inflammatory drugs (NSAIDs), ACE-inhibitors or AT1-receptor-antagonists (angioedema) and thiazolidinediones/ glitazones which are used as oral antidiabetics. This review focuses on drug-induced oedema, pathophysiological considerations and potential treatment and management strategies from a clinical-pharmacological perspective. Keywords
pathophysiology, treatment strategies, Glitazones, Drug-induced oedema, vasodilators, calcium channel blockers, loop-diuretics, ACE-inhibitors, AT1-receptor-blockers