See also
Drug-induced angioedema
Gleichs syndrome (unexplained angioedema with high eosinophil counts)
Ruconest (C1-inhibitor)

References
External links

Angioedema at Curlie
As plasma levels of epirubicinol are lower than those of the unchanged drug and the metabolite has an in vitro cytotoxic activity 10% of that of epirubicin, it is unlikely to reach in vivo concentration sufficient for cytotoxicity. No significant toxicity has been reported for the other metabolites. Epirubicinol is the 13(S)-dihydro derivative formed via the reduction of the C-13 keto-group. Both the unchanged drug and epirubicinol can be conjugated with glucuronic acid, creating the 2 glucuronides. This glucuronidation pathway is unique to epirubicin metabolism in humans  as epirubicin is the only anthracycline that serves as a substrate for beta-glucuronidation. This unique pathway might explain the better tolerability of this drug compared with doxorubicin.The 4 aglycones are formed by losing the amino sugar moiety through a hydrolytic process or redox process, creating the doxorubicin and doxorubicinol aglycones and 7-deoxy-doxorubicin and 7-deoxy-doxorubicinol aglycones, respectively. Excretion
Epirubicin and its metabolites are primarily eliminated through biliary excretion. About 11 to 15% of the administered dose is eliminated as an unchanged drug, which makes up 6 to 7% of the excreted compounds, and metabolites. Side effects
The most common side effects of the Epirubicin are alopecia, nausea/vomiting, cardiotoxicity, leukopenia, and stomatitis. Cardiotoxicity is a severe side effect and the exact pathway is still unknown. However, there is good evidence to suggest that cardiotoxicity is caused at least in part by the avid interaction of anthracyclines with iron, resulting in the formation of metal ion complexes.