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Dexrazoxane protects breast cancer patients with diabetes from chemotherapy-induced cardiotoxicity
Fangyi Sun1, Xiaoyong Qi, Cuizhi Geng
1Department of Internal Medicine, Hebei Medical University, Shijiazhuang, P. R. China (FS, XL), Department of Cardiology, Hebei General Hospital, Shijiazhuang, P. R. China (XQ), Department of surgical medicine, Fourth Hospital of Hebei Medical University, Shijiazhuang, P. R. China (CG), Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Background:
To evaluate the cardioprotective effect of dexrazoxane (DEX) on chemotherapy in patients with breast cancer with concurrent type 2 diabetes mellitus (DM2).
Methods:
Eighty female patients with breast cancer with DM2 were randomly assigned to receive chemotherapy only or chemotherapy plus DEX. All patients received 80 mg/m epirubicin and 500 mg/m cyclophosphamide by intravenous infusion every 3 weeks for a total of 6 cycles. The group assigned to receive chemotherapy alone received placebo 30 minutes before epirubicin administration. The group assigned to receive chemotherapy plus DEX received 800 mg/m DEX 30 minutes before epirubicin administration. Cardiac function and hematology before and after 6 cycles of chemotherapy were analyzed.
Results:
There was no difference in baseline systole or diastole function between the 2 DM2 groups. Patients receiving chemotherapy alone experienced significantly greater reductions in Ea and significantly greater elevations in E/Ea and Tei index in comparison with patients receiving chemotherapy plus DEX. After chemotherapy, superoxide dismutase was significantly reduced, and serum malondialdehyde (MDA) was significantly increased in patients with DM2. Serum superoxide dismutase levels were comparable between the 2 groups before and after chemotherapy, MDA levels were comparable between the 2 groups before chemotherapy, whereas serum MDA was significantly higher after chemotherapy in the chemotherapy alone group in comparison with the group that received DEX.
Conculsions:
DEX protects against cardiotoxicity induced by chemotherapy in patients with breast cancer with concurrent DM2.
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