Endothelial dysfunction as the pathogenetic factor of internal organ damage in polychemotherapy for the breast cancer

Objective: to evaluate the role of endothelial dysfunction in pathogenesis of toxic damage of internal organs caused by anthracyclinecontaining polychemotherapy (ACP) for breast cancer. The dynamic examination comprised 34 female patients aged 30 to 59 (V0,5=49.0; V0,25=45.0; V0,75=53.0 years) with the stage II B breast cancer who had received six courses of ACP under CAF scheme (cyclophosphamide 100 mg/m2 daily for 14 days from day 1 to day 14; doxorubicin 30 mg/m2 in days 1 and 8; 5fluorouracil 500 mg/m2 in days 1 and 8; the treatment courses were repeated every 28 days). During the period of study, the percentage of patients with augmented endothelin1(21) level and insufficient endothelium dependent vasodilatation significantly increased (McNemars test: X2=8.1 and X2=15.06; р=0.044 and p=0.001, respectively for endothelin1(21) level and endotheliumdependent vasodilatation). In detection of endothelial dysfunction during ACP, the test parameters revealed sensitivities of 100 and 94%; specificities of 64 and 65%; positive predictive values of 85 and 73%; and negative predictive values of 100 and 92% for endothelin1(21) and microalbumin levels, respectively. Moderate and weak correlation relationships were found between the laboratory and instrumental parameters reflecting the endothelium, heart, and kidney functions. ACP under CAF scheme causes endothelial dysfunction with the early markers such as augmentation of the endothelin1(21) and microalbumin levels. Determination of the endothelin1(21) and microalbumin levels represent affordable laboratory tests for endothelial dysfunction and may be widely used in clinical practice in case of ACP for breast cancer. High incidence of endothelial dysfunction and its pathogenetic significance for toxic damage of internal organ require clinical correction of the pathological changes in vascular endothelium during ACP for breast cancer.