Literature DB >> 26935039

Abnormal correlation of circulating endothelial progenitor cells and endothelin-1 concentration may contribute to the development of arterial hypertension in childhood acute lymphoblastic leukemia survivors.

Tomasz Ociepa1, Magdalena Bartnik1, Karolina Zielezinska1, Mai Prokowska2, Elzbieta Urasinska2, Tomasz Urasinski1.   

Abstract

It is well known that the rate of arterial hypertension (AH) in childhood acute lymphoblastic leukemia (ALL) survivors is significantly higher than that in the healthy pediatric population; however, the mechanism of this phenomenon is not fully understood. The developing cardiovascular system in children is thought to be highly susceptible to the toxic effects of chemotherapy, which causes damage to the blood vessel wall, including the endothelium. Endothelin-1 (ET-1) is a marker of endothelial damage, and it contributes to AH. Endothelial progenitor cells (EPCs) are derived from the bone marrow and participate in the process of blood vessel repair. The aim of this study was to determine the relationship between the rate of circulating EPCs and plasma levels of ET-1 with respect to hypertension in childhood ALL survivors. The study included 88 childhood ALL survivors and 44 healthy children as controls. All patients and controls had 24-h blood pressure monitoring with a HolCARD CR-07 device. The number of EPCs and the ET-1 serum concentration were measured in the peripheral blood of patients and controls using flow cytometry and enzyme-linked immunosorbent assay, respectively. A correlation was found between the number of EPCs and the ET-1 concentration in the peripheral blood of healthy children and normotensive ALL survivors. However, such a correlation was not found in hypertensive childhood ALL survivors. We conclude that dysregulation of the 'ET-1 and EPC axis' may contribute to the development of AH in some childhood ALL survivors.

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Year:  2016        PMID: 26935039     DOI: 10.1038/hr.2016.22

Source DB:  PubMed          Journal:  Hypertens Res        ISSN: 0916-9636            Impact factor:   3.872


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