Seker, MESUTISEN, Hayati C.Cevirme, NİDALAydin, SinemBilici, AhmetCOBAN, EZGİBulut, HURİYASIN, Ayse I.Demir, TARIKAliyev, ALTAYKocyigit, ABDÜRRAHİMTurk, Haci M.2019-10-052019-10-052018-01-01Seker M., ISEN H. C. , Cevirme N., Aydin S., Bilici A., Bulut H., YASIN A. I. , COBAN E., Demir T., Aliyev A., et al., -Role of Urotensin-2 in 5-Fluorouracil-Related Arterial Vasoconstriction in Cancer Patients-, ONCOLOGY RESEARCH AND TREATMENT, cilt.41, ss.545-549, 2018https://hdl.handle.net/20.500.12645/3417Background: The aim of this study was to identify the possible relationship of 5-fluorouracil (5-FU)-related arterial vasoconstriction with urotensin-2 (UT-2), which has a high potential as an endogenic vasoconstrictor. Methods: We assigned the patients to 1 of 3 groups. Patients in group 1 received a bolus of 5-FU, those in group 2 a continuous infusion (CI) of 5-FU, and those in group 3 no 5-FU, which was also a control group. Pre- and post-treatment UT-2 levels and brachial arterial diameters were measured and recorded in all patients. Results: 132 patients were included in the study. Pre-and post-treatment brachial artery diameters were similar in all groups: in group 1 (3.28 +/- 0.52 vs. 3.25 +/- 0.44 mm, p = 0.740), in group 2 (3.57 +/- 0.47 vs. 3.46 +/- 0.45 mm, p = 0.441) and in the control group (3.51 +/- 0.52 vs. 3.25 +/- 0.44 mm, p = 0.818). Pre-and post-treatment UT-2 levels were significantly different in each group: in group 1 (39.5 +/- 30.9 vs. 56.7 +/- 27.1 ng/ml, p = 0.0001), in group 2 (37.7 +/- 33.7 vs. 62.5 +/- 37.7 ng/ml, p = 0.0001) and in the control group (52.9 +/- 40.2 vs. 60.8 +/- 40.7 ng/ml, p = 0.006). Conclusion: Our findings suggest that UT-2 has a high potential as a vasoconstrictor agent in our bodies and its level increases through a bolus or CI 5-FU. Increased UT-2 levels are likely to play a role in 5-FU-related cardiac toxicity pathogenesis. (c) 2018 S. Karger GmbH, FreiburgenArticle