5-fluorourasile bağlı arteryel vazokonstrüksiyon etyolojisinde ürotensin-2'nin rolü

Background and Aim:5-Fluorouracil (5-FU) is a widely used drug in many malignancies alone or in multiple drug therapies, including gastrointestinal, breast, head and neck cancers. Cardiac toxicity associated with 5-FU may be rare but life-threatening. Although the pathogenesis of cardiac toxicity has not yet been fully elucidated, coronary vasospasm has long been regarded as the main triggering cause. In studies up to now, continuous 5-FU and bolus 5-FU applications were compared, but the most powerful known vasoconstrictor mediator, urotensin 2, was not considered. We aimed to find the role of urotensin 2 in 5-FU-bound arterial vasoconstriction by looking at brachial artery diameter measurements and urotensin 2 levels in patients treated with 5-FU, bolus 5-FU and 5-FU except(control group) treatment. Results: A total of 132 patients were included in the study. Of these, 42 were treated with bolus 5-FU (Group 1), 51 were treated with infusional 5-FU (Group 2) and the remaining 39 were treated with 5-FU except treatment (Group 3) . 31 patients in Group 1 were treated with FEC chemotherapy, 2 patients received bolus FUFA treatment, 7 patients in Group 2 received FOLFIRINOX treatment and 44 patients received FOLFOX (± Bevacizumab) therapy. 13 patients in Group 3 received carboplatin-paclitaxel, 6 patients received cisplatin-gemcitabine, 6 patients received EC, 3 patients received AC, 2 patients received cisplatin-etoposide, 2 patients received gemcitabine, and 7 patients received other treatments. Urotensin II, complete blood cell counts, liver and kidney function tests were analyzed in all blood samples taken before and after the chemotherapy treatment from all the patients participating in the study. There was no significant change in brachial artery diameters before and after chemotherapy. After chemotherapy, the levels of urotensin2 were increased in all three groups according to baseline, but the increase in Group 1 and 2 was significantly higher. The brachial artery diameters and urotensin 2 levels before and after chemotherapy are shown in. Conclusion: In conclusion, we showed that the most potent vasoconstrictor, urotensin 2, was increased by bolus or infusional 5-FU administration in this study. It may be that urotensin 2 increases have a role in the pathogenesis of 5-FU-associated cardiac toxicity. We think that the relationship between UII and 5-FU cardiac toxicity needs to be investigated in more detail. Keywords: Urotensin 2, brachial artery diameter, 5-fluoropyrimidine, vasoconstriction, toxicity