Akademik Veri Yönetim Sistemi
Süleyman Demirel Üniversitesi Tıp Fakültesi Dergisi, cilt.29, sa.2, ss.187-195, 2022 (Hakemli Dergi)
Objective Atherosclerosis, one of the prominent factors causing dysfunctional vascular events in stroke patients, is a multi-factorial and complex process in which endothelial dysfunction and vascular inflammation play significant roles. This study aimed to investigate the relationships between serum levels of IL-18 and adropin, associated with endothelial dysfunction and inflammatory processes in acute ischemic stroke patients, with epidemiological, clinical, radiological findings and stroke severity. Materials and Methods Sixty-one patients diagnosed with acute ischemic stroke and 30 healthy individuals were included in the study as the patient and control groups. In the patient group, the stroke sub-groups and severity were determined etiologically and clinically. Venous blood samples were obtained within the first 24 hours in the patient group, and at any time in the control group, their serums were separated and stored at -80°C. IL-8 and adropin levels were determined using the ELISA method. The relationships between patient and control groups’ IL-18 and adropin levels and ischemic stroke were analyzed statistically. Results The adropin level was statistically significantly lower in the patient group than the control group (398.01±403.51 and 509.42±1492.89, respectively; p=0.041). The IL-18 levels of the study and control groups were similar (24.87±14.26 and 21.11±14.93, respectively; p=0.112). There was no relationship between the IL-18 and adropin levels determined with stroke risk factors, stroke sub-groups, and stroke severity. Conclusion These results showed that low adropin levels could be used to indicate atherosclerosis in the risk prediction scales of ischemic stroke. The absence of a difference between the patient group with acute ischemic stroke and the control group regarding the first 24-hour mean serum IL-18 level suggested that IL-18 could play a role as a late-stage cytokine in ischemia-related inflammation.