IL-18 AND ADROPIN LEVELS IN PATIENTS WITH ACUTE ISCHEMIC STROKE

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.