Document Type : Short Communication

Authors

1 Clinical Neurology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

2 Department of Neurology, Shiraz University of Medical Sciences, Shiraz, Iran.

3 Laboratory of Basic Sciences, Mohammad Rasul Allah Research Tower, Shiraz University of Medical Sciences, Shiraz, Iran.

4 Department of Neurology, John Hunter Hospital, University of Newcastle, Newcastle, Australia.

5 Hunter Medical Research Institute and the University of Newcastle, Newcastle, Australia.

10.22034/iji.2023.96384.2432

Abstract

Background: The initial inflammatory reaction starts following occlusion in ischemic stroke (IS). Interleukin-1β (IL-1β) is a pro-inflammatory cytokine with a crucial role in the pathogenesis of neurodegenerative disorders.
Objective: To investigate the levels of IL-1β and vitamin D (VitD) in patients with IS compared with controls and their correlation.
Methods: The serum level of 25-OH VitD and IL-1β was assessed in 102 IS patients (0-24 h after stroke) and 102 controls with an enzyme-linked immunosorbent assay (ELISA) kit.
Results: We found a significant increase in IL-1β (80.14±6.8 vs. 60.32±4.1 pg/ml, p<0.05) and a decrease in VitD level (24.3±1.4 vs. 29.9±1.5 ng/ml, p<0.01) in the IS patients compared with the controls. There was a significantly positive correlation between the National Institutes of Health Stroke Scale (NIHSS) and IL-1β according to both the Spearman correlation (r=0.35, p=0.0003) and the linear regression (beta=0.255, p=0.014). Also, a significant negative association between VitD and NIHSS was detected by the Spearman correlation (r=-0.41, p<0.0001) and the linear regression (beta=-0.381, p=0.000). Moreover, we found a significant negative correlation (r=-0.26, p=0.006) between the serum levels of VitD and IL-1β in the patient group.
Conclusion: Ischemic stroke correlates positively with IL-1β and negatively with VitD levels. The speculated role of VitD deficiency in the evolution and severity of stroke may be justified by its role in the modification of inflammation.

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