A cross-sectional study to assess the association between major depression and inflammatory markers in patients with acute ischemic stroke

摘要

Background: Increased interest in the relationship between affective disorder and long-term health consequences has generated recent examinations of depression and stroke. Observations suggest that depressive disorder is associated with abnormal physiological and immunological responses and a resultant increase in inflammatory markers. Given the high prevalence of stroke and associated costs for the community, it is important to understand the mechanisms that may impact on the outcome to achieve the best possible prognosis. Aims: The view that inflammatory factors contribute to depression is predicated on findings that circulating cytokines and other inflammatory factors are increased in depressed patients. Therefore, it has been hypothesized that inflammation could be one of the mechanisms by which depression increases risk for ischemic stroke. Our aim was to determine whether there is any relationship between major depression and tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), IL-18, brain-derived neurotrophic factor (BDNF), and neuron-specific enolase (NSE) in patients with acute ischemic stroke (AIS). Study Design: This was as a cross-sectional design. Materials and Methods: This study has a cross-sectional design, and it was conducted in Necmettin Erbakan University, the Meram Faculty of Medicine in Konya, Turkey, between 2014 and 2015. Fifty-three AIS patients admitted to the hospital within the first 24 h after stroke onset were recruited. Major depression was ascertained by means of the structured clinical interview for the diagnostic and statistical manual of mental disorders, Fourth Edition/Clinical Version. The enzyme-linked immunosorbent assay was used to measure the serum levels of TNF-α, IL-1 β, IL-18, BDNF, and NSE at admission. Results: A total of 53 patients with a mean age of 65.9 years were recruited. Of these patients, 17 (32.1%) had major depression. Depressive and nondepressive patients had similar demographical and clinical features. There was no significant statistical difference between depressive and nondepressive patients with AIS with respect to levels of TNF-α, IL-1 β, IL-18, BDNF, and NSE. Conclusion: This study suggests that in patients who have experienced AIS, there is no significant relationship between major depression and basal proinflammatory cytokines (TNF-α, IL-1 β, IL-18), BDNF, and NSE.