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Impact of thyroid autoantibodies on functional outcome in patients with acute ischemic stroke
Han-Jin Cho1, Sang-Soo Kim2, Sang-Min Sung1
1Department of Neurology, Pusan National University Hospital, Pusan National University Graduate School of Medicine and Biomedical Research Institute, Busan, Korea.
Background:
Recent studies have shown that thyroid autoantibodies contribute to the development of cerebrovascular diseases, including atherosclerosis, moyamoya disease, and even arterial dissection, induced by immune-mediated endothelial dysfunction on the cerebral vasculature. The aim of this study was to investigate the impact of thyroid autoantibodies on functional outcome in patients with acute ischemic stroke.
Methods:
We reviewed the patients with acute ischemic stroke who consecutively underwent thyroid autoantibody tests. We divided the patients into positive thyroid autoantibody (PAB) and negative thyroid autoantibody (NAB) groups. Demographic profiles, risk factors, stroke subtypes, laboratory results, and functional outcomes were compared between the 2 groups. We performed the multivariate analysis to determine whether thyroid autoantibodies were independently associated with functional outcome.
Results:
Of the 763 patients, 121 (15.9%) were of the PAB group. Compared with the NAB group, higher baseline National Institutes of Health Stroke Scale score (P = .001) and prevalence of large-artery atherosclerosis (P = .014) were found in the PAB group. The PAB group had significantly higher proportion of unfavorable outcome at 3 months (modified Rankin Scale score ≥ 3) than the NAB group (P = .002). On multiple regression analysis, lower tri-iodothyronine level (odds ratio [OR] .985, 95% confidence interval [CI] .976-.995, P = .002) and PABs (OR 1.661, 95% CI 1.013-2.724, P = .044) were significant and independent predictors of unfavorable outcome.
Conclusions:
This study showed that elevated thyroid autoantibodies were independently associated with unfavorable outcome in patients with acute ischemic stroke. We speculate that immune-mediated vascular damage may contribute to the increased risk of unfavorable outcome by providing insufficient cerebral blood flow to the ischemic area.
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