Literature DB >> 18436156

Association of serum bilirubin with ischemic stroke outcomes.

Sandra Pineda1, Oh Young Bang, Jeffrey L Saver, Sidney Starkman, Susan W Yun, David S Liebeskind, Doojin Kim, Latisha K Ali, Samir H Shah, Bruce Ovbiagele.   

Abstract

BACKGROUND: Higher levels of serum bilirubin may offer a therapeutic advantage in oxidative stress-mediated diseases, but may also simply reflect intensity of oxidative stress. Little is known about the role of bilirubin in stroke. We assessed the relation of serum bilirubin levels with clinical presentation and outcomes among patients hospitalized with ischemic stroke.
METHODS: Data were collected prospectively during a 5-year period on consecutive ischemic stroke admissions to a university hospital. Serum bilirubin levels, total (Tbil) and direct (Dbil), were measured on admission. Presenting stroke severity was assessed with the National Institutes of Health Stroke Scale (NIHSS). Functional outcome at discharge was assessed using the modified Rankin scale.
RESULTS: Among 743 patients, mean age was 67.3 years and 47.5% were women. Median presenting NIHSS score was 4, and 24% had a poor (modified Rankin scale 4-6) functional outcome at discharge. Higher Dbil levels were associated with greater stroke severity (P = .001) and poorer discharge outcome (P = .034). Multivariable regression analyses showed that those with higher Dbil levels (> or =0.4 mg/dL) had significantly greater admission NIHSS scores compared with those with lower levels (< or =0.1 mg/dL) (odds ratio 2.79, 95% confidence interval 1.25-6.20, P = .012), but no independent relationship was confirmed between Dbil and discharge outcome. Although higher admission Tbil was associated with greater stroke severity in crude analyses (P = .003), no independent relationship between Tbil versus stroke severity or outcome was noted after adjusting for confounders.
CONCLUSIONS: Higher Dbil level is associated with greater stroke severity but not outcome among ischemic stroke patients, possibly reflecting the intensity of initial oxidative stress. Further study into the underlying pathophysiology of this relationship is needed.

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Year:  2008        PMID: 18436156      PMCID: PMC2731670          DOI: 10.1016/j.jstrokecerebrovasdis.2008.01.009

Source DB:  PubMed          Journal:  J Stroke Cerebrovasc Dis        ISSN: 1052-3057            Impact factor:   2.136


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