Abstract
Background: The adrenal glucocorticoid stress response in humans causes catabolism, increasing
blood glucose and heart rate, and possibly potentiates ischaemic damage to neurons.
These effects could induce secondary brain damage in acute stroke. Materials and Methods: This prospective study was based on a single determination of s-cortisol in 172
patients included within 24 h of stroke onset, 50% within 12 h of stroke onset. All
patients were admitted to hospital within 6 h of stroke onset. We investigated the
relations of s-cortisol to neurological deficit measured by Scandinavian Stroke Scale
(SSS), lesion volume on CT-scan, blood glucose on admission, pulse rate, blood pressure,
body temperature, deteriorating stroke, cytokines and cytokine receptors, and outcome.
Results: In a multivariate logistic regression analysis, s-cortisol was independently related
to death within 7 days of stroke onset, odds ratio (OR) Cortisol+100 nmol/l 1.9 (95% CI 1.01–3.8); serum-cortisol was, however, not a predictor of death or dependency
within 3 months. S-cortisol correlated to SSS (ρ=−0.45, p<0.001), body temperature (ρ=0.27, p<0.001), pulse rate (ρ=0.26, p<0.001), and lesion volume (ρ=0.33, p<0.001). S-cortisol was related to the presence of insular damage. Conclusion: Acute stroke mortality related to increasing serum-cortisol levels. S-cortisol was
associated with stroke severity and markers reflecting stroke severity.
Keywords
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Article info
Publication history
Accepted:
September 24,
2003
Received in revised form:
September 4,
2003
Received:
May 15,
2003
Footnotes
☆This study was funded by: Augustinus Fonden, Dagmar Marshalls Fond, Else og Mogens Wedel-Wedelsborgs Fond, Ludvig og Sara Elsass' Fond, Lykfeldts Legat, Aase og Ejnar Danielsens Fond. No conflicts of interest to reveal.
Identification
Copyright
© 2003 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
