Increased cortisol levels are associated with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.
BACKGROUND
Physiological reactions of the stress hormone cortisol include hyperglycemia, hypertension, and endothelium dysfunction. In patients with aneurysmal subarachnoid hemorrhage (SAH), hyperglycemia, hypertension, and endothelium dysfunction are associated with the occurrence of delayed cerebral ischemia (DCI). Therefore, the purpose of the present study was to investigate whether increased serum cortisol levels after aneurysmal SAH are associated with DCI occurrence.


METHODS
Blood samples were obtained at standard intervals after SAH. DCI was defined as the gradual onset of new focal neurological impairment, and/or a decreased level of consciousness of at least 2 points as recorded on the Glasgow Coma Scale. Correlation coefficients were calculated to investigate the associations between cortisol and serum glucose levels, and between cortisol and von Willebrand factor levels.


RESULTS
Thirty-one patients were included. Eleven patients (35%) developed DCI. Signs of DCI started at a median of 6 days (range 4-10 days). Patients who developed DCI had significantly higher cortisol levels than patients without DCI (P = 0.006). Statistically significant, but weak, correlations were observed between cortisol and serum glucose levels (r = 0.216, P = 0.006), and cortisol and von Willebrand factor levels (r = 0.282, P < 0.001).


CONCLUSIONS
Increased serum cortisol levels after SAH are associated with DCI occurrence and might be the link between the associations of hyperglycemia and endothelium dysfunction with DCI. It remains to be investigated whether the association between cortisol levels and DCI is independent from known prognostic baseline factors, such as amount of blood on admission CT scan.
Vergouwen
Mervyn D I
MD
Department of Neurology, H2-234, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. m.d.vergouwen@amc.uva.nl
van Geloven
Nan
N
de Haan
Rob J
RJ
Kruyt
Nyika D
ND
Vermeulen
Marinus
M
Roos
Yvo B W E M
YB
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000378:metabolism; D002545:Brain Ischemia / Q000097:blood* / Q000188:drug therapy; D003131:Combined Modality Therapy; D004311:Double-Blind Method; D004621:Embolization, Therapeutic; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D015600:Glasgow Coma Scale; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D006943:Hyperglycemia / Q000503:physiopathology; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D011379:Prognosis; D019821:Simvastatin / Q000627:therapeutic use; D020206:Subarachnoid Hemorrhage, Traumatic / Q000097:blood* / Q000188:drug therapy; D013525:Surgical Instruments; D014841:von Willebrand Factor / Q000378:metabolism
D001786:Blood Glucose; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014841:von Willebrand Factor; D019821:Simvastatin; D006854:Hydrocortisone