Evidence map›Paper›PMID 20069390›Full record

Trial reportNeurocritical care2010

Increased cortisol levels are associated with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Mervyn D I Vergouwen, Nan van Geloven, Rob J de Haan, Nyika D Kruyt, Marinus Vermeulen, Yvo B W E M Roos

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Neurocritical care, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Group-based trajectory modeling identifies distinct glycemic patterns predictive of mortality in aneurysmal subarachnoid hemorrhage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Endocrine function following acute SAH.Neurocritical care · 2011
    Review
  10. SAH pituitary adrenal dysfunction.Neurocritical care · 2011
    Review
  11. Article
  12. Article
  13. Hyperglycemia in aneurysmal subarachnoid hemorrhage: a potentially modifiable risk factor for poor outcome.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010
    Review
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Mervyn D I VergouwenDepartment of Neurology, H2-234, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands. m.d.vergouwen@amc.uva.nl
Nan van Geloven
Rob J de Haan
Nyika D Kruyt
Marinus Vermeulen
Yvo B W E M Roos

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPhysiological 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.

methodsBlood 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.

resultsThirty-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).

conclusionsIncreased 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.

Indexed as

AdultAgedBlood GlucoseBrain IschemiaCombined Modality TherapyDouble-Blind MethodEmbolization, TherapeuticEndothelium, VascularFemaleGlasgow Coma ScaleHumansHydrocortisoneHydroxymethylglutaryl-CoA Reductase InhibitorsHyperglycemiaHypertensionMaleBlood GlucoseHydrocortisoneHydroxymethylglutaryl-CoA Reductase InhibitorsSimvastatinvon Willebrand Factor

Identifiers

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.