ArticleNeurocritical care2011
Relation of serum TNF-α and TNF-α genotype with delayed cerebral ischemia and outcome in subarachnoid hemorrhage.
Article in Neurocritical care, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01865630 (Phase I Safety, Blood Brain Barrier Permeability and Potential Efficacy of Etanercept for Aneurysmal Subarachnoid Hemorrhage), which is not on this map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Phase I Safety, Blood Brain Barrier Permeability and Potential Efficacy of Etanercept for Aneurysmal Subarachnoid Hemorrhage
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Monitoring biomarkers of cellular injury and death in acute brain injury.Neurocritical care · 2014Pooled it
- Systemic Inflammation after Aneurysmal Subarachnoid Hemorrhage.International journal of molecular sciences · 2023Review
- Association between inflammatory response and outcome after subarachnoid haemorrhage.Acta neurologica Scandinavica · 2021Observational
- Biospecimens and Molecular and Cellular Biomarkers in Aneurysmal Subarachnoid Hemorrhage Studies: Common Data Elements and Standard Reporting Recommendations.Neurocritical care · 2019Article
- The role of inflammation and potential use of sex steroids in intracranial aneurysms and subarachnoid hemorrhage.Surgical neurology international · 2018Review
- Association of TNF-α-3959T/C Gene Polymorphisms in the Chinese Population with Intracranial Aneurysms.Journal of molecular neuroscience : MN · 2017Article
- Robust effects of genetic background on responses to subarachnoid hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Article
- Elevated IL-6 and TNF-α Levels in Cerebrospinal Fluid of Subarachnoid Hemorrhage Patients.Molecular neurobiology · 2016Article
- Monitoring inflammation (including fever) in acute brain injury.Neurocritical care · 2014Review
- Tumor necrosis factor-α modulates cerebral aneurysm formation and rupture.Translational stroke research · 2014Review
- Controversies and evolving new mechanisms in subarachnoid hemorrhage.Progress in neurobiology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe pathogenesis of delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) remains obscure. The authors assessed the relationship of tumor necrosis factor alpha (TNF-α) and TNF-α gene polymorphisms with occurrence of DCI and poor outcome at 3 months.
methodsSerum levels of TNF-α were measured every other day until discharge in 67 patients and the mean serum levels per patient during days 0-12 were dichotomized at the median value of the whole group. TNF-α genotyping was available in 31 patients and related to serum TNF-α by means of one-way ANOVA analysis. The authors calculated hazard ratio's (HR) with corresponding 95% confidence intervals (CI) for the association with DCI by means of Cox proportional hazard analysis and odds ratio's (OR) for the association with poor clinical outcome by means of logistic regression analysis. In both analyses the authors adjusted for sex, age, amount of blood, and clinical condition at admission. Leukocytes and CRP were investigated similarly for comparison.
resultsFor high-serum TNF-α levels during days 0-12 adjusted HR was 0.6 (95%CI: 0.1-2.4) for DCI and adjusted OR 2.0 (95%CI: 0.4-9.0) for clinical outcome. Serum TNF-α levels were 11.4 pg/ml for wildtype TNF-α genotype and 9.7 pg/ml for the non-wildtype TNF-α genotype (P = 0.15). For the non-wildtype TNF-α genotype the HR for DCI was 0.4 (95%CI: 0.1-2.6) and the OR for clinical outcome was 0.8 (95%CI: 0.1-4.0).
conclusionIt is unlikely that serum TNF-α or TNF-α genotype play an important role in the occurrence of DCI after SAH.
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Registered trials
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.