Evidence map›Paper›PMID 41499535›Full record

ArticleCNS neuroscience & therapeutics2026

Coagulation Pathways as Determinants of Acute Subdural Hematoma Resolution: Genetic Evidence From Human Data.

Qizhong Wu, Tingting Xu, Bo Tan

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Qizhong WuDepartment of Critical Care Medicine, Guangyuan Central Hospital, Guangyaun, Sichuan, China.
Tingting XuDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.
Bo TanDepartment of Neurosurgery, Guangyuan Central Hospital, Guangyuan, Sichuan, China.ORCID 0000-0001-5976-7546

Funding

Guangyuan Science and Technology Bureau Science and Technology Project 23ZDYF0053Health Commission of Sichuan Province Medical Science and Technology Program 24WSXT042Sichuan Provincial Clinical Key Specialty Construction Project 2024HSWKP001Wu Jieping Medical Foundation 320.6750.2024-6-113
6 · The paper itself

Abstract

backgroundAcute subdural hematoma (ASDH) is a severe complication of traumatic brain injury, with high mortality and disability. Spontaneous hematoma resolution is an important determinant of functional recovery, but the biological mechanisms underlying this process remain poorly understood. Coagulopathy, common in ASDH, may influence hematoma dynamics, but its causal role remains uncertain.

methodsWe conducted a two-sample Mendelian randomization (MR) study to investigate the causal effects of coagulation traits on hematoma resolution. Genetic instruments for fibrinogen isoforms, coagulation factors VIII, XI, V, VII, natural anticoagulants, and platelet traits were obtained from large genome-wide association studies. Due to the absence of ASDH-specific GWAS data, we used genetic susceptibility to intracerebral hemorrhage (ICH) and poststroke functional outcome as indirect proxies for hematoma persistence and clearance. We acknowledge that these proxies cannot fully capture the unique pathophysiology of ASDH, but they represent pragmatic, biologically relevant surrogates. Causal estimates were obtained using inverse-variance weighted MR with robust sensitivity analyses.

resultsGenetically higher fibrinogen γ' levels were associated with increased odds of hematoma resolution (OR 1.25, 95% CI 1.10-1.42). Higher factor VIII and XI levels were associated with reduced odds of Resolution (OR 0.82, 95% CI 0.72-0.94; OR 0.88, 95% CI 0.78-1.00). Secondary analyses using poststroke functional outcome yielded similar patterns but did not reach statistical significance (OR ~1.10, p = 0.15).

conclusionsOur findings provide genetic evidence suggesting coagulation pathways, particularly fibrinogen γ' and factors VIII and XI, may influence hematoma resolution in ASDH. However, due to the indirect nature of the proxies used, these results should be considered hypothesis-generating and require further validation in ASDH-specific cohorts.

Indexed as

Blood CoagulationHematoma, Subdural, AcuteFibrinogenFibrinogens, AbnormalGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideFibrinogenfibrinogen gamma'Fibrinogens, Abnormalacute subdural hematomacoagulationfactor VIIIfactor XIfibrinogen γ'Mendelian randomization

Identifiers

PMID41499535
PMCPMC12778947

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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.