ArticleThe journal of trauma and acute care surgery2018
Perhaps it's not the platelet: Ristocetin uncovers the potential role of von Willebrand factor in impaired platelet aggregation following traumatic brain injury.
Article in The journal of trauma and acute care surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- The hidden battlefield: platelet function in the wake of severe trauma.Frontiers in immunology · 2026Review
- Platelet recruitment kinetics are impacted by von Willebrand factor quality in hemostatic adjuncts.Blood vessels, thrombosis & hemostasis · 2025Article
- Traumatic brain injury: Advances in coagulopathy (Review).Biomedical reports · 2024Review
- Blood failure: traumatic hemorrhage and the interconnections between oxygen debt, endotheliopathy, and coagulopathy.Clinical and experimental emergency medicine · 2024Article
- Severe Trauma-Induced Coagulopathy: Molecular Mechanisms Underlying Critical Illness.International journal of molecular sciences · 2023Review
- Covid-19 and Liver Injury: Role of Inflammatory Endotheliopathy, Platelet Dysfunction, and Thrombosis.Hepatology communications · 2022Review
- Treatment with ddAVP improves platelet-based coagulation in a rat model of traumatic hemorrhagic shock.Trauma surgery & acute care open · 2022Article
- Effects of pathogen reduction technology and storage duration on the ability of cryoprecipitate to rescue induced coagulopathies in vitro.Transfusion · 2021Article
- Platelet Receptor Activity for Predicting Survival in Patients with Intracranial Bleeding.Journal of clinical medicine · 2021Article
- Trauma-induced coagulopathy.Nature reviews. Disease primers · 2021Review
- Review
- Dynamic effects of calcium on in vivo and ex vivo platelet behavior after trauma.The journal of trauma and acute care surgery · 2020Article
- Identification of injury and shock driven effects on ex vivo platelet aggregometry: A cautionary tale of phenotyping.The journal of trauma and acute care surgery · 2020Article
- Von Willebrand factor as a thrombotic and inflammatory mediator in critical illness.Transfusion · 2020Article
- A journey upstream: Fluctuating platelet-specific genes in cell-free plasma as proof-of-concept for using ribonucleic acid sequencing to improve understanding of postinjury platelet biology.The journal of trauma and acute care surgery · 2020Observational
- It's About Time: Transfusion effects on postinjury platelet aggregation over time.The journal of trauma and acute care surgery · 2019Article
- Targeting Tyrosine Phosphatases by 3-Bromopyruvate Overcomes Hyperactivation of Platelets from Gastrointestinal Cancer Patients.Journal of clinical medicine · 2019Article
- Trauma-induced coagulopathy: The past, present, and future.Journal of thrombosis and haemostasis : JTH · 2019Review
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundInjury to the blood-brain barrier exposes endothelium rich in von Willebrand factor (vWF), which may play a role in altered platelet aggregation following traumatic brain injury (TBI). Ristocetin is an antimicrobial substance that induces vWF-mediated aggregation of platelets. We examined these mechanisms in injured patients by measuring the aggregation response of platelets to stimulating agonists (including ristocetin) via whole-blood multiple-electrode platelet aggregometry. We hypothesized that patients with TBI have an altered platelet aggregation response to ristocetin stimulation compared with patients without TBI.
methodsBlood was collected from 233 trauma patients without thrombocytopenia. Platelet aggregation was assessed using multiple-electrode platelet aggregometry (Multiplate). Platelet aggregation response to stimulating agonists collagen, thrombin receptor-activating peptide 6, adenosine diphosphate, arachidonic acid, and ristocetin was measured. Factor activity was measured.
resultsOf the 233 patients, 23% had TBI. There were no differences in platelet aggregation responses to any agonists between TBI and non-TBI patients except ristocetin. Platelet aggregation response to ristocetin stimulation was significantly lower in TBI patients (p = 0.03). Patients with TBI also had higher factor VIII activity (215% vs. 156%, p = 0.01). In multivariate analysis, there was a significant independent association of impaired platelet aggregation response to ristocetin stimulation with TBI (odds ratio, 3.05; p = 0.04).
conclusionsGiven the importance of platelets in hemostasis, understanding the mechanisms of impaired platelet aggregation following injury is critical. The impaired platelet aggregation response to ristocetin stimulation and corresponding increase in factor VIII activity in TBI patients may be secondary to a TBI-induced effect on vWF quantity (due to injury-driven consumption of vWF) or vWF function with resultant increase in circulating factor VIII activity (due to impaired carrying capacity of vWF). Given there are multiple known therapies for vWF deficits including desmopressin, purified and recombinant vWF, and estrogens, these lines of investigation are particularly compelling in patients with TBI and hemorrhage. LEVEL OF EVIDENCE: Prognostic study, level II.
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