Journal of Thrombosis and Haemostasis最新文献

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Redefining emperipolesis: a controlled mechanism of megakaryocyte function 巨核细胞功能的控制机制

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.10.002

Alessandra Balduini , Christian A. Di Buduo

引用次数: 0

Modulating platelet checkpoints: from storage lesion to thrombo-inflammation 调节血小板检查点：从储存病变到血栓炎症

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.022

David Stegner

引用次数: 0

Antibody-mediated multicellular pathophysiology of heparin-induced thrombocytopenia and vaccine-induced thrombotic thrombocytopenia: the dynamic roles of platelets, neutrophils, endothelial cells, and monocytes 抗体介导的HIT和VITT的多细胞病理生理：血小板、中性粒细胞、内皮细胞和单核细胞的动态作用。

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.014

Romy T. Meier, Rick Kapur

Heparin-induced thrombocytopenia (HIT) is a severe immune-mediated reaction to heparin, characterized by thrombocytopenia and an increased risk of thrombosis. Its pathophysiology is centered around the formation of antibodies directed against platelet factor 4 (PF4)/heparin complexes. These PF4/heparin antibodies engage platelet-FcγRIIa, leading to platelet activation and subsequent degranulation, aggregation, and the release of procoagulant extracellular vesicles (EVs). Activation of neutrophils, monocytes, and endothelial cells have also been suggested to be important features of HIT; neutrophil extracellular traps (NETs) are increasingly recognized as key contributors to thrombus propagation, monocytes may stimulate a prothrombotic state via FcγRIIa-mediated generation of tissue factor and thrombin, and endothelial activation may lead to the exposure of von Willebrand factor, further enhancing platelet recruitment and thrombosis. Importantly, interactions between different cell types, directly or indirectly, for instance, via EVs or dynamic shuttling of PF4, may consequently influence HIT responses. Vaccine-induced thrombotic thrombocytopenia (VITT), also a rare but serious complication of thrombocytopenia and thrombosis reported after administration of adenoviral vector COVID-19 vaccines, shares mechanistic parallels with HIT but is initiated by antibodies directed against PF4. These VITT antibodies also activate platelets via the FcγRIIa and may also induce the release of NETs, which could contribute to thrombus formation. Overall, in both HIT and VITT there appears to be a complex antibody-mediated interplay between various cells in promoting the regulation of thromboinflammatory responses. However, critical gaps remain regarding the precise cellular interactions driving thrombosis and/or thrombocytopenia. Further research is essential for developing improved diagnostic and therapeutic strategies for these life-threatening complications.

肝素诱导的血小板减少症（HIT）是一种严重的免疫介导的肝素反应，以血小板减少和血栓形成的风险增加为特征。其病理生理机制以血小板因子4 (PF4)/肝素复合物抗体的形成为中心。这些PF4/肝素抗体参与血小板fc γ riia，导致血小板活化和随后的脱颗粒、聚集和促凝细胞外囊泡（EVs）的释放。中性粒细胞、单核细胞和内皮细胞的活化也被认为是HIT的重要特征；中性粒细胞胞外陷阱（NETs）越来越被认为是血栓传播的关键因素，单核细胞可以通过fc - γ riia介导的组织因子和凝血酶的产生刺激血栓形成前状态，内皮细胞激活可能导致血管性血友病因子的暴露，进一步增强血小板募集和血栓形成。重要的是，不同细胞类型之间直接或间接的相互作用，例如通过电动汽车或PF4的动态穿梭，可能因此影响HIT反应。疫苗诱导的血栓性血小板减少症（VITT）也是一种罕见但严重的血小板减少症和血栓形成并发症，在接种腺病毒载体COVID-19疫苗后报道，它与HIT有相似的机制，但由针对PF4的抗体引发。这些VITT抗体也通过FcγRIIa激活血小板，并可能诱导NETs的释放，从而促进血栓形成。总的来说，在HIT和VITT中，在促进血小板炎症反应调节的各种细胞之间似乎存在复杂的抗体介导的相互作用。然而，关于驱动血栓形成和/或血小板减少的精确细胞相互作用的关键差距仍然存在。进一步的研究对于制定针对这些危及生命的并发症的改进的诊断和治疗策略至关重要。

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引用次数: 0

Diverse career paths within thrombosis and hemostasis: perspectives from the ISTH early career committee 血栓和止血的不同职业道路：来自ISTH早期职业委员会的观点。

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.10.003

Julia S. Gauer , Nicola Potere , Thita Chiasakul , Sofija Dunjic Manevski , Shrey Kohli

引用次数: 0

Reducing the risk of venous thromboembolism in pregnant women with inherited antithrombin deficiency 降低遗传性抗凝血酶缺乏症孕妇静脉血栓栓塞的风险

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.10.001

Eva N. Hamulyák , Maria T. DeSancho

引用次数: 0

Standardization of scanning electron microscopy analysis of fibrin fiber diameter measurement: communication from the ISTH SSC subcommittee on FXIII and fibrinogen 纤维蛋白纤维直径测量的扫描电镜分析标准化：来自ISTH SSC FXIII和纤维蛋白原小组委员会的通讯。

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.013

Can Cai , Zelda De Lange-Loots , Stephen R. Baker , Rustem I. Litvinov , Albe C. Swanepoel , Chandrasekaran Nagaswami , John W. Weisel , Rita Marchi , Alessandro Casini , Marguerite Neerman-Arbez , Cedric Duval , Robert A.S. Ariens , Rebecca A. Risman , Valerie Tutwiler , Heather A. Belcher , Aravind Elangovan , Nathan E. Hudson , Anetta Undas , Michał Ząbczyk , Martin Guthold , Marlien Pieters

Background

The microscopic characteristics of the fibrin clot structure, such as fibrin fiber length and diameter, network fiber density, and pore size, can be correlated with mechanical properties, permeability, susceptibility to lysis, and diseases. Several of these properties are commonly assessed using scanning electron microscopy (SEM); however, there are currently no standardized protocols on clot preparation for fiber diameter determination using SEM. This has led to a large discrepancy in values reported for healthy individuals and precludes interlaboratory comparisons.

Objectives

To develop a standardized protocol for the preparation of blood plasma clots for SEM analysis and fibrin fiber diameter determination.

Methods

A standardized sample preparation protocol using widely available materials and matching fibrinogen concentration and molality of normal human blood was established. This protocol, in addition to in-house protocols, was reproduced and tested by 8 laboratories across the world. Testing also included evaluations of sample air drying with hexamethyldisilazane versus critical point drying, fiber diameter measurements on the surface and inside a fractured clot, and manual versus automated measurement of fiber diameter.

Results

Reported fiber diameter values were in good agreement across laboratories, with an average median diameter of 110 ± 13 nm, coefficient of variation = 12% (hexamethyldisilazane drying) and 99 ± 7 nm, coefficient of variation = 7% (critical point drying). There were only small, practically insignificant differences between the diameters of surface fibers and internal fibers. Manual and automated measurements showed reasonable agreement.

Conclusion

The standardized protocol is recommended as a reference point for preparing plasma clots from the blood of healthy individuals for SEM.

背景：纤维蛋白凝块的微观结构，如纤维蛋白纤维的长度和直径、网状纤维的密度和孔隙大小，可以与力学性能、渗透性、易裂解性和疾病相关。其中一些特性通常是用扫描电子显微镜（SEM）来评估的，然而，目前还没有用于测定纤维直径的扫描电子显微镜血块制备的标准化方案。这导致了健康个体报告值的巨大差异，并排除了实验室间比较。目的：建立用于扫描电镜分析和纤维蛋白纤维直径测定的血浆凝块制备的标准化方案。方法：采用广泛可获得的材料，并与正常人血液纤维蛋白原浓度和摩尔浓度相匹配，建立标准化的样品制备方案。除了内部协议外，该协议还由世界各地的八个实验室复制和测试。测试还包括用六甲基二氮杂烷（HMDS）和临界点干燥（CPD）对样品进行空气干燥的评估，对破裂凝块表面和内部的纤维直径进行测量，以及手工测量和自动测量纤维直径。结果：各实验室报告的纤维直径值一致，平均中位数直径为110±13 nm， CV = 12% （HMDS干燥）和99±7 nm， CV = 7% （CPD）。表面纤维和内部纤维的直径之间只有很小的，几乎不显著的差异。手动和自动测量结果显示出合理的一致性。结论：推荐标准化方案作为从健康人血液中制备用于扫描电镜的血浆凝块的参考点。

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引用次数: 0

A novel homozygous splice-site variant in VPS33B identified as a cause of bleeding 一种新的VPS33B纯合剪接位点变异被确定为出血的原因

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.036

Lorena Díaz-Ajenjo , Ana Marín-Quílez , Ana Lama-Villanueva , Pablo García-Jaén , Beatriz Rey-Bua , Jesús María Hernández-Rivas , Neil V. Morgan , José Ramón González-Porras , Rocío Benito , José Rivera , José María Bastida

Background

Mild-to-moderate bleeding disorders are underdiagnosed, with many individuals classified as having no clear cause for their bleeding. Accurate diagnosis remains challenging and requires comprehensive clinical assessment, detailed laboratory testing, and advanced genetic testing.

Objectives

This study aimed to elucidate the relevance of an integrated approach for diagnosing patients with mild-to-moderate bleeding disorders by reevaluating 2 cases previously labeled with an undefined cause.

Methods

Two young siblings with unexplained bleeding tendencies were referred for evaluation. Bleeding score were assessed using the International Society on Thrombosis and Haemostasis bleeding assessment tool questionnaire. Platelet phenotyping included blood count, blood film, coagulation tests, light transmission aggregometry, flow cytometry, western blotting, and transmission electron microscopy. Genetic analysis involved whole-exome sequencing (WES) and pathogenicity assessment of candidate variants.

Results

Both siblings exhibited mild-to-moderate bleeding (bleeding score, 11 and 3, respectively). Blood count, coagulation factor tests, and light transmission aggregometry response to several agonists were normal. Blood film showed large and hypogranular platelets. Flow cytometry revealed reduced α-granule secretion upon ADP and TRAP6 stimulation. WES identified a homozygous variant in VPS33B (c.1225+5G>C) predicted to disrupt splicing. Immunoblotting confirmed null VPS33B expression and reduced von Willebrand factor levels. Transmission electron microscopy showed abnormal vacuole content and significantly reduced α-granules, while δ-granules and mitochondria remained intact.

Conclusion

This study reports a novel homozygous variant in VPS33B, leading to platelet dysfunction and bleeding diathesis based on α-granule defect and syndromic manifestations. Our findings highlight the importance of an integrated diagnostic approach, including WES, and expand the clinical and genetic spectrum of arthrogryposis, renal dysfunction, and cholestasis syndrome.

背景：轻至中度出血性疾病（MBDs）的诊断不足，许多个体被归类为没有明确的出血原因。准确的诊断仍然具有挑战性，需要全面的临床评估、详细的实验室检测和先进的基因检测。目的：通过重新评估先前标记为不明原因的两个病例，阐明综合方法诊断MBDs患者的相关性。患者/方法：两名有不明原因出血倾向的年轻兄弟姐妹进行评估。采用ISTH-BAT问卷评估出血评分（BS）。血小板表型包括血细胞计数、血膜、凝血试验、光透射聚集（LTA）、流式细胞术（FC）、western blotting （WB）和透射电子显微镜（TEM）。遗传分析包括全外显子组测序（WES）和候选变异的致病性评估。结果和讨论：兄弟姐妹均表现为轻度至中度出血（分别为BS 11和BS 3）。血细胞计数、凝血因子测试和LTA对几种激动剂的反应正常。血膜显示大而小颗粒的血小板。在ADP和TRAP6刺激下，FC显示α-颗粒分泌减少。WES在VPS33B中发现了一个纯合变异（C .1225+5G>C），预计会破坏剪接。免疫印迹证实VPS33B表达为零，血管性血友病因子水平降低。透射电镜显示液泡含量异常，α-颗粒明显减少，而δ-颗粒和线粒体保持完整。结论：本研究报告了一种新的VPS33B纯合变异，该变异基于α-颗粒缺陷和综合征表现导致血小板功能障碍和出血。我们的研究结果强调了包括WES在内的综合诊断方法的重要性，并扩大了ARC综合征的临床和遗传谱。

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引用次数: 0

Treating von Willebrand disease without von Willebrand factor 无血管性血友病因子治疗血管性血友病

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.034

Giancarlo Castaman , Pier Mannuccio Mannucci

引用次数: 0

Thrombosis magnified—zooming in to get to the bottom of clot formation 血栓形成放大——放大到血栓形成的底部

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.08.041

Leo Nicolai

引用次数: 0

Mouse trials and human triumphs: recovery after hemarthrosis? 小鼠试验和人类的成功：血肿后的恢复？

IF 5 2区医学 Q1 HEMATOLOGY

Journal of Thrombosis and Haemostasis

Pub Date : 2026-01-01 DOI: 10.1016/j.jtha.2025.09.031

Leonard A. Valentino , Angela L. Forsyth

引用次数: 0

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