Pub Date : 2026-03-01Epub Date: 2026-01-22DOI: 10.1016/j.thromres.2026.109595
Mattea Pellerito , Abigail R. Dowling , Catherine E. Luke , Qing Cai , Antonio M. Pellerito , Andrew Quang , Lonnie Shea , Farouc Jaffer , Andrea Obi , Peter K. Henke
Background
Post thrombotic syndrome is a fibrotic disease related to inflammation resolution. There are no direct therapies that can ameliorate this disease. Monocyte/macrophages (Mo/MØ) are the primary leukocyte involved with later venous resolution, and likely direct vein wall responses and healing. Herein, we explored the vein wall response with Mo/MØ depletion by two methods.
Methods
Using two mouse models of venous thrombosis (VT), complete stasis and a flow restricted model, Mo/MØ depletion was accomplished using CD11b-DTR mice administered diphtheria toxin, and clodronate micelle administration in wild type mice. Tissue assays for structural histology, immunohistochemistry and western blotting were performed.
Results
Mo/MØ depletion resulted in significantly less vein wall fibrotic thickness, in the stasis model at day 14 in both the CD11b-DTR mice and those receiving clodronate micelles. No significant effect of Mo/MØ depletion was observed in the flow restricted VT model. The decrease in vein wall fibrosis was associated with fewer DDR2+ vein wall cells in the CD11b-DTR mice, but no difference in endothelial luminal coverage. Decreased cytokine and growth factor expression of IL-6, FSP-1, and VEGFa were associated with Mo/MØ depletion. Lastly, PMN depletion was associated with increased proinflammatory Mo/MØ, and a trend towards increased vein wall fibrosis as compared with controls.
Conclusion
Mo/MØ direct the post VT late fibrotic response, possibly by affecting fibroblasts and inflammatory cytokine expression. This effect was only found with the complete stasis model and is consistent with worsened PTS in humans with complete venous obstruction.
{"title":"Monocyte depletion reduces late experimental post-thrombotic fibrotic injury in a stasis mouse model","authors":"Mattea Pellerito , Abigail R. Dowling , Catherine E. Luke , Qing Cai , Antonio M. Pellerito , Andrew Quang , Lonnie Shea , Farouc Jaffer , Andrea Obi , Peter K. Henke","doi":"10.1016/j.thromres.2026.109595","DOIUrl":"10.1016/j.thromres.2026.109595","url":null,"abstract":"<div><h3>Background</h3><div>Post thrombotic syndrome is a fibrotic disease related to inflammation resolution. There are no direct therapies that can ameliorate this disease. Monocyte/macrophages (Mo/MØ) are the primary leukocyte involved with later venous resolution, and likely direct vein wall responses and healing. Herein, we explored the vein wall response with Mo/MØ depletion by two methods.</div></div><div><h3>Methods</h3><div>Using two mouse models of venous thrombosis (VT), complete stasis and a flow restricted model, Mo/MØ depletion was accomplished using CD11b-DTR mice administered diphtheria toxin, and clodronate micelle administration in wild type mice. Tissue assays for structural histology, immunohistochemistry and western blotting were performed.</div></div><div><h3>Results</h3><div>Mo/MØ depletion resulted in significantly less vein wall fibrotic thickness, in the stasis model at day 14 in both the CD11b-DTR mice and those receiving clodronate micelles. No significant effect of Mo/MØ depletion was observed in the flow restricted VT model. The decrease in vein wall fibrosis was associated with fewer DDR2+ vein wall cells in the CD11b-DTR mice, but no difference in endothelial luminal coverage. Decreased cytokine and growth factor expression of IL-6, FSP-1, and VEGFa were associated with Mo/MØ depletion. Lastly, PMN depletion was associated with increased proinflammatory Mo/MØ, and a trend towards increased vein wall fibrosis as compared with controls.</div></div><div><h3>Conclusion</h3><div>Mo/MØ direct the post VT late fibrotic response, possibly by affecting fibroblasts and inflammatory cytokine expression. This effect was only found with the complete stasis model and is consistent with worsened PTS in humans with complete venous obstruction.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109595"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146057467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-31DOI: 10.1016/j.thromres.2026.109604
Marieke J.A. Verhagen , Saskia E.M. Schols , Sanna R. Rijpma , An K Stroobants
{"title":"Monitoring the Hemostatic Balance: measuring thrombin generation in a patient with acquired hemophilia A on combined pro- and anticoagulant therapy","authors":"Marieke J.A. Verhagen , Saskia E.M. Schols , Sanna R. Rijpma , An K Stroobants","doi":"10.1016/j.thromres.2026.109604","DOIUrl":"10.1016/j.thromres.2026.109604","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109604"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146133027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-01DOI: 10.1016/j.thromres.2026.109608
Andaleb Kholmukhamedov
{"title":"Simplifying the next-generation of anticoagulants: Elexians – Why a unified nomenclature for FXI/XIa inhibitors is needed","authors":"Andaleb Kholmukhamedov","doi":"10.1016/j.thromres.2026.109608","DOIUrl":"10.1016/j.thromres.2026.109608","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109608"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146114125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-19DOI: 10.1016/j.thromres.2026.109626
Giuseppe Guglielmini , Emanuela Falcinelli , Michelantonio De Fano , Anna Maria Mezzasoma , Loredana Bury , Gabriele Perriello , Pietro Minuz , Carmine Giuseppe Fanelli , Paolo Gresele
Background
Platelet hyperreactivity and in vivo platelet activation, effectors of increased cardiovascular risk, have been associated with both type 2 diabetes (T2DM) and obesity, however, whether T2DM and obesity when combined further enhance platelet activation has not been explored.
Materials and methods
We assessed several parameters of platelet reactivity and in vivo platelet activation, VWF activity and adipokine levels in 40 well characterized obese subjects without T2DM (metabolically healthy obese, MHO), non obese T2DM patients (metabolically unhealthy normal weight, MUNW), obese and T2DM patients (metabolically unhealthy obese, MUO) and age and sex-matched healthy controls (metabolically healthy normal weight, MHNW).
Results
Both MUNW and MHO subjects showed enhanced platelet thrombus formation, increased response to collagen and ADP at light transmission aggregometry, raised urinary 11-dehydro-TxB2, higher production of platelet reactive oxygen species and impaired platelet nitric oxide formation compared to MHNW, which were further significantly worsened in MUO. VWF activity and resistin levels were significantly higher in MUO patients compared to the other groups.
Conclusions
Our data show that the concomitant presence of T2DM and obesity exert a significant additive effect on platelet hyperreactivity and in vivo platelet activation compared with only one of these risk factors, and suggest that enhanced VWF and resistin levels in MUO subjects play a pathogenic role in the modulation of the platelet response to stimuli leading to a strong platelet hyperreactivity and in vivo platelet activation, in turn favoring enhanced cardiovascular risk.
{"title":"Obesity and type 2 diabetes mellitus add up to induce platelet hyperreactivity and platelet activation","authors":"Giuseppe Guglielmini , Emanuela Falcinelli , Michelantonio De Fano , Anna Maria Mezzasoma , Loredana Bury , Gabriele Perriello , Pietro Minuz , Carmine Giuseppe Fanelli , Paolo Gresele","doi":"10.1016/j.thromres.2026.109626","DOIUrl":"10.1016/j.thromres.2026.109626","url":null,"abstract":"<div><h3>Background</h3><div>Platelet hyperreactivity and in vivo platelet activation, effectors of increased cardiovascular risk, have been associated with both type 2 diabetes (T2DM) and obesity, however, whether T2DM and obesity when combined further enhance platelet activation has not been explored.</div></div><div><h3>Materials and methods</h3><div>We assessed several parameters of platelet reactivity and in vivo platelet activation, VWF activity and adipokine levels in 40 well characterized obese subjects without T2DM (metabolically healthy obese, MHO), non obese T2DM patients (metabolically unhealthy normal weight, MUNW), obese and T2DM patients (metabolically unhealthy obese, MUO) and age and sex-matched healthy controls (metabolically healthy normal weight, MHNW).</div></div><div><h3>Results</h3><div>Both MUNW and MHO subjects showed enhanced platelet thrombus formation, increased response to collagen and ADP at light transmission aggregometry, raised urinary 11-dehydro-TxB<sub>2</sub>, higher production of platelet reactive oxygen species and impaired platelet nitric oxide formation compared to MHNW, which were further significantly worsened in MUO. VWF activity and resistin levels were significantly higher in MUO patients compared to the other groups.</div></div><div><h3>Conclusions</h3><div>Our data show that the concomitant presence of T2DM and obesity exert a significant additive effect on platelet hyperreactivity and in vivo platelet activation compared with only one of these risk factors, and suggest that enhanced VWF and resistin levels in MUO subjects play a pathogenic role in the modulation of the platelet response to stimuli leading to a strong platelet hyperreactivity and in vivo platelet activation, in turn favoring enhanced cardiovascular risk.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109626"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147310489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-01-30DOI: 10.1016/j.thromres.2026.109586
Ji Yoon Kim , Taiju Hwang , Sang Kyu Park , Ki-Young Yoo , Eun Jin Choi , Soyon Kim , Chur Woo You , Eungsun Kim , Aeran Jung , Young-Shil Park
{"title":"Corrigendum to “Real-world safety and effectiveness of rurioctocog alfa pegol in 338 patients with hemophilia A in South Korea: A postmarketing surveillance study” [Thromb. Res. 253 (2025) 109402]","authors":"Ji Yoon Kim , Taiju Hwang , Sang Kyu Park , Ki-Young Yoo , Eun Jin Choi , Soyon Kim , Chur Woo You , Eungsun Kim , Aeran Jung , Young-Shil Park","doi":"10.1016/j.thromres.2026.109586","DOIUrl":"10.1016/j.thromres.2026.109586","url":null,"abstract":"","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109586"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Congenital fibrinogen deficiency is a rare inherited coagulation disorder characterized by partial or total lack of plasma fibrinogen (hypo- or afibrinogenemia), or expression of dysfunctional fibrinogen (dysfibrinogenemia), which may cause plasma level reduction (hypodysfibrinogenemia). Loss of functional fibrinogen causes bleeding disposition. In case of trauma or surgical intervention, supplementation of human fibrinogen is required to stop or prevent extensive bleeding events.
Study design
A prospective, open-label, uncontrolled, multi-center phase I/III trial was performed to investigate pharmacokinetics, efficacy and safety of single and/or repetitive intravenous infusions of a human fibrinogen concentrate (BT524) for on-demand prophylaxis (ODP) and/or on-demand treatment (ODT) of bleeding events in patients with congenital fibrinogen deficiency.
Patients
In the phase III part of the trial reported here, 36 patients (3 children <6 years, 9 children 6–12 years, 4 adolescents and 20 adults) were treated with BT524 for 175 bleeding events, either for ODP or ODT.
Results
Fibrinogen concentrate infusion substantially improved maximum clot firmness (MCF). The overall hemostatic response was rated as good or excellent in 98.9% of bleedings. Loss of blood was considered normal in the majority of surgical interventions, and wound healing was also positively assessed. Additional evaluations, including blood product consumption and adverse events, further supported the efficacy and confirmed the favorable safety profile of the novel fibrinogen product.
Conclusion
BT524 represents a novel human fibrinogen concentrate provenly efficacious and safe both for the treatment of bleeding and for peri-operative bleeding prophylaxis in patients with congenital fibrinogen deficiency of all ages.
{"title":"Efficacy and safety of prophylaxis and treatment of bleeding events with a novel fibrinogen concentrate from human plasma in patients with congenital fibrinogen deficiency","authors":"Claudia Djambas Khayat , Amal El-Beshlawy , Naglaa Omar , Emna Gouider Belhadjali , Abderrahim Khelif , Sonia Adolf , Wolfgang Miesbach , Silke Aigner , Salomon Abraha , Joerg Schuettrumpf , Heike Boehm","doi":"10.1016/j.thromres.2026.109616","DOIUrl":"10.1016/j.thromres.2026.109616","url":null,"abstract":"<div><h3>Background</h3><div>Congenital fibrinogen deficiency is a rare inherited coagulation disorder characterized by partial or total lack of plasma fibrinogen (hypo- or afibrinogenemia), or expression of dysfunctional fibrinogen (dysfibrinogenemia), which may cause plasma level reduction (hypodysfibrinogenemia). Loss of functional fibrinogen causes bleeding disposition. In case of trauma or surgical intervention, supplementation of human fibrinogen is required to stop or prevent extensive bleeding events.</div></div><div><h3>Study design</h3><div>A prospective, open-label, uncontrolled, multi-center phase I/III trial was performed to investigate pharmacokinetics, efficacy and safety of single and/or repetitive intravenous infusions of a human fibrinogen concentrate (BT524) for on-demand prophylaxis (ODP) and/or on-demand treatment (ODT) of bleeding events in patients with congenital fibrinogen deficiency.</div></div><div><h3>Patients</h3><div>In the phase III part of the trial reported here, 36 patients (3 children <6 years, 9 children 6–12 years, 4 adolescents and 20 adults) were treated with BT524 for 175 bleeding events, either for ODP or ODT.</div></div><div><h3>Results</h3><div>Fibrinogen concentrate infusion substantially improved maximum clot firmness (MCF). The overall hemostatic response was rated as good or excellent in 98.9% of bleedings. Loss of blood was considered normal in the majority of surgical interventions, and wound healing was also positively assessed. Additional evaluations, including blood product consumption and adverse events, further supported the efficacy and confirmed the favorable safety profile of the novel fibrinogen product.</div></div><div><h3>Conclusion</h3><div>BT524 represents a novel human fibrinogen concentrate provenly efficacious and safe both for the treatment of bleeding and for peri-operative bleeding prophylaxis in patients with congenital fibrinogen deficiency of all ages.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109616"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146214278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-19DOI: 10.1016/j.thromres.2026.109625
Caoimhe Kenny , Fiona Curran , Olive Lennon , Ann-marie O'Neill , Frederikus A. Klok , James Matthews , Fionnuala Ni Ainle , Rachel P. Rosovsky , Grainne O'Donoghue , Caoimhe Kenny
Background
People living with post-pulmonary embolism syndrome (PPES) commonly experience persistent dyspnoea, fatigue, reduced exercise tolerance, anxiety, and fear of recurrence. When symptoms continue beyond three months after effective anticoagulation, quality of life can be substantially impaired. Although healthy lifestyle behaviours may improve PPES symptoms, little is known about the barriers and facilitators influencing behaviour change from the perspective of those affected.
Aim
To explore patients' perceived barriers and facilitators to adopting healthy lifestyle behaviours following PE, in order to inform the future development of rehabilitation interventions for people with PPES.
Methodology
A purposive sample of adults with PPES took part in semi-structured interviews informed by the Theoretical Domains Framework (TDF) and the Capability, Opportunity, Motivation–Behaviour (COMB) model. Interviews were transcribed and analysed using a framework approach with inductive and deductive coding. Codes were grouped into categories and mapped to the 14 TDF domains and six COM-B constructs to identify behavioural influences and key barriers and facilitators.
Findings
Thirty-one participants (18 women, 13 men; aged 25–67 years) were interviewed. Ninety-eight codes were identified and organised into 35 categories, which were mapped to TDF and COM-B domains. The most frequently represented domains were Knowledge, Beliefs about Capabilities, Beliefs about Consequences, and Emotion. Key barriers and facilitators included pain, dyspnoea, healthcare professional knowledge and training, financial resources, and access to education and rehabilitation services.
Conclusions
Engagement in healthy lifestyle behaviours after PE is shaped by interacting physical, emotional, socioeconomic, and environmental factors. These findings highlight the need for comprehensive, theory-informed rehabilitation strategies that address both individual and contextual influences on behaviour change in people with PPES.
{"title":"Barriers and facilitators to healthy lifestyle behaviours for people living with post pulmonary embolism syndrome. A qualitative study exploring participants lived experiences","authors":"Caoimhe Kenny , Fiona Curran , Olive Lennon , Ann-marie O'Neill , Frederikus A. Klok , James Matthews , Fionnuala Ni Ainle , Rachel P. Rosovsky , Grainne O'Donoghue , Caoimhe Kenny","doi":"10.1016/j.thromres.2026.109625","DOIUrl":"10.1016/j.thromres.2026.109625","url":null,"abstract":"<div><h3>Background</h3><div>People living with post-pulmonary embolism syndrome (PPES) commonly experience persistent dyspnoea, fatigue, reduced exercise tolerance, anxiety, and fear of recurrence. When symptoms continue beyond three months after effective anticoagulation, quality of life can be substantially impaired. Although healthy lifestyle behaviours may improve PPES symptoms, little is known about the barriers and facilitators influencing behaviour change from the perspective of those affected.</div></div><div><h3>Aim</h3><div>To explore patients' perceived barriers and facilitators to adopting healthy lifestyle behaviours following PE, in order to inform the future development of rehabilitation interventions for people with PPES.</div></div><div><h3>Methodology</h3><div>A purposive sample of adults with PPES took part in semi-structured interviews informed by the Theoretical Domains Framework (TDF) and the Capability, Opportunity, Motivation–Behaviour (COM<img>B) model. Interviews were transcribed and analysed using a framework approach with inductive and deductive coding. Codes were grouped into categories and mapped to the 14 TDF domains and six COM-B constructs to identify behavioural influences and key barriers and facilitators.</div></div><div><h3>Findings</h3><div>Thirty-one participants (18 women, 13 men; aged 25–67 years) were interviewed. Ninety-eight codes were identified and organised into 35 categories, which were mapped to TDF and COM-B domains. The most frequently represented domains were Knowledge, Beliefs about Capabilities, Beliefs about Consequences, and Emotion. Key barriers and facilitators included pain, dyspnoea, healthcare professional knowledge and training, financial resources, and access to education and rehabilitation services.</div></div><div><h3>Conclusions</h3><div>Engagement in healthy lifestyle behaviours after PE is shaped by interacting physical, emotional, socioeconomic, and environmental factors. These findings highlight the need for comprehensive, theory-informed rehabilitation strategies that address both individual and contextual influences on behaviour change in people with PPES.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109625"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147284965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-13DOI: 10.1016/j.thromres.2026.109619
Lan Sun , Jia Wang , Yi-Dan Yan , Long-Tu Li , Lin-Yu Cao , Ruo-Fei Li , Shan Chong , Meng Hu , Hou-Wen Lin , Yi-Min Cui , Zhi-Chun Gu , Qian Xiang
The pathological hypercoagulable state and associated risk of thrombosis in colorectal cancer (CRC) persist throughout the disease course. Accurate identification of patients at high risk of venous thromboembolism (VTE) and judiciously applying drug or mechanical prevention measures can significantly reduce the incidence of VTE. The review details a range of biomarkers, including platelet count, soluble P-selectin, D-dimer, and vascular endothelial growth factor (VEGF), which have been shown to correlate with increased VTE risk in CRC patients. In addition to the biomarker analysis, the review makes important recommendations for the routine monitoring of these biomarkers in CRC patients, especially those at higher risk for VTE. Furthermore, it discusses the integration of these biomarkers into clinical VTE risk prediction models, advocating for personalized and targeted thromboprophylaxis strategies. The review also explores future research directions, emphasizing the potential of antiplatelet and anticoagulant therapies in improving the prognosis of CRC patients by reducing thromboembolic events. This narrative review not only deepens our understanding of the molecular mechanisms driving cancer-associated thrombosis but also paves the way for novel therapeutic interventions aimed at preventing VTE in CRC patients.
{"title":"Evolving biomarkers and risk prediction models in colorectal cancer-associated venous thromboembolism","authors":"Lan Sun , Jia Wang , Yi-Dan Yan , Long-Tu Li , Lin-Yu Cao , Ruo-Fei Li , Shan Chong , Meng Hu , Hou-Wen Lin , Yi-Min Cui , Zhi-Chun Gu , Qian Xiang","doi":"10.1016/j.thromres.2026.109619","DOIUrl":"10.1016/j.thromres.2026.109619","url":null,"abstract":"<div><div>The pathological hypercoagulable state and associated risk of thrombosis in colorectal cancer (CRC) persist throughout the disease course. Accurate identification of patients at high risk of venous thromboembolism (VTE) and judiciously applying drug or mechanical prevention measures can significantly reduce the incidence of VTE. The review details a range of biomarkers, including platelet count, soluble P-selectin, D-dimer, and vascular endothelial growth factor (VEGF), which have been shown to correlate with increased VTE risk in CRC patients. In addition to the biomarker analysis, the review makes important recommendations for the routine monitoring of these biomarkers in CRC patients, especially those at higher risk for VTE. Furthermore, it discusses the integration of these biomarkers into clinical VTE risk prediction models, advocating for personalized and targeted thromboprophylaxis strategies. The review also explores future research directions, emphasizing the potential of antiplatelet and anticoagulant therapies in improving the prognosis of CRC patients by reducing thromboembolic events. This narrative review not only deepens our understanding of the molecular mechanisms driving cancer-associated thrombosis but also paves the way for novel therapeutic interventions aimed at preventing VTE in CRC patients.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109619"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146221222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-03-01Epub Date: 2026-02-16DOI: 10.1016/j.thromres.2026.109622
Angela Di Giorgio , Claudia Carnuccio , Antonio Nesci , Valerio De Stefano , Angelo Santoliquido
Antiphospholipid syndrome (APS) is an acquired coagulation disorder with an unclear pathogenesis, diagnosed in the presence of thrombotic events, obstetric complications, or non-thrombotic manifestations, alongside persistently detectable antiphospholipid antibodies. aPLs seroconversion, defined as the transition from persistent antibody positivity to sustained antibody negativity, is typically confirmed by at least two negative tests ≥12 weeks apart and maintained for over one year. This phenomenon is distinct from seronegative APS (SNAPS), in which patients present with APS-like clinical features but never fulfill laboratory criteria. Thrombotic risk remains significant in APS, particularly in patients with prior events or persistently elevated aPLs titers. Immunomodulatory therapies, such as hydroxychloroquine, rituximab, eculizumab, sirolimus, or other agents, may reduce antibody levels and contribute to improved outcomes, though evidence is limited. Among these, hydroxychloroquine is the most established agent, particularly in refractory or recurrent thrombotic cases, and is recommended as adjunctive therapy alongside anticoagulation in high-risk thrombotic and obstetric APS. While these therapies may allow cautious adjustments in anticoagulation for low-risk patients, anticoagulants should not be discontinued solely based on seroconversion or adjunctive treatment. Overall, immunomodulatory drugs should be considered strictly as adjuncts, with patient selection guided by clinical phenotype, thrombotic risk, and available evidence.
{"title":"aPLs seroconversion in antiphospholipid syndrome: from definition to clinical relevance","authors":"Angela Di Giorgio , Claudia Carnuccio , Antonio Nesci , Valerio De Stefano , Angelo Santoliquido","doi":"10.1016/j.thromres.2026.109622","DOIUrl":"10.1016/j.thromres.2026.109622","url":null,"abstract":"<div><div>Antiphospholipid syndrome (APS) is an acquired coagulation disorder with an unclear pathogenesis, diagnosed in the presence of thrombotic events, obstetric complications, or non-thrombotic manifestations, alongside persistently detectable antiphospholipid antibodies. aPLs seroconversion, defined as the transition from persistent antibody positivity to sustained antibody negativity, is typically confirmed by at least two negative tests ≥12 weeks apart and maintained for over one year. This phenomenon is distinct from seronegative APS (SNAPS), in which patients present with APS-like clinical features but never fulfill laboratory criteria. Thrombotic risk remains significant in APS, particularly in patients with prior events or persistently elevated aPLs titers. Immunomodulatory therapies, such as hydroxychloroquine, rituximab, eculizumab, sirolimus, or other agents, may reduce antibody levels and contribute to improved outcomes, though evidence is limited. Among these, hydroxychloroquine is the most established agent, particularly in refractory or recurrent thrombotic cases, and is recommended as adjunctive therapy alongside anticoagulation in high-risk thrombotic and obstetric APS. While these therapies may allow cautious adjustments in anticoagulation for low-risk patients, anticoagulants should not be discontinued solely based on seroconversion or adjunctive treatment. Overall, immunomodulatory drugs should be considered strictly as adjuncts, with patient selection guided by clinical phenotype, thrombotic risk, and available evidence.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"259 ","pages":"Article 109622"},"PeriodicalIF":3.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146776650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}