Pub Date : 2025-12-01Epub Date: 2025-11-01DOI: 10.1016/j.thromres.2025.109528
Wanru Yao , Di Ai , Qing Zhang , Xiaojing Li , Min Zhou , Ningning Zhang , Yan Wang , Sheng Yang , Zhenping Chen , Gang Li , Koon-Hung Luke , Runhui Wu
The management of severe haemophilia A (SHA) in China has evolved significantly from on-demand treatment to low-dose prophylaxis, substantially reducing bleeding rates. The Chinese Haemophilia Individualized Prophylaxis Study (CHIPS) protocol was developed as a standardized, cost-effective framework to pursue zero joint bleeding and long-term joint health preservation. This review provides a comprehensive overview of the CHIPS protocol, synthesizing evidence from three interrelated studies that demonstrate the efficacy of a structured, individualized approach incorporating pharmacokinetic-guided dosing and multimodal joint assessment. The results indicate that this strategy achieves near-zero bleeding rates, improves quality of life, and maintains joint health while optimizing factor consumption. Furthermore, the review discusses the expanding role of the CHIPS framework in the current treatment landscape, highlighting its utility as a practical platform for monitoring patients transitioning to non-factor therapies, such as emicizumab, in resource-conscious settings. The CHIPS protocol represents a timely and scalable prophylaxis framework that optimizes factor replacement therapy and adapts to novel agents. Its structured monitoring and individualized dosing offer a critical solution for protecting joint health in boys with SHA until non-factor and gene therapies become widely accessible in China.
{"title":"The Chinese Haemophilia Individualized Prophylaxis (CHIPS): A cost-effective regimen for zero joint bleeding and long-term joint health in boys with Severe Haemophilia A (SHA) on factor replacement","authors":"Wanru Yao , Di Ai , Qing Zhang , Xiaojing Li , Min Zhou , Ningning Zhang , Yan Wang , Sheng Yang , Zhenping Chen , Gang Li , Koon-Hung Luke , Runhui Wu","doi":"10.1016/j.thromres.2025.109528","DOIUrl":"10.1016/j.thromres.2025.109528","url":null,"abstract":"<div><div>The management of severe haemophilia A (SHA) in China has evolved significantly from on-demand treatment to low-dose prophylaxis, substantially reducing bleeding rates. The Chinese Haemophilia Individualized Prophylaxis Study (CHIPS) protocol was developed as a standardized, cost-effective framework to pursue zero joint bleeding and long-term joint health preservation. This review provides a comprehensive overview of the CHIPS protocol, synthesizing evidence from three interrelated studies that demonstrate the efficacy of a structured, individualized approach incorporating pharmacokinetic-guided dosing and multimodal joint assessment. The results indicate that this strategy achieves near-zero bleeding rates, improves quality of life, and maintains joint health while optimizing factor consumption. Furthermore, the review discusses the expanding role of the CHIPS framework in the current treatment landscape, highlighting its utility as a practical platform for monitoring patients transitioning to non-factor therapies, such as emicizumab, in resource-conscious settings. The CHIPS protocol represents a timely and scalable prophylaxis framework that optimizes factor replacement therapy and adapts to novel agents. Its structured monitoring and individualized dosing offer a critical solution for protecting joint health in boys with SHA until non-factor and gene therapies become widely accessible in China<strong>.</strong></div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109528"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145517455","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 : 2025-12-01Epub Date: 2025-10-27DOI: 10.1016/j.thromres.2025.109522
Xiaoxiao Chen , Yuntao Mao , Yuxin Ge , Dandan Ju
Objective
The systemic immune-inflammation index (SII), a new inflammatory marker, is considered a predictive indicator for multiple malignant tumors and inflammatory illnesses. Its relationship with deep vein thrombosis (DVT) has garnered growing attention. This research seeks to systematically examine the relationship between SII and DVT.
Methods
Embase, Web of Science, Cochrane Library, and PubMed were searched up to January 6, 2025, for observational studies examining the link between SII and DVT. Two reviewers separately screened the retrieved articles, extracted data, and appraised the quality of the enrolled studies. MetaDisc version 1.4 and StataMP 15 were utilized to carry out statistical analyses.
Results
14 studies involving 13,655 individuals were included. The meta-analysis demonstrated that individuals with DVT exhibited elevated SII in comparison to those without DVT (WMD = 938.60; 95 % CI: 466.55–1410.64; p < 0.001). Moreover, individuals with elevated SII had a 4.73-fold greater risk of DVT than those with low SII (95 % CI: 2.19–10.19; p < 0.001). The pooled diagnostic performance revealed a specificity of 78 % (95 % CI: 71 %–84 %), sensitivity of 69 % (95 % CI: 56 %–79 %), negative likelihood ratio of 0.40 (95 % CI: 0.26–0.60), positive likelihood ratio of 3.18 (95 % CI: 2.12–4.76), and diagnostic odds ratio of 7.96 (95 % CI: 3.66–17.30). The area under the receiver operating characteristic curve was 0.81 (95 % CI: 0.77–0.84). Sensitivity analyses were carried out by sequentially excluding individual studies, and no substantial changes were observed in the mean differences, odds ratios, or diagnostic estimates, indicating the stability of the results. No substantial publication bias was detected in the analyses of mean differences, odds ratios, or diagnostic measures.
Conclusion
Elevated SII is related to a higher likelihood of DVT, suggesting its potential as a valuable predictor of DVT risk.
{"title":"Predictive value of the systemic immuane-inflammation index for deep vein thrombosis: A meta-analysis","authors":"Xiaoxiao Chen , Yuntao Mao , Yuxin Ge , Dandan Ju","doi":"10.1016/j.thromres.2025.109522","DOIUrl":"10.1016/j.thromres.2025.109522","url":null,"abstract":"<div><h3>Objective</h3><div>The systemic immune-inflammation index (SII), a new inflammatory marker, is considered a predictive indicator for multiple malignant tumors and inflammatory illnesses. Its relationship with deep vein thrombosis (DVT) has garnered growing attention. This research seeks to systematically examine the relationship between SII and DVT.</div></div><div><h3>Methods</h3><div>Embase, Web of Science, Cochrane Library, and PubMed were searched up to January 6, 2025, for observational studies examining the link between SII and DVT. Two reviewers separately screened the retrieved articles, extracted data, and appraised the quality of the enrolled studies. MetaDisc version 1.4 and StataMP 15 were utilized to carry out statistical analyses.</div></div><div><h3>Results</h3><div>14 studies involving 13,655 individuals were included. The meta-analysis demonstrated that individuals with DVT exhibited elevated SII in comparison to those without DVT (WMD = 938.60; 95 % CI: 466.55–1410.64; <em>p</em> < 0.001). Moreover, individuals with elevated SII had a 4.73-fold greater risk of DVT than those with low SII (95 % CI: 2.19–10.19; <em>p</em> < 0.001). The pooled diagnostic performance revealed a specificity of 78 % (95 % CI: 71 %–84 %), sensitivity of 69 % (95 % CI: 56 %–79 %), negative likelihood ratio of 0.40 (95 % CI: 0.26–0.60), positive likelihood ratio of 3.18 (95 % CI: 2.12–4.76), and diagnostic odds ratio of 7.96 (95 % CI: 3.66–17.30). The area under the receiver operating characteristic curve was 0.81 (95 % CI: 0.77–0.84). Sensitivity analyses were carried out by sequentially excluding individual studies, and no substantial changes were observed in the mean differences, odds ratios, or diagnostic estimates, indicating the stability of the results. No substantial publication bias was detected in the analyses of mean differences, odds ratios, or diagnostic measures.</div></div><div><h3>Conclusion</h3><div>Elevated SII is related to a higher likelihood of DVT, suggesting its potential as a valuable predictor of DVT risk.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109522"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145419432","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 : 2025-12-01Epub Date: 2025-10-11DOI: 10.1016/j.thromres.2025.109507
Wen-jing Ge , Teng-fei Zhu , Wen-jie Ge , Xin-yi Zhu , Ai-qin Chu
Objective
This systematic review aims to evaluate the methodological quality, performance, and clinical applicability of machine learning (ML) models for predicting the risk of venous thromboembolism (VTE) in hospitalized patients. Specifically, we aim to assess the methodological quality and reporting transparency of the included studies, with a focus on their risk of bias and adherence to reporting guidelines.
Methods
A systematic review by use of the databases Cochrane Library, Web of Science, Embase, PubMed, CNKI, VIP Journal Database, Wanfang Database, and the Chinese Biomedical Literature Database. The study was registered at PROSPERO before data collection and PRISMA guidelines were followed. The search was conducted to identify all relevant studies published from the inception of database up to August 1, 2024. Two independent researchers screened the literature and extracted data. Model quality was assessed using the PROBAST appraisal tool and a modified TRIPOD+AI framework, alongside reported model performance metrics.
Results
A total of seventeen studies were included, comprising 65 VTE ML models with sample sizes ranging from 120 to 9213. All models demonstrated an area under the curve (AUC) >0.7. Twenty-three ML algorithms were employed, with logistic regression (LR) being the most frequently used (n = 11), followed by XGBoost (n = 10) and random forests (RF) (n = 9). Thirteen studies utilized various stochastic algorithms. Most studies used Bootstrap or 10-fold cross-validation for internal validation, but lacked external validation, leading to a high overall risk of bias. Key predictors in these models included D-dimer, history of thrombosis, history of hypertension, age, and complications.
Conclusions
Existing evidence suggests that ML models can effectively predict VTE outcomes. However, most models suffer from poor methodological quality, lack of external validation, and limited generalizability. Future research should focus on large-scale, multi-center prospective studies that are based on clinical practice, improve external validation, and develop optimized local VTE risk assessment and decision support tools for better integration into clinical practice.
{"title":"Systematic review of a machine learning model for prediction of venous thromboembolism risk","authors":"Wen-jing Ge , Teng-fei Zhu , Wen-jie Ge , Xin-yi Zhu , Ai-qin Chu","doi":"10.1016/j.thromres.2025.109507","DOIUrl":"10.1016/j.thromres.2025.109507","url":null,"abstract":"<div><h3>Objective</h3><div>This systematic review aims to evaluate the methodological quality, performance, and clinical applicability of machine learning (ML) models for predicting the risk of venous thromboembolism (VTE) in hospitalized patients. Specifically, we aim to assess the methodological quality and reporting transparency of the included studies, with a focus on their risk of bias and adherence to reporting guidelines.</div></div><div><h3>Methods</h3><div>A systematic review by use of the databases Cochrane Library, Web of Science, Embase, PubMed, CNKI, VIP Journal Database, Wanfang Database, and the Chinese Biomedical Literature Database. The study was registered at PROSPERO before data collection and PRISMA guidelines were followed. The search was conducted to identify all relevant studies published from the inception of database up to August 1, 2024. Two independent researchers screened the literature and extracted data. Model quality was assessed using the PROBAST appraisal tool and a modified TRIPOD+AI framework, alongside reported model performance metrics.</div></div><div><h3>Results</h3><div>A total of seventeen studies were included, comprising 65 VTE ML models with sample sizes ranging from 120 to 9213. All models demonstrated an area under the curve (AUC) >0.7. Twenty-three ML algorithms were employed, with logistic regression (LR) being the most frequently used (<em>n</em> = 11), followed by XGBoost (<em>n</em> = 10) and random forests (RF) (<em>n</em> = 9). Thirteen studies utilized various stochastic algorithms. Most studies used Bootstrap or 10-fold cross-validation for internal validation, but lacked external validation, leading to a high overall risk of bias. Key predictors in these models included D-dimer, history of thrombosis, history of hypertension, age, and complications.</div></div><div><h3>Conclusions</h3><div>Existing evidence suggests that ML models can effectively predict VTE outcomes. However, most models suffer from poor methodological quality, lack of external validation, and limited generalizability. Future research should focus on large-scale, multi-center prospective studies that are based on clinical practice, improve external validation, and develop optimized local VTE risk assessment and decision support tools for better integration into clinical practice.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109507"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145419433","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 : 2025-12-01Epub Date: 2025-11-03DOI: 10.1016/j.thromres.2025.109525
Claudia Iglesias-Perez , Paula Jimenez-Fonseca , Javier López Robles , Silvia García Adrián , Isaura Fernández Pérez , Purificación Martínez del Prado , Jaime Rubio Pérez , Eva Martínez de Castro , Carmen Díaz Pedroche , Marta García de Herreros , Marta Carmona Campos , Ana Belén Rupérez Blanco , Mercedes Salgado Fernández , Teresa Quintanar Verdúguez , David Marrupe González , Marta Covela Rúa , Jose Antonio Santiago Crespo , María Nieva Muñoz , Andrés Muñoz , Alberto Carmona-Bayonas
Background
Cancer-associated venous thromboembolism (VTE) is a major adverse prognostic factor with heterogeneous outcomes across tumor types. We aimed to describe the characteristics of lung cancer patients with VTE, compare outcomes across malignancies, and assess their association with complications, progression, and survival.
Methods
We analyzed TESEO-SEOM, a prospective multicenter registry including patients with active cancer and VTE. Patients were stratified by tumor site, with lung as reference. Outcomes included recurrent VTE, bleeding, and survival. Analyses were stratified by tumor type and VTE presentation (clinically suspected, symptomatic/asymptomatic incidental). Complications were estimated using competing-risk methods.
Results
Among 3855 patients, the most frequent cancers were gastrointestinal (39.4 %), lung (22.2 %), and breast (10.4 %). Pulmonary embolism predominated (55 %), especially in lung cancer (69.8 %). Overall, 48.9 % of events were clinically suspected and 50.9 % incidental; suspected were more common in lung cancer (53.9 %), whereas incidental diagnoses predominated in gastrointestinal tumors (58.8 %).
Complications occurred in 17.6 % (10.2 % bleeding, 7.4 % recurrent VTE). Recurrence was highest in gastrointestinal cancers (11.4 %, Gray's p = 0.022), while bleeding did not differ (p = 0.213). VTE-related mortality was low (1 %), while mixed-cause mortality was highest in lung cancer (17.2 %). Median PFS and OS were shortest in lung cancer (4.5 and 7.7 months, p < 0.0001). Incidental asymptomatic events conferred longer survival, particularly in lung cancer (OS 11.5 vs. 7.3 months for symptomatic incidental and 5.6 for suspected, p < 0.001).
Conclusion
VTE in lung cancer is associated with more severe presentation, higher mixed-cause mortality, and worse survival than in other tumors. Incidental asymptomatic VTE predicts better outcomes, supporting risk stratification by tumor type and presentation.
癌症相关静脉血栓栓塞（VTE）是一种主要的不良预后因素，不同肿瘤类型的预后不尽相同。我们的目的是描述肺癌静脉血栓栓塞患者的特征，比较不同恶性肿瘤的预后，并评估其与并发症、进展和生存的关系。方法我们分析了TESEO-SEOM，一项前瞻性多中心登记，包括活动性癌症和静脉血栓栓塞患者。按肿瘤部位分层，以肺为参照。结果包括静脉血栓栓塞复发、出血和生存。根据肿瘤类型和静脉血栓栓塞表现（临床怀疑、有症状/无症状偶发）对分析进行分层。采用竞争风险法估计并发症。结果3855例患者中，最常见的肿瘤为胃肠道（39.4%）、肺癌（22.2%）和乳腺癌（10.4%）。肺栓塞占多数（55%），尤其是肺癌（69.8%）。总体而言，48.9%的事件为临床怀疑，50.9%为偶然事件；疑似多见于肺癌（53.9%），而偶然诊断主要见于胃肠道肿瘤（58.8%）。并发症发生率为17.6%（10.2%出血，7.4%静脉血栓栓塞复发）。胃肠道肿瘤复发率最高（11.4%,Gray’s p = 0.022），而出血无差异（p = 0.213）。静脉血栓栓塞相关死亡率较低（1%），而肺癌的混合原因死亡率最高（17.2%）。肺癌患者的中位PFS和OS最短（4.5个月和7.7个月，p < 0.0001）。偶发无症状事件可延长生存期，尤其是肺癌患者（偶发症状患者生存期11.5个月，疑似患者生存期7.3个月，p < 0.001）。结论与其他肿瘤相比，vte在肺癌中的表现更严重，混合原因死亡率更高，生存期更差。偶发无症状静脉血栓栓塞预测更好的预后，支持肿瘤类型和表现的风险分层。
{"title":"Venous thrombosis in lung cancer compared with other tumors: results from the TESEO-SEOM registry","authors":"Claudia Iglesias-Perez , Paula Jimenez-Fonseca , Javier López Robles , Silvia García Adrián , Isaura Fernández Pérez , Purificación Martínez del Prado , Jaime Rubio Pérez , Eva Martínez de Castro , Carmen Díaz Pedroche , Marta García de Herreros , Marta Carmona Campos , Ana Belén Rupérez Blanco , Mercedes Salgado Fernández , Teresa Quintanar Verdúguez , David Marrupe González , Marta Covela Rúa , Jose Antonio Santiago Crespo , María Nieva Muñoz , Andrés Muñoz , Alberto Carmona-Bayonas","doi":"10.1016/j.thromres.2025.109525","DOIUrl":"10.1016/j.thromres.2025.109525","url":null,"abstract":"<div><h3>Background</h3><div>Cancer-associated venous thromboembolism (VTE) is a major adverse prognostic factor with heterogeneous outcomes across tumor types. We aimed to describe the characteristics of lung cancer patients with VTE, compare outcomes across malignancies, and assess their association with complications, progression, and survival.</div></div><div><h3>Methods</h3><div>We analyzed TESEO-SEOM, a prospective multicenter registry including patients with active cancer and VTE. Patients were stratified by tumor site, with lung as reference. Outcomes included recurrent VTE, bleeding, and survival. Analyses were stratified by tumor type and VTE presentation (clinically suspected, symptomatic/asymptomatic incidental). Complications were estimated using competing-risk methods.</div></div><div><h3>Results</h3><div>Among 3855 patients, the most frequent cancers were gastrointestinal (39.4 %), lung (22.2 %), and breast (10.4 %). Pulmonary embolism predominated (55 %), especially in lung cancer (69.8 %). Overall, 48.9 % of events were clinically suspected and 50.9 % incidental; suspected were more common in lung cancer (53.9 %), whereas incidental diagnoses predominated in gastrointestinal tumors (58.8 %).</div><div>Complications occurred in 17.6 % (10.2 % bleeding, 7.4 % recurrent VTE). Recurrence was highest in gastrointestinal cancers (11.4 %, Gray's <em>p</em> = 0.022), while bleeding did not differ (<em>p</em> = 0.213). VTE-related mortality was low (1 %), while mixed-cause mortality was highest in lung cancer (17.2 %). Median PFS and OS were shortest in lung cancer (4.5 and 7.7 months, <em>p</em> < 0.0001). Incidental asymptomatic events conferred longer survival, particularly in lung cancer (OS 11.5 vs. 7.3 months for symptomatic incidental and 5.6 for suspected, <em>p</em> < 0.001).</div></div><div><h3>Conclusion</h3><div>VTE in lung cancer is associated with more severe presentation, higher mixed-cause mortality, and worse survival than in other tumors. Incidental asymptomatic VTE predicts better outcomes, supporting risk stratification by tumor type and presentation.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109525"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145517380","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 : 2025-12-01Epub Date: 2025-11-07DOI: 10.1016/j.thromres.2025.109531
Sarah E. Tashbook , Tomasz W. Kaminski , Claudette M. St. Croix , Simon C. Watkins , Prithu Sundd , Tomasz Brzoska
In situ pulmonary arterial thrombosis (iPAT), occurring without concurrent deep vein thrombosis, is a life-threatening complication associated with various pathological conditions. The etiological mechanisms underlying iPAT remain poorly understood. Several studies suggest that circulating tissue factor (cTF) may contribute to the development of thrombotic complications; however, there is no direct in vivo evidence supporting the role of cTF in the pathogenesis of iPAT. Furthermore, although in vitro studies suggest that platelet anionic phospholipids enable cTF-initiated coagulation, how platelets contribute to cTF-dependent iPAT in vivo remains unknown. In the current study, we used quantitative fluorescence intravital lung microscopy to investigate the development of cTF-induced iPAT in live mice following intravascular administration of thromboplastin. To dissect the interplay between coagulation and platelet procoagulant activity, we assessed the effects of coagulation and platelet inhibition on iPAT development in vivo. Additionally, we conducted an in vitro clotting time assay using mouse plasma samples. Thromboplastin triggered iPAT in mice in a dose-dependent manner. IPAT involved the formation of platelet-rich thrombi at the bottle-neck junctions of pulmonary arterioles and capillaries, which was prevented by heparin. Notably, pretreatment of mice with annexin A5 or eptifibatide also completely abrogated thromboplastin-induced iPAT. These intravital microscopy findings were further corroborated by the in vitro clotting time assay. Our study provides in vivo evidence that cTF contributes to the development of iPAT. We demonstrate that the prothrombotic effect of cTF is dependent on platelet-αIIbβ3 signaling, which enhances platelet procoagulant activity, leading to accelerated coagulation and development of iPAT.
{"title":"αIIbβ3-dependent platelet procoagulant activity promotes pulmonary arterial thrombosis triggered by circulating tissue factor","authors":"Sarah E. Tashbook , Tomasz W. Kaminski , Claudette M. St. Croix , Simon C. Watkins , Prithu Sundd , Tomasz Brzoska","doi":"10.1016/j.thromres.2025.109531","DOIUrl":"10.1016/j.thromres.2025.109531","url":null,"abstract":"<div><div><em>In situ</em> pulmonary arterial thrombosis (iPAT), occurring without concurrent deep vein thrombosis, is a life-threatening complication associated with various pathological conditions. The etiological mechanisms underlying iPAT remain poorly understood. Several studies suggest that circulating tissue factor (cTF) may contribute to the development of thrombotic complications; however, there is no direct <em>in vivo</em> evidence supporting the role of cTF in the pathogenesis of iPAT. Furthermore, although <em>in vitro</em> studies suggest that platelet anionic phospholipids enable cTF-initiated coagulation, how platelets contribute to cTF-dependent iPAT <em>in vivo</em> remains unknown. In the current study, we used quantitative fluorescence intravital lung microscopy to investigate the development of cTF-induced iPAT in live mice following intravascular administration of thromboplastin. To dissect the interplay between coagulation and platelet procoagulant activity, we assessed the effects of coagulation and platelet inhibition on iPAT development <em>in vivo</em>. Additionally, we conducted an <em>in vitro</em> clotting time assay using mouse plasma samples. Thromboplastin triggered iPAT in mice in a dose-dependent manner. IPAT involved the formation of platelet-rich thrombi at the bottle-neck junctions of pulmonary arterioles and capillaries, which was prevented by heparin. Notably, pretreatment of mice with annexin A5 or eptifibatide also completely abrogated thromboplastin-induced iPAT. These intravital microscopy findings were further corroborated by the <em>in vitro</em> clotting time assay. Our study provides <em>in vivo</em> evidence that cTF contributes to the development of iPAT. We demonstrate that the prothrombotic effect of cTF is dependent on platelet-αIIbβ3 signaling, which enhances platelet procoagulant activity, leading to accelerated coagulation and development of iPAT.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109531"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145496865","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 : 2025-12-01Epub Date: 2025-11-10DOI: 10.1016/j.thromres.2025.109537
Tian Gao , Ling Wang , Boheng Wang , Rui Yin , Li Qian , Aiqin Zhai , Vakkas Qureshi , Can Yang , Fei Han , Shuo Wang , Dan Wang , Xueping Xu , Xiujuan Wang , Kang Han , Ping Li , Xinjian Zhou , Xiaoman Ye , Runkai Shao , Lu Chen , Wei Wang , Yuan Mao
<div><h3>Background</h3><div>Pneumonia-related sepsis is frequently complicated by coagulation disorders, which significantly increase mortality risk. The current ISTH criteria demonstrate limited sensitivity in diagnosing pneumonia-specific coagulopathy, and the mechanisms underlying clinical phenotypic heterogeneity remain poorly understood. There is a growing need to identify novel biomarkers that can enhance the early detection and stratification of disseminated intravascular coagulation (DIC), particularly in its non-overt stages.</div></div><div><h3>Aims</h3><div>The study aimed to evaluate the prognostic value of antithrombin (AT) and activated protein C (aPC) testing for predicting clinical deterioration and early DIC progression in adults with severe pneumonia-related sepsis.</div></div><div><h3>Methods</h3><div>We conducted a prospective observational cohort study of 86 adults with severe pneumonia-related sepsis admitted to the Intensive Care Unit (ICU). All patients underwent testing of AT and aPC upon enrollment. The predictive value of this biomarker combination was evaluated for the development of overt DIC within 72 h and 28-day all-cause mortality using receiver operating characteristic (ROC) analysis.</div></div><div><h3>Results</h3><div>Among 86 adults with severe pneumonia-related sepsis (median age 65 years; 56.9 % male), 18 (20.9 %) progressed to overt DIC within 72 h, and the 28-day mortality rate was 26.7 % (23/86). Compared with survivors, non-survivors exhibited significantly lower antithrombin activity (median 65 % vs. 78 %; <em>P</em> = 0.005) and higher activated protein C levels (median 127 pg/mL vs. 93.9 pg/mL; <em>P</em> < 0.001). Notably, the presence of overt DIC was the strongest predictor of mortality (OR = 144, 95 % CI: 18.66–1111.07). Similarly, patients with overt DIC exhibited markedly elevated aPC (P < 0.001). Among non-survivors, aPC was positively correlated with the 24-hour vasoactive-inotropic score (VIS; <em>r</em> = 0.567, <em>P</em> = 0.005). ROC analysis revealed that for predicting mortality, both aPC (AUC = 0.804, 95 % CI: 0.709–0.900) and the combined AT/aPC model (AUC = 0.814, 95 % CI: 0.714–0.913) significantly outperformed AT alone (AUC = 0.736, 95 % CI: 0.595–0.878).For predicting overt DIC, aPC (AUC = 0.859, 95 % CI: 0.778–0.939) and the combined model (AUC = 0.850, 95 % CI: 0.764–0.935) both demonstrated high accuracy. Notably, only the combined model effectively identified non-overt DIC (AUC = 0.850, 95 % CI: 0.768–0.932), whereas AT (AUC = 0.723) and aPC (AUC = 0.742) alone showed suboptimal performance.</div></div><div><h3>Conclusion</h3><div>In conclusion, this preliminary study identifies a combined AT/aPC model as a promising early predictor of DIC progression and mortality in pneumonia-sepsis. If validated in larger, multicentre cohorts, this simple two-biomarker approach provides a potential biomarker foundation for future studies investigating personalised anticoagulation st
{"title":"Superiority of a combined antithrombin and activated protein C model for predicting coagulopathy and mortality in pneumonia-related sepsis: A prospective cohort study","authors":"Tian Gao , Ling Wang , Boheng Wang , Rui Yin , Li Qian , Aiqin Zhai , Vakkas Qureshi , Can Yang , Fei Han , Shuo Wang , Dan Wang , Xueping Xu , Xiujuan Wang , Kang Han , Ping Li , Xinjian Zhou , Xiaoman Ye , Runkai Shao , Lu Chen , Wei Wang , Yuan Mao","doi":"10.1016/j.thromres.2025.109537","DOIUrl":"10.1016/j.thromres.2025.109537","url":null,"abstract":"<div><h3>Background</h3><div>Pneumonia-related sepsis is frequently complicated by coagulation disorders, which significantly increase mortality risk. The current ISTH criteria demonstrate limited sensitivity in diagnosing pneumonia-specific coagulopathy, and the mechanisms underlying clinical phenotypic heterogeneity remain poorly understood. There is a growing need to identify novel biomarkers that can enhance the early detection and stratification of disseminated intravascular coagulation (DIC), particularly in its non-overt stages.</div></div><div><h3>Aims</h3><div>The study aimed to evaluate the prognostic value of antithrombin (AT) and activated protein C (aPC) testing for predicting clinical deterioration and early DIC progression in adults with severe pneumonia-related sepsis.</div></div><div><h3>Methods</h3><div>We conducted a prospective observational cohort study of 86 adults with severe pneumonia-related sepsis admitted to the Intensive Care Unit (ICU). All patients underwent testing of AT and aPC upon enrollment. The predictive value of this biomarker combination was evaluated for the development of overt DIC within 72 h and 28-day all-cause mortality using receiver operating characteristic (ROC) analysis.</div></div><div><h3>Results</h3><div>Among 86 adults with severe pneumonia-related sepsis (median age 65 years; 56.9 % male), 18 (20.9 %) progressed to overt DIC within 72 h, and the 28-day mortality rate was 26.7 % (23/86). Compared with survivors, non-survivors exhibited significantly lower antithrombin activity (median 65 % vs. 78 %; <em>P</em> = 0.005) and higher activated protein C levels (median 127 pg/mL vs. 93.9 pg/mL; <em>P</em> < 0.001). Notably, the presence of overt DIC was the strongest predictor of mortality (OR = 144, 95 % CI: 18.66–1111.07). Similarly, patients with overt DIC exhibited markedly elevated aPC (P < 0.001). Among non-survivors, aPC was positively correlated with the 24-hour vasoactive-inotropic score (VIS; <em>r</em> = 0.567, <em>P</em> = 0.005). ROC analysis revealed that for predicting mortality, both aPC (AUC = 0.804, 95 % CI: 0.709–0.900) and the combined AT/aPC model (AUC = 0.814, 95 % CI: 0.714–0.913) significantly outperformed AT alone (AUC = 0.736, 95 % CI: 0.595–0.878).For predicting overt DIC, aPC (AUC = 0.859, 95 % CI: 0.778–0.939) and the combined model (AUC = 0.850, 95 % CI: 0.764–0.935) both demonstrated high accuracy. Notably, only the combined model effectively identified non-overt DIC (AUC = 0.850, 95 % CI: 0.768–0.932), whereas AT (AUC = 0.723) and aPC (AUC = 0.742) alone showed suboptimal performance.</div></div><div><h3>Conclusion</h3><div>In conclusion, this preliminary study identifies a combined AT/aPC model as a promising early predictor of DIC progression and mortality in pneumonia-sepsis. If validated in larger, multicentre cohorts, this simple two-biomarker approach provides a potential biomarker foundation for future studies investigating personalised anticoagulation st","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109537"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145517332","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 : 2025-12-01Epub Date: 2025-10-13DOI: 10.1016/j.thromres.2025.109506
Mohammad Reza Moghaddasnejad , Negar Sadat Sherafat , Najmaldin Saki
Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of immune regulatory cells that play crucial roles in suppressing immune responses and promoting immune tolerance in autoimmune diseases. Platelets, historically recognized for their role in hemostasis, have recently attracted significant attention for their immune regulatory functions, mainly through their interactions with immune cells, including MDSCs. In patients with immune thrombocytopenia (ITP), both the quantity and suppressive function of MDSCs are decreased. However, following treatment and subsequent elevation of platelet counts, the mean level and suppressive capacity of MDSCs increase. Studies have indicated that platelet-derived products can increase the suppressive capacity of MDSCs in ITP, thereby promoting immune tolerance and reducing inflammation. Conversely, specific platelet-secreted molecules such as TGF-β and histamine play complex roles and are capable of both augmenting and inhibiting MDSC activity, depending on the context. Understanding these interactions reveals potential targets in platelet-MDSC signaling pathways as novel approaches for ITP management. Future research could investigate targeted therapies that modulate MDSC function by enhancing or inhibiting specific platelet-derived mediators, leading to the development of innovative treatments for autoimmune diseases such as ITP.
{"title":"The role of platelets in the regulation of myeloid-derived suppressor cells in immune thrombocytopenia","authors":"Mohammad Reza Moghaddasnejad , Negar Sadat Sherafat , Najmaldin Saki","doi":"10.1016/j.thromres.2025.109506","DOIUrl":"10.1016/j.thromres.2025.109506","url":null,"abstract":"<div><div>Myeloid-derived suppressor cells (MDSCs) are a heterogeneous group of immune regulatory cells that play crucial roles in suppressing immune responses and promoting immune tolerance in autoimmune diseases. Platelets, historically recognized for their role in hemostasis, have recently attracted significant attention for their immune regulatory functions, mainly through their interactions with immune cells, including MDSCs. In patients with immune thrombocytopenia (ITP), both the quantity and suppressive function of MDSCs are decreased. However, following treatment and subsequent elevation of platelet counts, the mean level and suppressive capacity of MDSCs increase. Studies have indicated that platelet-derived products can increase the suppressive capacity of MDSCs in ITP, thereby promoting immune tolerance and reducing inflammation. Conversely, specific platelet-secreted molecules such as TGF-β and histamine play complex roles and are capable of both augmenting and inhibiting MDSC activity, depending on the context. Understanding these interactions reveals potential targets in platelet-MDSC signaling pathways as novel approaches for ITP management. Future research could investigate targeted therapies that modulate MDSC function by enhancing or inhibiting specific platelet-derived mediators, leading to the development of innovative treatments for autoimmune diseases such as ITP.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109506"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145365125","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 : 2025-12-01Epub Date: 2025-10-24DOI: 10.1016/j.thromres.2025.109521
Roman Kotlín , Žofie Sovová , Tereza Sklenářová , Marek Havlíček , Jiří Suttnar , Leona Chrastinová , Ingrid Hrachovinová , Alžběta Hlaváčková
Introduction
Variants in genes coding fibrinogen chains may lead to a quantitative fibrinogen disorder—hypofibrinogenemia. The aim of the study was to determine the cause of congenital hypofibrinogenemia and characterize the underlying structure and function of fibrinogen.
Methods
Genetic and proteomic analyses were performed to determine fibrinogen variants and detect their presence in plasma. Scanning electron microscopy was used to study fibrin clot morphology, and polymerization experiments were used to determine its effect on fibrin formation. Bioinformatics and in silico structural biology techniques were used to predict the impact of variant on the protein's stability and function.
Results
We identified three previously undescribed variants of the fibrinogen-related domain (FReD) of the fibrinogen Bβ chain—FGB:p.Asp350His, FGB:p.Arg436Lys, and FGB:p.Tyr447Cys. Fibrin structure and fibrin polymerization were very slightly affected in FGB:p.Asp350His and FGB: p.Arg436Lys cases. The FGB:p.Tyr447Cys variant could have physiological manifestations because it destabilizes the binding site of the fibrinogen Bβ chain. The FGB:Arg436Lys variant does not destabilize the protein's structure, but it may disturb fibrin polymerization. High conservation of Arg436 may indicate its importance in fibrinogen biosynthesis or secretion. FGB:p.Asp350His is situated in the N-terminal residue of the third β-strand of the central antiparallel β-sheet of the FReD, forming a hydrogen bond with Asp346, and Asp350 seems to have a negligible effect on the formation of the correct Bβ chain structure.
Conclusion
The analyzed variants in the FReD of the fibrinogen Bβ chain seems to have an impact on the proper structure of the fibrinogen-related domain of the fibrinogen Bβ chain.
{"title":"Three new variants of the fibrinogen-related domain of the fibrinogen Bβ chain","authors":"Roman Kotlín , Žofie Sovová , Tereza Sklenářová , Marek Havlíček , Jiří Suttnar , Leona Chrastinová , Ingrid Hrachovinová , Alžběta Hlaváčková","doi":"10.1016/j.thromres.2025.109521","DOIUrl":"10.1016/j.thromres.2025.109521","url":null,"abstract":"<div><h3>Introduction</h3><div>Variants in genes coding fibrinogen chains may lead to a quantitative fibrinogen disorder—hypofibrinogenemia. The aim of the study was to determine the cause of congenital hypofibrinogenemia and characterize the underlying structure and function of fibrinogen.</div></div><div><h3>Methods</h3><div>Genetic and proteomic analyses were performed to determine fibrinogen variants and detect their presence in plasma. Scanning electron microscopy was used to study fibrin clot morphology, and polymerization experiments were used to determine its effect on fibrin formation. Bioinformatics and <em>in silico</em> structural biology techniques were used to predict the impact of variant on the protein's stability and function.</div></div><div><h3>Results</h3><div>We identified three previously undescribed variants of the fibrinogen-related domain (FReD) of the fibrinogen Bβ chain—<em>FGB</em>:p.Asp350His, <em>FGB</em>:p.Arg436Lys, and <em>FGB</em>:p.Tyr447Cys. Fibrin structure and fibrin polymerization were very slightly affected in <em>FGB</em>:p.Asp350His and <em>FGB</em>: p.Arg436Lys cases. The <em>FGB</em>:p.Tyr447Cys variant could have physiological manifestations because it destabilizes the binding site of the fibrinogen Bβ chain. The <em>FGB</em>:Arg436Lys variant does not destabilize the protein's structure, but it may disturb fibrin polymerization. High conservation of Arg436 may indicate its importance in fibrinogen biosynthesis or secretion. <em>FGB</em>:p.Asp350His is situated in the N-terminal residue of the third β-strand of the central antiparallel β-sheet of the FReD, forming a hydrogen bond with Asp346, and Asp350 seems to have a negligible effect on the formation of the correct Bβ chain structure.</div></div><div><h3>Conclusion</h3><div>The analyzed variants in the FReD of the fibrinogen Bβ chain seems to have an impact on the proper structure of the fibrinogen-related domain of the fibrinogen Bβ chain.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109521"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145419431","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 : 2025-12-01Epub Date: 2025-11-03DOI: 10.1016/j.thromres.2025.109527
Yingying Li , Jiachen Liu , Lili Luo , Lijuan Zhou , Zhong Wu , Wei Sang , Huiwen Jiang , Jingming Wang , Xindi Wang , Peiru Li , Zhaozhao Chen , Jinhui Shu , Wenjing Luo , Yu Hu , Yuhua Li , Heng Mei
Background
Chimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment of relapsed/refractory (r/r) B-cell acute lymphoblastic leukemia (B-ALL). While CAR-T-associated coagulopathy (CARAC) remains a critical complication, significantly increasing the risk of hemorrhage and disseminated intravascular coagulation (DIC).
Aims
To develop an effective CARAC risk stratification and outcome prediction model.
Methods
This multicenter retrospective study enrolled r/r B-ALL patients who received CD19 CAR-T therapy between January 2016 and July 2025. Machine learning, logistic regression and cutoff values were utilized to select key variables and develop predictive models. Model performance and clinical applicability were evaluated by receiver operating characteristic, calibration, and clinical decision curves. Survival analyses evaluated the impact of CARAC severity on overall survival (OS) and progression-free survival (PFS) and to validate the prognostic value of the prediction model.
Results
Bone marrow (BM) blasts and the modified endothelial activation and stress index (mEASIX) were independent predictors for CARAC. Patients with mEASIX<4.0 were identified as low-risk CARAC. For patients with mEASIX≥4.0, CARAC was stratified by BM blast percentage (blast%). Blast% between 10 % and 44 % indicated high-risk CARAC-nonDIC, and a blast% ≥ 44 % indicated high-risk CARAC-DIC. Moreover, compared to non-CARAC patients, CARAC patients had inferior OS (hazard ratio [HR]: 2.62, p = 0.002) and PFS (HR: 2.11, p = 0.002). The stratified prediction model revealed progressively worse OS and PFS from low-risk CARAC patients to high-risk CARAC-nonDIC, with high-risk CARAC-DIC patients demonstrating the most unfavorable outcomes.
Conclusions
An effective CARAC risk prediction and stratification model was established. High-risk CARAC patients, particularly CARAC-DIC, were associated with significantly worse outcomes.
{"title":"Bone marrow blasts- and modified EASIX-guided risk stratification for coagulopathy and outcomes after CAR-T therapy in relapsed/refractory B-ALL","authors":"Yingying Li , Jiachen Liu , Lili Luo , Lijuan Zhou , Zhong Wu , Wei Sang , Huiwen Jiang , Jingming Wang , Xindi Wang , Peiru Li , Zhaozhao Chen , Jinhui Shu , Wenjing Luo , Yu Hu , Yuhua Li , Heng Mei","doi":"10.1016/j.thromres.2025.109527","DOIUrl":"10.1016/j.thromres.2025.109527","url":null,"abstract":"<div><h3>Background</h3><div>Chimeric antigen receptor (CAR) T-cell therapy has revolutionized the treatment of relapsed/refractory (r/r) B-cell acute lymphoblastic leukemia (B-ALL). While CAR-T-associated coagulopathy (CARAC) remains a critical complication, significantly increasing the risk of hemorrhage and disseminated intravascular coagulation (DIC).</div></div><div><h3>Aims</h3><div>To develop an effective CARAC risk stratification and outcome prediction model.</div></div><div><h3>Methods</h3><div>This multicenter retrospective study enrolled r/r B-ALL patients who received CD19 CAR-T therapy between January 2016 and July 2025. Machine learning, logistic regression and cutoff values were utilized to select key variables and develop predictive models. Model performance and clinical applicability were evaluated by receiver operating characteristic, calibration, and clinical decision curves. Survival analyses evaluated the impact of CARAC severity on overall survival (OS) and progression-free survival (PFS) and to validate the prognostic value of the prediction model.</div></div><div><h3>Results</h3><div>Bone marrow (BM) blasts and the modified endothelial activation and stress index (mEASIX) were independent predictors for CARAC. Patients with mEASIX<4.0 were identified as low-risk CARAC. For patients with mEASIX≥4.0, CARAC was stratified by BM blast percentage (blast%). Blast% between 10 % and 44 % indicated high-risk CARAC-nonDIC, and a blast% ≥ 44 % indicated high-risk CARAC-DIC. Moreover, compared to non-CARAC patients, CARAC patients had inferior OS (hazard ratio [HR]: 2.62, <em>p</em> = 0.002) and PFS (HR: 2.11, p = 0.002). The stratified prediction model revealed progressively worse OS and PFS from low-risk CARAC patients to high-risk CARAC-nonDIC, with high-risk CARAC-DIC patients demonstrating the most unfavorable outcomes.</div></div><div><h3>Conclusions</h3><div>An effective CARAC risk prediction and stratification model was established. High-risk CARAC patients, particularly CARAC-DIC, were associated with significantly worse outcomes.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109527"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145496851","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 : 2025-12-01Epub Date: 2025-10-20DOI: 10.1016/j.thromres.2025.109516
Juliette Hugueny , Anna de Ricolfis , Nicolaï Johnson , Nathalie Chabbert-Buffet , Sarra Cristofari
Objective
This review aimed to synthesize recent data on venous thromboembolism (VTE) risk in the context of masculinizing hormone therapy with testosterone.
Methods
An electronic search was performed in MEDLINE/PubMed without date restrictions. Eligible articles were peer-reviewed observational and interventional studies and had to be written in English. Results are presented by theme of analysis.
Results
Most recent large-scale studies investigating trans masculine populations have not found a statistically significant change in the risk of VTE. However, most of the available data relate to younger individuals with minimal cardiovascular risk factors. For patients with a personal or family history of VTE, the introduction of testosterone therapy should be discussed within a multidisciplinary team specializing in transgender health, balancing the risk-benefit ratio in a population where the risk of suicide is high and is largely reduced by gender-affirming hormone therapy.
Conclusions
Most of the studies did not found a significant change in the risk of venous thromboembolism in trans masculine persons taking testosterone. However, data are limited, and further robust studies are warranted to clarify these data and to generalize these results to higher veinous thromboembolic risk groups.
{"title":"Assessing the risk of venous thromboembolism in trans masculine persons on gender-affirming hormone therapy: A literature review","authors":"Juliette Hugueny , Anna de Ricolfis , Nicolaï Johnson , Nathalie Chabbert-Buffet , Sarra Cristofari","doi":"10.1016/j.thromres.2025.109516","DOIUrl":"10.1016/j.thromres.2025.109516","url":null,"abstract":"<div><h3>Objective</h3><div>This review aimed to synthesize recent data on venous thromboembolism (VTE) risk in the context of masculinizing hormone therapy with testosterone.</div></div><div><h3>Methods</h3><div>An electronic search was performed in MEDLINE/PubMed without date restrictions. Eligible articles were peer-reviewed observational and interventional studies and had to be written in English. Results are presented by theme of analysis.</div></div><div><h3>Results</h3><div>Most recent large-scale studies investigating trans masculine populations have not found a statistically significant change in the risk of VTE. However, most of the available data relate to younger individuals with minimal cardiovascular risk factors. For patients with a personal or family history of VTE, the introduction of testosterone therapy should be discussed within a multidisciplinary team specializing in transgender health, balancing the risk-benefit ratio in a population where the risk of suicide is high and is largely reduced by gender-affirming hormone therapy.</div></div><div><h3>Conclusions</h3><div>Most of the studies did not found a significant change in the risk of venous thromboembolism in trans masculine persons taking testosterone. However, data are limited, and further robust studies are warranted to clarify these data and to generalize these results to higher veinous thromboembolic risk groups.</div></div>","PeriodicalId":23064,"journal":{"name":"Thrombosis research","volume":"256 ","pages":"Article 109516"},"PeriodicalIF":3.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145365189","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}
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