Journal of thrombosis and haemostasis : JTH最新文献

{"title":"Management of catheter-related upper extremity deep vein thrombosis in patients with cancer: A systematic review and meta-analysis.","authors":"Tzu-Fei Wang, Roger Kou, M. Carrier, A. Delluc","doi":"10.1182/blood-2023-187817","DOIUrl":"https://doi.org/10.1182/blood-2023-187817","url":null,"abstract":"BACKGROUND Patients with cancer commonly require a central venous catheter, which is associated with an increased risk of venous thromboembolism (VTE). Despite the frequent occurrence, the optimal anticoagulation management and outcomes for patients with cancer and catheter-related upper extremity deep vein thrombosis (DVT) are unclear. OBJECTIVE We performed a systematic review and meta-analysis to evaluate the rates of recurrent VTE and bleeding in patients with cancer and catheter-related upper extremity DVT. METHODS We searched MEDLINE, Embase, Scopus, and CENTRAL from inception to June 2, 2023. The primary efficacy outcome was recurrent VTE, and the primary safety outcome was major bleeding. The incidence rates (with 95% confidence interval [CI]) of outcomes were pooled using random effects model. RESULTS We included 29 studies (N=2,836), among which 5 were prospective. The duration of follow-up and anticoagulation varied considerably. The main long-term anticoagulant used was low-molecular-weight heparin, followed by direct oral anticoagulants. The pooled 3-month recurrent VTE rate from 14 studies (N=1128) was 0.56% (95% CI 0.10-3.01%, I2 = 0%). The pooled 3-month major bleeding rate from 10 studies (N=834) was 2.34% (95% CI 1.14-4.76%, I2 = 0%). We were unable to pool event rates beyond 3 months given high heterogeneity. All studies had serious risk of bias. CONCLUSIONS Our study demonstrated a relatively low rate of recurrent VTE and moderate rate of major bleeding events within the first 3 months in patients with cancer and catheter-related upper extremity DVT. However, there was significant heterogeneity in the management and reporting after 3 months.","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139216498","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extravascular Factor IX pool fed by prophylaxis is a true hemostatic barrier against bleeding.","authors":"Alexandre Leuci, N. Enjolras, Muriel Marano, Melanie Daniel, Marie Brevet, Philippe Connes, Y. Dargaud","doi":"10.1182/blood-2023-179522","DOIUrl":"https://doi.org/10.1182/blood-2023-179522","url":null,"abstract":"BACKGROUND Factor IX (FIX) can bind to type-IV collagen in the endothelial basement membrane and diffuse into extravascular spaces. Previous studies in rodents have reported a large biodistribution of FIX. OBJECTIVE the aim of the study was to evaluate the potential hemostatic activity of extravascular FIX and its role in protecting against joint bleeds. METHODS The capacity of 4 different FIX molecules (plasma derived [pd] and recombinants) to bind type I and type IV collagen was studied here. FIX molecules were also administered intravenously at doses of 50 to 3000 IU/kg in FIX knock-out mice. RESULTS A specific FIX signal was detected in immunohistochemistry in the liver as well as in muscles and knee joints with recombinant FIX molecules injected at 1000 and 3000 IU/kg but not at the usual clinical doses of 50-100 IU/kg, while pdFIX generated a FIX signal at all doses including 50 IU/kg. Such a signal was also detected after five 100 IU/kg daily infusions of rFIX, suggesting that FIX can accumulate in the extravascular space during prophylaxis. The extravascular procoagulant activity of FIX, assessed in saphenous vein bleeding assays, was significantly higher in hemophilia B mice after these five days of prophylaxis compared to a single infusion of FIX 100 IU/kg and assessment of FIX activity seven days later. CONCLUSION Taken together, these results show that in individuals with severe hemophilia B receiving regular prophylaxis with FIX, extravascular accumulation of FIX over time may have a significant impact on the coagulation capacity and protection towards bleeding.","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"57 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139223537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Limited concordance of heparin/PF4 antibody assays for the diagnosis of heparin-induced thrombocytopenia: an analysis of the TORADI-HIT study.","authors":"A. Hammerer-Lercher, H. Nilius, J. Studt, D. Tsakiris, A. Greinacher, Adriana Méndez, A. Schmidt, W. Wuillemin, B. Gerber, J. K. Kremer Hovinga, P. Vishnu, L. Graf, T. Bakchoul, M. Nagler","doi":"10.1055/s-0042-1760496","DOIUrl":"https://doi.org/10.1055/s-0042-1760496","url":null,"abstract":"BACKGROUND\u0000Anecdotal reports suggest that the correlation between heparin/PF4 antibody assays for the diagnosis of heparin-induced thrombocytopenia (HIT) is limited. To address this issue, we investigated the correlation between widely used assays and examined possible factors contributing to variability.\u0000\u0000\u0000METHODS\u0000This is a large, prospective cohort study with 10 participating tertiary care hospitals including 1'393 patients with suspected HIT in clinical practice. HIT was defined by a positive heparin-induced platelet activation assay (HIPA; washed-platelet reference standard test). Three different immunoassays were used to measure heparin/PF4 antibodies: chemiluminescent immunoassay (CLIA), enzyme-linked immunosorbent assay (ELISA), and particle gel immunoassay (PaGIA). Various factors that could influence the assays were examined: sex (male, female), age (< 65 years, ≥ 65 years), unfractionated heparin exposure, presence of thrombosis, cardiovascular surgery, and intensive care unit. Spearman's correlation coefficients were calculated. Z-scores, and diagnostic odds ratios (DOR) were determined in above-mentioned subgroups of patients.\u0000\u0000\u0000RESULTS\u0000Among 1,393 patients, 119 were classified as HIT positive (prevalence 8.5%). The median 4Ts score was 5 in patients with HIT (interquartile range, IQR, 4-6), compared to 3 in patients without (IQR 2-4). Correlations (rs) between immunoassays were weak (0.53 to 0.65). Inconsistencies between immunoassays could not be explained by further analyses of z-scored test results and DOR in subgroups of patients.\u0000\u0000\u0000CONCLUSIONS\u0000The correlation between widely used heparin/PF4 antibody assays was weak and key factors could not explain this variability. Standardization of immunoassays is requested to improve comparability.","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"49 32","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"113934111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Von-Willebrand factor antigen: a biomarker for severe pregnancy complications in women with hereditary TTP?","authors":"Sharon Davidesko, O. Pikovsky, K. Al-Athamen, R. Hackmon, O. Erez, Shayna Miodownik, A. Rabinovich","doi":"10.1016/j.ajog.2021.11.582","DOIUrl":"https://doi.org/10.1016/j.ajog.2021.11.582","url":null,"abstract":"","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133670612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-9 contributes to the developmental differences in CXCR-4 expression in human megakaryocytes.","authors":"F Ferrer-Marin,&nbsp;R Gutti,&nbsp;Z-J Liu,&nbsp;M Sola-Visner","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":" ","pages":"282-5"},"PeriodicalIF":10.4,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32266138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-factor IXa/X bispecific antibody (ACE910): hemostatic potency against ongoing bleeds in a hemophilia A model and the possibility of routine supplementation.","authors":"A Muto,&nbsp;K Yoshihashi,&nbsp;M Takeda,&nbsp;T Kitazawa,&nbsp;T Soeda,&nbsp;T Igawa,&nbsp;Y Sakamoto,&nbsp;K Haraya,&nbsp;Y Kawabe,&nbsp;M Shima,&nbsp;A Yoshioka,&nbsp;K Hattori","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>We previously reported that a humanized anti-factor IXa/X bispecific antibody, hBS23, mimics the function of FVIII even in the presence of FVIII inhibitors, and has preventive hemostatic activity against bleeding in an animal model of acquired hemophilia A. After further molecular engineering of hBS23, we recently identified an improved humanized bispecific antibody, ACE910, for clinical investigation.</p><p><strong>Objectives: </strong>To elucidate the in vivo hemostatic potency of ACE910 by examining its effect against ongoing bleeds, and to determine its pharmacokinetic parameters for discussion of its potency for prophylactic use.</p><p><strong>Methods: </strong>A nonhuman primate model of acquired hemophilia A was established by injecting anti-primate FVIII neutralizing antibody. When bleeds emerged following an artificial bleed-inducing procedure, either ACE910 or recombinant porcine FVIII (rpoFVIII) was intravenously administered. rpoFVIII was additionally administered twice daily on the following 2 days. Bleeding symptoms were monitored for 3 days. A pharmacokinetic study and multiple-dosing simulations of ACE910 were also performed.</p><p><strong>Results: </strong>A single bolus of 1 or 3 mg kg⁻¹ ACE910 showed hemostatic activity comparable to that of 10 U kg⁻¹ (twice daily) rpoFVIII against ongoing bleeds. The determined ACE910 pharmacokinetic parameters included a long half-life (3 weeks) and high subcutaneous bioavailability (nearly 100%). The simulation results based on pharmacokinetic parameters indicated that the above hemostatic level could be maintained with once-weekly subcutaneous administration of ACE910, suggesting the possibility of more effective prophylaxis.</p><p><strong>Conclusions: </strong>ACE910 may offer an alternative on-demand treatment option for patients with hemophilia A, as well as user-friendly and aggressive routine supplementation.</p>","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":" ","pages":"206-13"},"PeriodicalIF":10.4,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32266136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-coupled receptor kinase 2 moderates recruitment of THP-1 cells to the endothelium by limiting histamine-invoked Weibel-Palade body exocytosis.","authors":"N L Stevenson, B Martin-Martin, J Freeman, J Kriston-Vizi, R Ketteler, D F Cutler","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>G protein-coupled receptors (GP-CRs) are a major family of signaling molecules, central to the regulation of inflammatory responses. Their activation upon agonist binding is attenuated by GPCR kinases (GRKs), which desensitize the receptors through phosphorylation. G protein-coupled receptor kinase 2(GRK2) down-regulation in leukocytes has been closely linked to the progression of chronic inflammatory disorders such as rheumatoid arthritis and multiple sclerosis. Because leukocytes must interact with the endothelium to infiltrate inflamed tissues, we hypothesized that GRK2 down-regulation in endothelial cells would also be pro-inflammatory.</p><p><strong>Objectives: </strong>To determine whether GRK2 down-regulation in endothelial cells is pro-inflammatory.</p><p><strong>Methods: </strong>siRNA-mediated ablation of GRK2 in human umbilical vein endothelial cells (HUVECs) was used in analyses of the role of this kinase. Microscopic and biochemical analyses of Weibel-Palade body (WPB) formation and functioning, live cell imaging of calcium concentrations and video analyses of adhesion of monocyte-like THP-1 cells provide clear evidence of GRK2 function in histamine activation of endothelial cells.</p><p><strong>Results: </strong>G protein-coupled receptor kinase 2 depletion in HUVECs increases WPB exocytosis and P-selectin-dependent adhesion of THP-1 cells to the endothelial surface upon histamine stimulation, relative to controls. Further, live imaging of intracellular calcium concentrations reveals amplified histamine receptor signaling in GRK2-depleted cells, suggesting GRK2 moderates WPB exocytosis through receptor desensitization.</p><p><strong>Conclusions: </strong>G protein-coupled receptor kinase 2 deficiency in endothelial cells results in increased pro-inflammatory signaling and enhanced leukocyte recruitment to activated endothelial cells. The ability of GRK2 to modulate initiation of inflammatory responses in endothelial cells as well as leukocytes now places GRK2 at the apex of control of this finely balanced process.</p>","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":" ","pages":"261-72"},"PeriodicalIF":0.0,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32266137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk assessment of venous thrombosis in families with known hereditary thrombophilia: the MARseilles-NImes prediction model.","authors":"W Cohen,&nbsp;C Castelli,&nbsp;P Suchon,&nbsp;S Bouvet,&nbsp;M F Aillaud,&nbsp;D Brunet,&nbsp;M C Barthet,&nbsp;M C Alessi,&nbsp;D A Trégouët,&nbsp;P E Morange","doi":"","DOIUrl":"","url":null,"abstract":"<p><strong>Background: </strong>Although predicting the risk of venous thrombosis (VT) in an individual from a family with inherited thrombophilia is of major importance, it is often not feasible.</p><p><strong>Objectives: </strong>To develop a simple risk assessment model that improves prediction of the risk of VT for individuals of families with inherited thrombophilia.</p><p><strong>Patients/methods: </strong>1201 relatives from 430 families with inherited thrombophilia (deficiencies of antithrombin, protein C or protein S, and the factor V Leiden and F2 20210A mutations) were recruited at the referral center for thrombophilia in Marseilles, France, from 1986 to 2008. One hundred and twenty-two individuals had a personal history of VT. Sixteen preselected clinical and laboratory variables were used to derive the VT risk score.</p><p><strong>Results: </strong>The scores based on the 16 variables and on the five most strongly associated variables performed similarly (areas under receiver operating characteristic curves of 0.85 and 0.83, respectively). For the five-variable score, named the MARNI score, derived from family history score of VT, von Willebrand factor antigen levels, age, severity of thrombophilia, and FGG rs2066865, the risk of VT ranged from 0.2% for individuals with a score of 0 (n = 186) to > 70% for individuals with a score of ≥ 7 (n = 27). The model was validated with an internal bootstrap method.</p><p><strong>Conclusions: </strong>With the use of a simple scoring system, assessment of the risk of VT in subjects from families with inherited thrombophilia can be greatly improved. External validation is now needed to replicate these findings.</p>","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":" ","pages":"138-46"},"PeriodicalIF":10.4,"publicationDate":"2014-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32267539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The active metabolite of prasugrel inhibits adenosine diphosphate- and collagen-stimulated platelet procoagulant activities.","authors":"A. Frelinger, J. Jakubowski, Y. Li, M. Barnard, M. Linden, I. Tarnow, M. Fox, A. Sugidachi, K. Winters, M. Furman, A. Michelson","doi":"10.1111/J.1538-7836.2007.02838.X","DOIUrl":"https://doi.org/10.1111/J.1538-7836.2007.02838.X","url":null,"abstract":"BACKGROUND\u0000Prasugrel is a novel antiplatelet prodrug of the same thienopyridine class as clopidogrel and ticlopidine. Metabolism of prasugrel generates the active metabolite R-138727, an antagonist of the platelet P2Y(12) adenosine diphosphate (ADP) receptor, leading to inhibition of ADP-mediated platelet activation and aggregation. ADP also enhances the platelet response to collagen, and these two agonists contribute to the generation of platelet procoagulant activity. We therefore examined whether R-138727 inhibits ADP- and collagen-triggered platelet procoagulant activities.\u0000\u0000\u0000METHODS AND RESULTS\u0000As shown by whole blood flow cytometry, R-138727 inhibited surface phosphatidylserine expression on ADP plus collagen-stimulated platelets and tissue factor (TF) expression on ADP-, collagen-, and ADP plus collagen-stimulated monocyte-platelet aggregates. R-138727 reduced monocyte-platelet aggregate formation, thereby further inhibiting TF expression. ADP, collagen, and ADP plus collagen accelerated the kinetics of thrombin generation in recalcified whole blood and R-138727 significantly inhibited this acceleration. Clot strength in a modified thromboelastograph system was also inhibited by R-138727 (IC50 0.7 +/- 0.1 microM).\u0000\u0000\u0000CONCLUSIONS\u0000In addition to its previously known inhibitory effects on platelet activation and aggregation, the active metabolite of prasugrel, R-138727, inhibits platelet procoagulant activity in whole blood (as determined by phosphatidylserine expression on platelets and TF expression on monocyte-platelet aggregates), resulting in the functional consequences of delayed thrombin generation and impaired clot development.","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"141 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115902277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The international normalized ratio to prioritize patients for liver transplantation: problems and possible solutions.","authors":"A. Tripodi, V. Chantarangkul, P. Mannucci","doi":"10.1111/J.1538-7836.2007.02827.X","DOIUrl":"https://doi.org/10.1111/J.1538-7836.2007.02827.X","url":null,"abstract":"The prothrombin time (PT) test once designed by Dr Quick to investigate patients with obstructive jaundice was later adapted and standardized by means of the international normalized ratio (INR) to monitor patients on treatment with vitamin K antagonists (VKA). After more than 70 years from its introduction it is now time to think about its standardization for those very patients for whom it was intended at the beginning of its history. Two studies carried out independently and published recently in the same issue of a specialized journal do exploit the very same idea on how to accomplish this standardization. Both of them confirm previous anecdotal observations that the INR as devised for patients on VKA (INR(vka)) is not valid to harmonize PT results for patients with chronic liver disease. This fact, that at first sight may appear academic, has important consequences because the PT INR is used to construct the model for end-stage liver disease (MELD) scores, which is widely used to prioritize patients for liver transplantation. The two studies further demonstrate that an alternative calibration model, modified from that recommended by the World Health Organization for patients on VKA, may be feasible also for patients with chronic liver disease. This alternative calibration model, which calls for the substitution of plasmas from patients on VKA with those from patients with chronic liver disease, may be highly beneficial to harmonize the calculation of the MELD score, with important implications for the prioritization of patients for liver transplantation.","PeriodicalId":161374,"journal":{"name":"Journal of thrombosis and haemostasis : JTH","volume":"9 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2008-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127027731","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}