Evidence map›Paper›PMID 24815347›Full record

ArticleJournal of thrombosis and haemostasis : JTH2014

Abnormal plasma clot structure and stability distinguish bleeding risk in patients with severe factor XI deficiency.

M Zucker, U Seligsohn, O Salomon, A S Wolberg

Open access · greenAbstract read
In one paragraph

Article in Journal of thrombosis and haemostasis : JTH, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Inhibition of fibrinolysisResearch and practice in thrombosis and haemostasis · 2026
    Article
  3. Observational
  4. Hypoalbuminemia increases fibrin clot density and impairs fibrinolysis.Journal of thrombosis and haemostasis : JTH · 2026
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. TH open : companion journal to thrombosis and haemostasis · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Fibrin(ogen) as a Therapeutic Target: Opportunities and Challenges.International journal of molecular sciences · 2021
    Review
  20. [Congenital factor Ⅺ deficiency: a retrospective analysis of 80 cases].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 3 countries.

M ZuckerThrombosis and Hemostasis Unit, Amalia Biron Research Institute of Thrombosis and Hemostasis, Sheba Medical Center, Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
U Seligsohn
O Salomon
A S Wolberg
Thrombosis Research Institute · GBUniversity of North Carolina at Chapel Hill · US

Funding

Cellular Determinants of Fibrin Structure and StabilityR01HL094740 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WOLBERG, ALISA S. · 2009 to 2013
$1.6M
NHLBI NIH HHS R01 HL094740NHLBI NIH HHS R01HL094740
6 · The paper itself

Abstract

backgroundFactor XI (FXI) deficiency is a rare autosomal recessive disorder. Many patients with even very low FXI levels (< 20 IU dL(-1) ) are asymptomatic or exhibit only mild bleeding, whereas others experience severe bleeding, usually following trauma. Neither FXI antigen nor activity predicts the risk of bleeding in FXI-deficient patients.

objectives(i) Characterize the formation, structure and stability of plasma clots from patients with severe FXI deficiency and (ii) determine whether these assays can distinguish asymptomatic patients ('non-bleeders') from those with a history of bleeding ('bleeders').

methodsPlatelet-poor plasmas were prepared from 16 severe FXI-deficient patients who were divided into bleeders or non-bleeders, based on bleeding associated with at least two tooth extractions without prophylaxis. Clot formation was triggered by recalcification and addition of tissue factor and phospholipids in the absence or presence of tissue plasminogen activator and/or thrombomodulin. Clot formation and fibrinolysis were measured by turbidity and fibrin network structure by laser scanning confocal microscopy.

resultsNon-bleeders and bleeders had similarly low FXI levels, normal prothrombin times, normal levels of fibrinogen, factor VIII, von Willebrand factor and factor XIII, and normal platelet number and function. Compared with non-bleeders, bleeders exhibited lower fibrin network density and lower clot stability in the presence of tissue plasminogen activator. In the presence of thrombomodulin, seven of eight bleeders failed to form a clot, whereas only three of eight non-bleeders did not clot.

conclusionsPlasma clot structure and stability assays distinguished non-bleeders from bleeders. These assays may reveal hemostatic mechanisms in FXI-deficient patients and have clinical utility for assessing the risk of bleeding.

Indexed as

Blood CoagulationAdultAgedCohort StudiesFactor XIFactor XI DeficiencyFactor XIIIFemaleFibrinolysisHemorrhageHumansMaleMicroscopy, ConfocalMiddle AgedPhospholipidsPlasmaFactor XIFactor XIIIPhospholipidsThrombinvon Willebrand Factorbleedingfactor XIfactor XI deficiencyfibrin clot lysis timeplasma clot lysis time

Identifiers

PMID24815347
PMCPMC4107079
OpenAlexW1998485366

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.