Evidence map›Paper›PMID 22389132›Full record

ReviewAmerican journal of hematology2012

von Willebrand disease: clinical and laboratory lessons learned from the large von Willebrand disease studies.

Paula D James, David Lillicrap

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 48 citations in OpenAlex.

  1. Von Willebrand disease: A century of progress.Research and practice in thrombosis and haemostasis · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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  10. Article
  11. Article
  12. Article
  13. Thrombosis journal · 2016
    Article
  14. Review
  15. Article
  16. On the versatility of von Willebrand factor.Mediterranean journal of hematology and infectious diseases · 2013
    Article
  17. Von Willebrand Factor Abnormalities Studied in the Mouse Model: What We Learned about VWF Functions.Mediterranean journal of hematology and infectious diseases · 2013
    Article
  18. Article
  19. Review
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

2 authors at 1 institution in 1 country.

Paula D JamesDepartment of Pathology and Molecular Medicine, Queen's University, Kingston, Ontario, Canada K7L 3N6.
David Lillicrap
Queen's University · CA

Funding

Zimmerman Program for the Molecular and Clinical Biology of VWDP01HL081588 · NHLBI · VERSITI WISCONSIN, INC. · PI MONTGOMERY, ROBERT R · 2005 to 2016
$19.3M
CIHR MOP97849NHLBI NIH HHS HL081588NHLBI NIH HHS P01 HL081588
6 · The paper itself

Abstract

During the past 25 years, our knowledge concerning the pathogenesis, diagnostic strategies, and treatment of von Willebrand disease (VWD) has increased significantly. Following the immunological differentiation of factor VIII (FVIII) and von Willebrand factor (VWF) in the 1970s and the cloning of the FVIII and VWF genes in the mid-1980s, substantial progress has been made in our understanding of this, the most common inherited bleeding disorder. We now recognize that VWD represents a range of genetic diseases all with the clinical endpoint of increased mucocutaneous bleeding. The molecular pathology of Type 2 and 3 VWD is now comprehensively documented and involves rare sequence variants at the VWF locus. In contrast, the genetic causation of Type 1 disease remains incompletely defined and in many cases appears to involve genetic determinants in addition to or instead of VWF. The diagnostic triad of a personal history of excessive mucocutaneous bleeding, laboratory tests for VWF that are consistent with VWD, and a family history of the condition remain the keystone to VWD identification. In the laboratory, measurement of VWF antigen and function continue to be the most important diagnostic studies, and while our understanding of the molecular genetic pathology of VWD has advanced considerably in the past decade, genetic testing as a component of diagnosis is limited to certain distinct subtypes of the disorder. Treatment of VWD has been relatively unchanged for the past decade and continues to involve either stimulation of the release of intrinsic VWF with desmopressin or the infusion of VWF concentrates.

Indexed as

von Willebrand DiseasesCloning, MolecularDeamino Arginine VasopressinFactor VIIIGenetic TestingHemorrhageHemostaticsHumansvon Willebrand FactorDeamino Arginine VasopressinFactor VIIIHemostaticsvon Willebrand Factor

Identifiers

PMID22389132
PMCPMC3934369
OpenAlexW1967239210

What OpenQuestion holds

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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.