Evidence map›Paper›PMID 32685901›Full record

ArticleResearch and practice in thrombosis and haemostasis2020

Determination of von Willebrand factor level in patient with sickle cell diseasein vaso-occlusive crisis.

Kingsley Akaba, Benedict Nwogoh, Olukayode Oshatuyi

Open access · goldAbstract read
In one paragraph

Article in Research and practice in thrombosis and haemostasis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Contribution of ADAMTS13-independent VWF regulation in sickle cell disease.Journal of thrombosis and haemostasis : JTH · 2022
    Article
  3. 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

3 authors at 3 institutions in 1 country.

Kingsley AkabaDepartment of Haematology University of Calabar Teaching Hospital Calabar Nigeria.ORCID https://orcid.org/0000-0002-4573-1187
Benedict NwogohDepartment of Haematology University of Benin Teaching Hospital Benin Nigeria.
Olukayode OshatuyiDepartment of Biochemistry Ebonyi State University Abakaliki Nigeria.
University of Calabar · NGEbonyi State University · NGUniversity of Benin Teaching Hospital · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSickle cell anemia (SCA) is a hypercoagulable state characterized by a significant alteration in hemostatic parameters that may predispose to increased risk of vaso-occlusive crisis (VOC). The role of von Willebrand factor (VWF) in the pathogenesis of VOC has not been fully investigated in Nigeria.

objectiveThe objective of this study was to evaluate the level of VWF in subjects with sickle cell disease (SCD) in Calabar, Nigeria, to determine its role in the pathogenesis of VOC.

methodsThis was a comparative study carried out at the University of Calabar Teaching Hospital, Calabar, Nigeria. Sixty patients with SCA in VOC and 50 healthy controls were included. VWF levels were measured using Assaypro enzyme-linked immunosorbent assay kits.

resultsThe mean age of patients with SCA in VOC and controls was 23.5 ± 7.2 years and 26.5 ± 5.6 years, respectively. The means (standard deviations) of VWF in patients in VOC and controls were 2.52 ± 0.34 IU/mL and 1.41 ± 0.23 IU/mL, respectively. There was no correlation of hematocrit and VWF in VOC (

conclusionsLevels of VWFare elevated in a VOC state and thus may be implicated in the pathogenesis of VOC.

Indexed as

sickle cell anemiavaso‐occlusive crisisvon Willebrand factor

Identifiers

PMID32685901
PMCPMC7354399
OpenAlexW3041703776

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.