Evidence map›Paper›PMID 29895622›Full record

ArticleBlood advances2018

Prothrombin conversion is accelerated in the antiphospholipid syndrome and insensitive to thrombomodulin.

Romy M W Kremers, Stéphane Zuily, Hilde Kelchtermans, Tessa C Peters, Saartje Bloemen, Véronique Regnault, H Coenraad Hemker, Philip G de Groot, Denis Wahl, Bas de Laat

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  4. Review
  5. How We Interpret Thrombosis with Thrombocytopenia Syndrome?International journal of molecular sciences · 2024
    Review
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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

10 authors at 3 institutions in 3 countries.

Romy M W KremersSynapse Research Institute and.ORCID 0000-0001-6526-0338
Stéphane ZuilyVascular Medicine Division, Centre Hospitalier Régional Universitaire de Nancy, Nancy, France.
Hilde KelchtermansSynapse Research Institute and.
Tessa C PetersSynapse Research Institute and.
Saartje BloemenSynapse Research Institute and.ORCID 0000-0003-3297-8196
Véronique RegnaultVascular Medicine Division, Centre Hospitalier Régional Universitaire de Nancy, Nancy, France.
H Coenraad HemkerDepartment of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands; and.ORCID 0000-0003-1669-2358
Philip G de GrootSynapse Research Institute and.
Denis WahlVascular Medicine Division, Centre Hospitalier Régional Universitaire de Nancy, Nancy, France.
Bas de LaatSynapse Research Institute and.
Maastricht University · NLCentre Hospitalier Régional et Universitaire de Nancy · FRSynapse Biomedical (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antiphospholipid syndrome (APS) is a condition in which the presence of antibodies against phospholipid-binding proteins is associated with thrombophilia and/or pregnancy morbidity. Although antiphospholipid antibodies have anticoagulant characteristics in vitro, they are associated with thromboembolic complications. Thrombin generation (TG) is a sensitive global test of coagulation, and elevated TG is associated with thrombosis. Increased TG can be caused by increased prothrombin conversion, decreased thrombin inactivation, or a combination of both. In this study, we measured TG in APS patients and healthy controls with and without vitamin K antagonist (VKA) treatment at 1 and 5 pM tissue factor and with thrombomodulin. Prothrombin conversion and thrombin inactivation were determined by thrombin dynamics analysis. The TG peak was increased in nontreated APS patients at 1 pM TF compared with nontreated controls. Prothrombin conversion was significantly increased in nontreated APS patients. In contrast, prothrombin conversion did not differ in controls and patients that were on VKA therapy. Thrombin inactivation was comparable between controls and APS patients in the presence and absence of VKAs. Both TG (peak and ETP) and prothrombin conversion were significantly higher in APS patients with prior thrombosis compared with patients without a history of thrombosis. In this study, we demonstrate that in APS, the hemostatic balance shifts toward a more prothrombotic phenotype due to elevated prothrombin conversion but unchanged thrombin inactivation rates. Within the group of APS patients, increased TG and prothrombin conversion are associated with a history of thrombosis.

Indexed as

AdultAntiphospholipid SyndromeFemaleHumansMaleMiddle AgedProthrombinThrombomodulinThrombosisVitamin KProthrombinTHBD protein, humanThrombomodulinVitamin K

Identifiers

PMID29895622
PMCPMC5998936
OpenAlexW2808392656

What OpenQuestion holds

Textmetadata
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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.