Evidence map›Paper›PMID 35317658›Full record

ReviewClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis

The Pathophysiology of The Antiphospholipid Syndrome: A Perspective From The Blood Coagulation System.

R Arreola-Diaz, A Majluf-Cruz, L E Sanchez-Torres, J Hernandez-Juarez

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

35 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. C4b-binding protein as an antigenic target in the pathogenesis of antiphosphatidylethanolamine autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  7. Cardiac Involvement in Systemic Lupus Erythematosus.Reviews in cardiovascular medicine · 2025
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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

4 authors at 3 institutions in 1 country.

R Arreola-DiazDepartamento de Inmunologia, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, Ciudad de Mexico, Mexico.
A Majluf-CruzUnidad de Investigacion Medica en Trombosis, Hemostasia y Aterogenesis, Instituto Mexicano del Seguro Social, Ciudad de Mexico, Mexico.
L E Sanchez-TorresDepartamento de Inmunologia, Escuela Nacional de Ciencias Biologicas, Instituto Politecnico Nacional, Ciudad de Mexico, Mexico.
J Hernandez-JuarezCONACyT-Facultad de Odontologia, Universidad Autonoma Benito Juarez de Oaxaca, Oaxaca de Juarez, Mexico.ORCID https://orcid.org/0000-0002-5505-1097
Instituto Politécnico Nacional · MXBenito Juárez Autonomous University of Oaxaca · MXMexican Social Security Institute · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The antiphospholipid syndrome (APS), a systemic autoimmune disease characterized by a hypercoagulability associated to vascular thrombosis and/or obstetric morbidity, is caused by the presence of antiphospholipid antibodies such as lupus anticoagulant, anti-β-2-glycoprotein 1, and/or anticardiolipin antibodies. In the obstetrical APS, antiphospholipid antibodies induce the production of proinflammatory cytokines and tissue factor by placental tissues and recruited neutrophils. Moreover, antiphospholipid antibodies activate the complement system which, in turn, induces a positive feedback leading to recruitment of neutrophils as well as activation of the placenta. Activation of these cells triggers myometrial contractions and cervical ripening provoking the induction of labor. In thrombotic and obstetrical APS, antiphospholipid antibodies activate endothelial cells, platelets, and neutrophils and they may alter the multimeric pattern and concentration of von Willebrand factor, increase the concentration of thrombospondin 1, reduce the inactivation of factor XI by antithrombin, increase the activation of factor XII, and reduce the activity of tissue plasminogen activator with the subsequent production of plasmin. All these effects result in less permeable clots, denser, thinner, and with more branched fibrin fibers which are more difficult to lysate. As a consequence, thrombosis, the defining clinical criterion of APS, complicates the clinical course of the patient.

Indexed as

Antiphospholipid SyndromeTissue Plasminogen ActivatorBlood CoagulationEndothelial CellsFemaleHumansPlacentaPregnancyTissue Plasminogen Activatorantiphospholipid syndromeautoantibodiesautoimmunitymiscarriagethrombosis

Identifiers

PMID35317658
PMCPMC8950029
OpenAlexW4221090489

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.