Evidence map›Paper›PMID 39066233›Full record

ArticleViruses2024

IgA Anti-β2-Glycoprotein I Antibodies as Markers of Thrombosis and Severity in COVID-19 Patients.

Susana Mellor-Pita, Pablo Tutor-Ureta, Paula Velasco, Aresio Plaza, Itziar Diego, José Vázquez-Comendador, Ana Paula Vionnet, Pedro Durán-Del Campo, Víctor Moreno-Torres, Juan Antonio Vargas and 1 more

Abstract read
In one paragraph

Article in Viruses, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. 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

11 authors.

Susana Mellor-PitaSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Pablo Tutor-UretaSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Paula VelascoSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Aresio PlazaDepartment of Immunology, Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Itziar DiegoSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.ORCID 0000-0002-3457-8359
José Vázquez-ComendadorSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Ana Paula VionnetDepartment of Immunology, Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Pedro Durán-Del CampoSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Víctor Moreno-TorresSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.ORCID 0000-0002-9798-4514
Juan Antonio VargasSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.
Raquel CastejonSystemic Autoimmune Diseases Unit, Department of Internal Medicine, IDIPHIM (Puerta de Hierro University Hospital Research Institute), Hospital Universitario Puerta de Hierro Majadahonda, 28222 Madrid, Spain.ORCID 0000-0002-9765-0303

Funding

Comunidad de Madrid HealthstartPlus Program, REACT-EU
6 · The paper itself

Abstract

Patients with COVID-19 may develop a hypercoagulable state due to tissue and endothelial injury, produced by an unbalanced immune response. Therefore, an increased number of thromboembolic events has been reported in these patients. The aim of this study is to investigate the presence of antiphospholipid antibodies (aPL) in COVID-19 patients, their role in the development of thrombosis and their relationship with the severity of the disease. In this retrospective study, serum samples from 159 COVID-19 patients and 80 healthy donors were analysed for the presence of aPL. A total of 29 patients (18.2%) and 14 healthy donors (17.5%) were positive for aPL. Nineteen COVID-19 patients (12%) but no healthy donor presented a positive percentage of the IgA isotype aPL. IgA anti-β2-glycoprotein I antibodies (anti-β2GPI) were the most frequent type (6.3%) in patients but was not detected in any healthy donor. The positivity of this antibody was found to be significantly elevated in patients with thromboembolic events (25% vs. 5%,

Indexed as

Antibodies, Antiphospholipidbeta 2-Glycoprotein IBiomarkersCOVID-19Immunoglobulin ASARS-CoV-2Severity of Illness IndexThrombosisAdultAgedAged, 80 and overFemaleHumansMaleMiddle AgedRetrospective StudiesAntibodies, Antiphospholipidbeta 2-Glycoprotein IBiomarkersImmunoglobulin Aantiphospholipid antibodiesCOVID-19severitythrombosis

Identifiers

PMID39066233
PMCPMC11281419

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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.