Evidence map›Paper›PMID 37656328›Full record

ArticleGeroScience2024

Distinct subsets of anti-pulmonary autoantibodies correlate with disease severity and survival in severe COVID-19 patients.

Emese Tóth, Miklós Fagyas, Béla Nagy, Ivetta Mányiné Siket, Blanka Szőke, Lilla Mártha, Mohamed Mahdi, Gábor Erdősi, Zsófia Pólik, János Kappelmayer and 9 more

Open access · hybridAbstract read
In one paragraph

Article in GeroScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

19 authors at 1 institution in 1 country.

Emese TóthDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary.
Miklós FagyasDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Béla NagyDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Ivetta Mányiné SiketDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Blanka SzőkeDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Lilla MárthaDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Mohamed MahdiDepartment of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gábor ErdősiDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zsófia PólikDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
János KappelmayerDepartment of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán PappDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Attila BorbélyDivision of Cardiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamás SzabóDepartment of Pediatrics, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
József BallaELKH-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
György BallaELKH-UD Vascular Biology and Myocardial Pathophysiology Research Group, Hungarian Academy of Sciences, Budapest, Hungary.
Attila BácsiDepartment of Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán SzekaneczDepartment of Rheumatology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Péter BaiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, 4032, Debrecen, Hungary. baip@med.unideb.hu.
Attila TóthDivision of Clinical Physiology, Department of Cardiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. atitoth@med.unideb.hu.ORCID 0000-0001-6503-3653
University of Debrecen · HU

Funding

Hungarian Academy of Sciences POST-COVID2021-16Hungarian Academy of Sciences POST-COVID2021-33Hungarian Scientific Research Fund FK135327Hungarian Scientific Research Fund K132623Hungarian Scientific Research Fund K142141Magyar Tudományos Akadémia NKM2022-30National Research, Development and Innovation Office TKP2020-NKA-04National Research, Development and Innovation Office TKP2021-EGA-19National Research, Development and Innovation Office TKP2021-EGA-20NKFIH K147243
6 · The paper itself

Abstract

Autoantibodies targeting the lung tissue were identified in severe COVID-19 patients in this retrospective study. Fifty-three percent of 104 patients developed anti-pulmonary antibodies, the majority of which were IgM class, suggesting that they developed upon infection with SARS-CoV-2. Anti-pulmonary antibodies correlated with worse pulmonary function and a higher risk of multiorgan failure that was further aggravated if 3 or more autoantibody clones were simultaneously present (multi-producers). Multi-producer patients were older than the patients with less or no autoantibodies. One of the identified autoantibodies (targeting a pulmonary protein of ~ 50 kDa) associated with worse clinical outcomes, including mortality. In summary, severe COVID-19 is associated with the development of lung-specific autoantibodies, which may worsen the clinical outcome. Tissue proteome-wide tests, such as the ones applied here, can be used to detect autoimmunity in the post-COVID state to identify the cause of symptoms and to reveal a new target for treatment.

Indexed as

AutoantibodiesCOVID-19HumansLungPatient AcuityRetrospective StudiesSARS-CoV-2AutoantibodiesAutoantibodyClinical outcomeIgGIgMLungMortalityMulti-producerPost-COVIDSARS-CoV-2Severe COVID-19

Identifiers

PMID37656328
PMCPMC10828368
OpenAlexW4386346928

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.