Evidence map›Paper›PMID 32720260›Full record

ReviewClinical rheumatology2020

Concomitant new diagnosis of systemic lupus erythematosus and COVID-19 with possible antiphospholipid syndrome. Just a coincidence? A case report and review of intertwining pathophysiology.

Eduardo Mantovani Cardoso, Jasmin Hundal, Dominique Feterman, John Magaldi

Open access · bronzeAbstract readCase ReportsReview
In one paragraph

Review in Clinical rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 5 pooled it
2.7field-weighted citation impact, top 6% 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

62 citing papers in PubMed, 5 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  6. Trial
  7. Article
  8. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Catastrophic Antiphospholipid Syndrome.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Article
  17. Review
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  20. Article

2 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Eduardo Mantovani CardosoInternal Medicine Residency, University of Connecticut School of Medicine, Farmington, CT, USA. mantovanicardoso@uchc.edu.ORCID http://orcid.org/0000-0003-3353-2831
Jasmin HundalInternal Medicine Residency, University of Connecticut School of Medicine, Farmington, CT, USA.
Dominique FetermanInternal Medicine Residency, University of Connecticut School of Medicine, Farmington, CT, USA.
John MagaldiHartford Hospital, Hartford, CT, USA.
University of Connecticut · USHartford Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the midst of the COVID-19 pandemic, further understanding of its complications points towards dysregulated immune response as a major component. Systemic lupus erythematosus (SLE) is also a disease of immune dysregulation leading to multisystem compromise. We present a case of new-onset SLE concomitantly with COVID-19 and development of antiphospholipid antibodies. An 18-year-old female that presented with hemodynamic collapse and respiratory failure, progressed to cardiac arrest, and had a pericardial tamponade drained. She then progressed to severe acute respiratory distress syndrome, severe ventricular dysfunction, and worsening renal function with proteinuria and hematuria. Further studies showed bilateral pleural effusions, positive antinuclear and antidouble-stranded DNA antibodies, lupus anticoagulant, and anticardiolipin B. C3 and C4 levels were low. SARS-Cov-2 PCR was positive after 2 negative tests. She also developed multiple deep venous thrombosis, in the setting of positive antiphospholipid antibodies and lupus anticoagulant. In terms of pathophysiology, COVID-19 is believed to cause a dysregulated cytokine response which could potentially be exacerbated by the shift in Th1 to Th2 response seen in SLE. Also, it is well documented that viral infections are an environmental factor that contributes to the development of autoimmunity; however, COVID-19 is a new entity, and it is not known if it could trigger autoimmune conditions. Additionally, it is possible that SARS-CoV-2, as it happens with other viruses, might lead to the formation of antiphospholipid antibodies, potentially contributing to the increased rates of thrombosis seen in COVID-19.

Indexed as

AdolescentAnemiaAntibodies, AnticardiolipinAntibodies, AntinuclearAntibodies, Monoclonal, HumanizedAntiphospholipid SyndromeAnuriaBetacoronavirusCardiac TamponadeComplement C3Complement C4Coronavirus InfectionsCOVID-19DNAEchocardiographyFatal OutcomeAntibodies, AnticardiolipinAntibodies, AntinuclearAntibodies, Monoclonal, HumanizedComplement C3Complement C4DNALupus Coagulation InhibitortocilizumabAntiphospholipid syndromeAutoimmunityCOVID-19Cytokine release syndromeSystemic lupus erythematosus

Identifiers

PMID32720260
PMCPMC7384868
OpenAlexW3046068155

What OpenQuestion holds

Textmetadata
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.