Evidence map›Paper›PMID 34677484›Full record

ArticleMedicines (Basel, Switzerland)2021

Autoimmune Disorders & COVID-19.

Leonardo Freire-de-Lima, Aline Miranda Scovino, Camilla Cristie Barreto Menezes, Leonardo Marques da Fonseca, Jhenifer Santos Dos Reis, Marcos André Rodrigues da Costa Santos, Kelli Monteiro da Costa, Carlos Antonio do Nascimento Santos, Celio Geraldo Freire-de-Lima, Alexandre Morrot

Open access · goldAbstract read
In one paragraph

Article in Medicines (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. 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

10 authors at 2 institutions in 1 country.

Leonardo Freire-de-LimaInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.ORCID 0000-0003-3013-3173
Aline Miranda ScovinoInstituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Camilla Cristie Barreto MenezesInstituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro 21040-360, Brazil.
Leonardo Marques da FonsecaInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Jhenifer Santos Dos ReisInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Marcos André Rodrigues da Costa SantosInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Kelli Monteiro da CostaInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Carlos Antonio do Nascimento SantosInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.
Celio Geraldo Freire-de-LimaInstituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-170, Brazil.ORCID 0000-0002-4148-3657
Alexandre MorrotInstituto Oswaldo Cruz, FIOCRUZ, Rio de Janeiro 21040-360, Brazil.
Universidade Federal do Rio de Janeiro · BRFundação Oswaldo Cruz · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) can progress to severe pneumonia with respiratory failure and is aggravated by the deregulation of the immune system causing an excessive inflammation including the cytokine storm. Since 2019, several studies regarding the interplay between autoimmune diseases and COVID-19 infections is increasing all over the world. In addition, thanks to new scientific findings, we actually know better why certain conditions are considered a higher risk in both situations. There are instances when having an autoimmune disease increases susceptibility to COVID-19 complications, such as when autoantibodies capable of neutralizing type I IFN are present, and other situations in which having COVID-19 infection precedes the appearance of various autoimmune and autoinflammatory diseases, including multisystem inflammatory syndrome in children (MIS-C), Guillain-Barré syndrome, and Autoimmune haemolytic anaemia (AIHA), thus, adding to the growing mystery surrounding the SARS-CoV-2 virus and raising questions about the nature of its link with autoimmune and autoinflammatory sequelae. Herein, we discuss the role of host and virus genetics and some possible immunological mechanisms that might lead to the disease aggravation.

Indexed as

autoimmunitycoronavirus disease 19immune systemviral infections

Identifiers

PMID34677484
PMCPMC8541336
OpenAlexW3203684100

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.