Evidence map›Paper›PMID 31819081›Full record

ArticleScientific reports2019

A Gene-Environment Interaction Between Smoking and Gene polymorphisms Provides a High Risk of Two Subgroups of Sarcoidosis.

Natalia V Rivera, Karina Patasova, Susanna Kullberg, Lina Marcela Diaz-Gallo, Tomoko Iseda, Camilla Bengtsson, Lars Alfredsson, Anders Eklund, Ingrid Kockum, Johan Grunewald and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
–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

24 citing papers in PubMed.

  1. Article
  2. Americas Association of Sarcoidosis and other granulomatous disorders 2024 conference highlights.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2025
    Article
  3. Review
  4. Review
  5. Comparison between diffuse and partial involvement of thoracic lymph nodes on the outcome of sarcoidosis patients.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2024
    Article
  6. Article
  7. Review
  8. Epidemiology of Sarcoidosis in U.S. Veterans from 2003 to 2019.Annals of the American Thoracic Society · 2023
    Article
  9. Article
  10. Observational
  11. Article
  12. Article
  13. Genetics of neurosarcoidosis.Journal of neuroimmunology · 2022
    Review
  14. Article
  15. Article
  16. Review
  17. Observational
  18. The intersection of women's health, lung health, and disease.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  19. Epigenetics and sarcoidosis.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  20. 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

11 authors.

Natalia V RiveraDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden. natalia.rivera@ki.se.ORCID http://orcid.org/0000-0002-1298-1243
Karina PatasovaDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Susanna KullbergDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Lina Marcela Diaz-GalloDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Tomoko IsedaDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Camilla BengtssonInstitute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden.
Lars AlfredssonInstitute of Environmental Medicine (IMM), Karolinska Institutet, SE-171 77, Stockholm, Sweden.
Anders EklundDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Ingrid KockumNeuroimmunology Unit, Department of Clinical Neuroscience, Karolinska Institutet, SE-171 76, Stockholm, Sweden.
Johan GrunewaldDivision of Respiratory Medicine, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.
Leonid PadyukovDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, SE-171 76, Stockholm, Sweden.ORCID http://orcid.org/0000-0003-2950-5670

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influence and effect of cigarette smoking in sarcoidosis is unclear. Here, we evaluated gene-environment interaction between multiple genetic variants including HLA genes and smoking in sarcoidosis defined by two clinical phenotypes, Löfgren's syndrome (LS) and patients without Löfgren's syndrome (non-LS). To quantify smoking effects in sarcoidosis, we performed a gene-environment interaction study in a Swedish population-based case-control study consisting of 3,713 individuals. Cases and controls were classified according to their cigarette smoking status and genotypes by Immunochip platform. Gene-smoking interactions were quantified by an additive interaction model using a logistic regression adjusted by sex, age and first two principal components. The estimated attributable proportion (AP) was used to quantify the interaction effect. Assessment of smoking effects with inclusion of genetic information revealed 53 (in LS) and 34 (in non-LS) SNP-smoking additive interactions at false discovery rate (FDR) below 5%. The lead signals interacting with smoking were rs12132140 (AP = 0.56, 95% CI = 0.22-0.90), p = 1.28e-03) in FCRL1 for LS and rs61780312 (AP = 0.62, 95% CI = 0.28-0.90), p = 3e-04) in IL23R for non-LS. We further identified 16 genomic loci (in LS) and 13 (in non-LS) that interact with cigarette smoking. These findings suggest that sarcoidosis risk is modulated by smoking due to genetic susceptibility. Therefore, patients having certain gene variants, are at a higher risk for the disease. Consideration of individual's genetic predisposition is crucial to quantify effects of smoking in sarcoidosis.

Indexed as

Gene-Environment InteractionAdultFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMembrane ProteinsMiddle AgedPhenotypePolymorphism, GeneticPolymorphism, Single NucleotideReceptors, InterleukinSarcoidosisSmokingSwedenFCRL1 protein, humanIL23R protein, humanMembrane ProteinsReceptors, Interleukin

Identifiers

PMID31819081
PMCPMC6901455

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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.