Evidence map›Paper›PMID 29703532›Full record

ArticleSeminars in arthritis and rheumatism2018

The effect of cigarette smoking on the clinical and serological phenotypes of polymyositis and dermatomyositis.

Adam Schiffenbauer, Sara Faghihi-Kashani, Terrence P O'Hanlon, Willy A Flegel, Sharon D Adams, Ira N Targoff, Chester V Oddis, Steven R Ytterberg, Rohit Aggarwal, Lisa Christopher-Stine and 5 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Seminars in arthritis and rheumatism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 3 pooled it
3.1field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  4. Observational
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  10. Article
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  12. Article
  13. The Genetics of Autoimmune Myositis.Frontiers in immunology · 2022
    Review
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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

15 authors at 8 institutions in 1 country.

Adam SchiffenbauerEnvironmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD. Electronic address: schiffenbauera2@niehs.nih.gov.
Sara Faghihi-KashaniEnvironmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD.
Terrence P O'HanlonEnvironmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD.
Willy A FlegelDepartment of Transfusion Medicine, NIH Clinical Center, National Institutes of Health, Bethesda, MD.
Sharon D AdamsDepartment of Transfusion Medicine, NIH Clinical Center, National Institutes of Health, Bethesda, MD.
Ira N TargoffVeterans Affairs Medical Center, University of Oklahoma Health Sciences Center, Oklahoma Medical Research Foundation, Oklahoma City, OK.
Chester V OddisMyositis Center, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Steven R YtterbergDivision of Rheumatology, Mayo Clinic, Rochester, MN.
Rohit AggarwalMyositis Center, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Lisa Christopher-StineJohns Hopkins Myositis Center, Johns Hopkins University School of Medicine, Baltimore, MD; Departments of Neurology and Medicine, Johns Hopkins University School of Medicine, Baltimore, MD.
Ejaz A ShamimDepartment of Neurology, Mid-Atlantic Permanente Research Institute, Kaiser Permanente, Rockville, MD.
Paul F DellaripaDivision of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA.
Sonye K DanoffDivision of Pulmonary and Critical Care Medicine, Johns Hopkins School of Medicine, Baltimore, MD.
Andrew L MammenDepartments of Neurology and Medicine, Johns Hopkins University School of Medicine, Baltimore, MD; National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD.
Frederick W MillerEnvironmental Autoimmunity Group, National Institute of Environmental Health Sciences, National Institutes of Health, Bethesda, MD.
National Institutes of Health · USJohns Hopkins University · USNational Institutes of Health Clinical Center · USUniversity of Pittsburgh · USBrigham and Women's Hospital · USKaiser Permanente · USMayo Clinic in Arizona · USOklahoma Medical Research Foundation · US

Funding

Intramural NIH HHS Z99 CL999999Intramural NIH HHS Z99 ES999999NULL Z99 ES999999
6 · The paper itself

Abstract

objectiveCigarette smoking is associated with immune-mediated disorders. We explored the contribution of smoking to polymyositis (PM) and dermatomyositis (DM) phenotypes and attempted to determine whether cigarette smoking effects differ by race and genotype.

methodsAssociations of tobacco smoking with disease features, autoantibodies, HLA types, and race were evaluated using multiple logistic regressions in 465 patients.

resultsCaucasian ever-smokers (n = 140) were more likely to have PM (adjusted OR = 2.24, 95% CI: 1.41\x963.57), anti-synthetase (adjusted OR = 1.93, 95% CI: 1.12\x963.34) and anti-Jo-1 autoantibodies (adjusted OR = 1.94, 95% CI: 1.08\x963.46) and less likely to have anti-p155/140 autoantibodies (adjusted OR = 0.36, 95% CI: 0.14\x960.92). In Caucasians, ever-smokers had a greater interstitial lung disease (ILD) frequency than never-smokers, while in African-Americans this relationship was inverted, but neither trend reached statistical significance. Pack-years of cigarette smoking showed significant positive associations with PM (adjusted OR = 1.02, 95% CI: 1.002\x961.04) and ILD (adjusted OR = 1.02, 95% CI: 1.001\x961.03) and was inversely associated with anti-p155/140 autoantibodies (adjusted OR = 0.93, 95% CI: 0.87\x960.99) in Caucasians. Caucasian heavy smokers (=20 pack-years) were more likely to have PM (adjusted OR = 2.52, 95% CI: 1.25\x965.09), ILD (adjusted OR = 2.48, 95% CI: 1.23\x965.00) and anti-Jo-1 autoantibodies (adjusted OR = 2.65, 95% CI: 1.16\x966.08) than never-smokers. In Caucasians, compared to never-smokers without HLA-DRB1*03:01 allele, ever-smokers with HLA-DRB1*03:01 allele had the highest odds of PM, ILD, ASA, and anti-Jo-1 autoantibodies. Risks for those with only one of these two factors were intermediate. An inverse pattern was observed regarding anti-p155/140 autoantibodies.

conclusionTobacco smoking was associated with clinical and autoantibody phenotypes in Caucasians. Our findings also suggest possible interactions among HLA-DRB1*03:01 and smoking on the risk of PM and ILD, as well as, anti-synthetase, anti-Jo-1, and anti-p155/140 autoantibodies in Caucasians.

Indexed as

AdultAutoantibodiesCigarette SmokingDermatomyositisFemaleHumansMaleMiddle AgedPhenotypePolymyositisAutoantibodiesAutoantibodyAutoimmunityCigarette smokingDermatomyositisPolymyositisSmoking

Identifiers

PMID29703532
PMCPMC6133760
OpenAlexW2790161929

What OpenQuestion holds

Textmetadata
LicenceTDM
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.