Evidence map›Paper›PMID 25629975›Full record

ArticlePloS one2015

Serum amyloid A is a marker for pulmonary involvement in systemic sclerosis.

Katja Lakota, Mary Carns, Sofia Podlusky, Katjusa Mrak-Poljsak, Monique Hinchcliff, Jungwha Lee, Matija Tomsic, Snezna Sodin-Semrl, John Varga

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Emerging therapeutic targets in systemic sclerosis.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The ubiquitin proteasome system as a potential therapeutic target for systemic sclerosis.Translational research : the journal of laboratory and clinical medicine · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Innate Immunity in Systemic Sclerosis.Current rheumatology reports · 2017
    Review
  15. Article
  16. Review
  17. Role of innate immune system in systemic sclerosis.Seminars in immunopathology · 2015
    Review
  18. 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

9 authors at 3 institutions in 2 countries.

Katja LakotaDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia; Division of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Mary CarnsDivision of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Sofia PodluskyDivision of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Katjusa Mrak-PoljsakDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Monique HinchcliffDivision of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Jungwha LeeDepartment of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Matija TomsicDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia.
Snezna Sodin-SemrlDepartment of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia; University of Primorska, Faculty of Mathematics, Natural Sciences and Information Technology, Koper, Slovenia.
John VargaDivision of Rheumatology, Feinberg School of Medicine, Northwestern University, Chicago, United States of America.
Northwestern University · USLjubljana University Medical Centre · SIUniversity of Primorska · SI

Funding

Northwestern University Clinical and Translational Science Institute (NUCATS)UL1TR001422 · NCATS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI D'AQUILA, RICHARD · 2015 to 2023
$56.8M
REGULATION OF COLLAGEN GENE EXPRESSION BY TGF-BETAR01AR042309 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VARGA, JOHN · 1994 to 2014
$4.4M
Aberrant TLR responses driving organ fibrosis in systemic sclerosisR56AR042309 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VARGA, JOHN · 2018 to 2018
$477k
Predictive Ability of Gene Expression Signatures In Skin as SSc BiomarkersK23AR059763 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HINCHCLIFF, MONIQUE EVANGELINE · 2013 to 2015
$390k
NCATS NIH HHS UL1 TR001422NIAMS NIH HHS AR-42309NIAMS NIH HHS K23 AR059763NIAMS NIH HHS R01 AR042309NIAMS NIH HHS R56 AR042309
6 · The paper itself

Abstract

Inflammation in systemic sclerosis (SSc) is a prominent, but incompletely characterized feature in early stages of the disease. The goal of these studies was to determine the circulating levels, clinical correlates and biological effects of the acute phase protein serum amyloid A (SAA), a marker of inflammation, in patients with SSc. Circulating levels of SAA were determined by multiplex assays in serum from 129 SSc patients and 98 healthy controls. Correlations between SAA levels and clinical and laboratory features of disease were analyzed. The effects of SAA on human pulmonary fibroblasts were studied ex vivo. Elevated levels of SAA were found in 25% of SSc patients, with the highest levels in those with early-stage disease and diffuse cutaneous involvement. Significant negative correlations of SAA were found with forced vital capacity and diffusion capacity for carbon monoxide. Patients with elevated SAA had greater dyspnea and more frequent interstitial lung disease, and had worse scores on patient-reported outcome measures. Incubation with recombinant SAA induced dose-dependent stimulation of IL-6 and IL-8 in normal lung fibroblasts in culture. Serum levels of the inflammatory marker SAA are elevated in patients with early diffuse cutaneous SSc, and correlate with pulmonary involvement. In lung fibroblasts, SAA acts as a direct stimulus for increased cytokine production. These findings suggest that systemic inflammation in SSc may be linked to lung involvement and SAA could serve as a potential biomarker for this complication.

Indexed as

BiomarkersBlood SedimentationCase-Control StudiesC-Reactive ProteinFibroblastsHumansInterleukin-6LungPatient Outcome AssessmentRespiratory Function TestsScleroderma, SystemicSelf ReportSerum Amyloid A ProteinBiomarkersC-Reactive ProteinInterleukin-6Serum Amyloid A Protein

Identifiers

PMID25629975
PMCPMC4321755
OpenAlexW2021050982

What OpenQuestion holds

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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.