Evidence map›Paper›PMID 22683422›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2012

The clinical and immunologic features of pulmonary fibrosis in sarcoidosis.

Karen C Patterson, Kyle Hogarth, Aliya N Husain, Anne I Sperling, Timothy B Niewold

Abstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.5field-weighted citation impact, top 18% 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, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Sarcoidosis-associated pulmonary fibrosis: joining the dots.European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  4. Pulmonary fibrosis in sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2023
    Article
  5. Review
  6. Article
  7. Emerging insights in sarcoidosis: moving forward through reverse translational research.American journal of physiology. Lung cellular and molecular physiology · 2022
    Review
  8. The ability to predict the clinical course of pulmonary sarcoidosis from data that is right in front of us.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Potential immunotherapies for sarcoidosis.Expert opinion on biological therapy · 2018
    Review
  14. Identification of apolipoprotein A-I in BALF as a biomarker of sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2018
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  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

5 authors at 1 institution in 1 country.

Karen C PattersonSection of Pulmonary and Critical Care, University of Chicago, Chicago, Ill. karenpatterson100@gmail.com
Kyle Hogarth
Aliya N Husain
Anne I Sperling
Timothy B Niewold
University of Chicago · US

Funding

Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
Genetic Regulation of interferon Alpha in Human LupusK08AI083790 · NIAID · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2009 to 2013
$616k
NIAID NIH HHS K08 AI083790NIAID NIH HHS L30 AI071651NIAMS NIH HHS R01 AR060861
6 · The paper itself

Abstract

Sarcoidosis is a multisystem, granulomatous disease that most often affects the lungs. The clinical course is highly variable; many patients undergo spontaneous remission, but up to a third of patients progresses to a chronic disease course. The development of pulmonary fibrosis (PF) in a subset of patients with chronic disease has a negative impact on morbidity and mortality. While sarcoidosis-associated PF can be progressive, it is often referred to as "burnt out" disease, a designation reflecting inactive granulomatous inflammation. The immune mechanisms of sarcoidosis-associated PF are not well understood. It is not clear if fibrotic processes are active from the onset of sarcoidosis in predisposed individuals, or whether a profibrotic state develops as a response to ongoing inflammation. Transforming growth factor β (TGF-β) is an important profibrotic cytokine, and in sarcoidosis, distinct genotypes of TGF-β have been identified in those with PF. The overall cytokine profile in sarcoidosis-associated PF has not been well characterized, although a transition from a T helper 1 to a T helper 2 signature has been proposed. Macrophages have important regulatory interactions with fibroblasts, and the role of alveolar macrophages in sarcoidosis-associated PF is a compelling target for further study. Elucidating the natural history of sarcoidosis-associated PF will inform our understanding of the fundamental derangements, and will enhance prognostication and the development of therapeutic strategies.

Indexed as

CytokinesDisease ProgressionHumansLungPulmonary FibrosisRadiographySarcoidosis, PulmonaryCytokines

Identifiers

PMID22683422
PMCPMC3910531
OpenAlexW2122322821

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.