Evidence map›Paper›PMID 3953768›Full record

ArticleThe American journal of pathology1986

Intraluminal fibrosis in interstitial lung disorders.

F Basset, V J Ferrans, P Soler, T Takemura, Y Fukuda, R G Crystal

Abstract read
In one paragraph

Article in The American journal of pathology, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing 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

68 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?American journal of respiratory and critical care medicine · 2019
    Review
  10. Article
  11. Idiopathic Pulmonary Fibrosis (IPF): An Overview.Journal of clinical medicine · 2018
    Review
  12. Fibrogenic Lung Injury Induces Non-Cell-Autonomous Fibroblast Invasion.American journal of respiratory cell and molecular biology · 2016
    Article
  13. Article
  14. Reduced FoxO3a expression causes low autophagy in idiopathic pulmonary fibrosis fibroblasts on collagen matrices.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  15. Article
  16. Lymphangiogenesis and Lesion Heterogeneity in Interstitial Lung Diseases.Clinical medicine insights. Circulatory, respiratory and pulmonary medicine · 2015
    Review
  17. Review
  18. Review
  19. MicroRNA-96 inhibits FoxO3a function in IPF fibroblasts on type I collagen matrix.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article
  20. miR-210 promotes IPF fibroblast proliferation in response to hypoxia.American journal of physiology. Lung cellular and molecular physiology · 2014
    Article

8 more citing papers are in PubMed but not listed here.

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

6 authors.

F Basset
V J Ferrans
P Soler
T Takemura
Y Fukuda
R G Crystal

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The histopathologic and ultrastructural features of intraluminal organizing and fibrotic changes were studied in open lung biopsies and autopsy specimens from 373 patients with interstitial lung disorders, including hypersensitivity pneumonitis (n = 44), idiopathic pulmonary fibrosis (n = 92), collagen-vascular diseases (n = 20), chronic eosinophilic pneumonia (n = 10), pulmonary histiocytosis X (n-90), pulmonary sarcoidosis (n = 62), pneumoconioses (n = 25), Legionnaire's disease (n = 5), drug- and toxin-induced pneumonitis (n = 4), radiation-induced pneumonitis (n = 2), lymphangioleiomyomatosis (n = 11), and chronic organizing pneumonia of unknown cause (n = 8). Three patterns of intraluminal organization and fibrosis were recognized: 1) intraluminal buds, which partially filled the alveoli, alveolar ducts and/or distal bronchioles; 2) obliterative changes, in which loose connective tissue masses obliterated the lumens of alveoli, alveolar ducts or distal bronchioles, and 3) mural incorporation of previously intraluminal connective tissue masses, which fused with alveolar, alveolar ductal, or bronchiolar structures and frequently became reepithelialized. All three patterns had common morphologic features, suggesting that, regardless of their severity, they resulted from a common pathogenetic mechanism, ie, the migration of activated connective tissue cells, through defects in the epithelial lining and its basement membrane, from the interstitial into the intraluminal compartment. Intraluminal buds were observed most frequently in hypersensitivity pneumonitis, chronic eosinophilic pneumonia, and organizing pneumonia of unknown cause. Mural incorporation and, to a lesser extent, obliterative changes were observed in most interstitial disorders and were very prominent in idiopathic pulmonary fibrosis. Mural incorporation and obliterative changes play an important role in pulmonary remodeling, especially when several adjacent alveoli and/or other air spaces are involved. Under these circumstances, intraluminal organization can mediate the fusion of adjacent alveolar structures by intraluminal connective tissue.

Indexed as

Alveolitis, Extrinsic AllergicConnective TissueExudates and TransudatesHumansLung DiseasesMicroscopy, ElectronPulmonary AlveoliPulmonary FibrosisTime Factors

Identifiers

PMID3953768
PMCPMC1888228

What OpenQuestion holds

Textmetadata
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.