Evidence map›Paper›PMID 23951234›Full record

ArticlePloS one2013

Human hemorrhagic pulmonary leptospirosis: pathological findings and pathophysiological correlations.

Thales De Brito, Vera Demarchi Aiello, Luis Fernando Ferraz da Silva, Ana Maria Gonçalves da Silva, Wellington Luiz Ferreira da Silva, Jussara Bianchi Castelli, Antonio Carlos Seguro

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

21 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Frontiers in molecular biosciences · 2022
    Article
  5. PathogenicFrontiers in microbiology · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. A simple score to predict severe leptospirosis.PLoS neglected tropical diseases · 2019
    Article
  10. Pathology and pathogenesis of human leptospirosis: a commented review.Revista do Instituto de Medicina Tropical de Sao Paulo · 2018
    Review
  11. Article
  12. Article
  13. Article
  14. Frontiers in cellular and infection microbiology · 2017
    Article
  15. Frontiers in microbiology · 2017
    Article
  16. Article
  17. High frequency oscillatory ventilation in leptospirosis pulmonary hemorrhage syndrome: A case series study.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2016
    Review
  18. Article
  19. Article
  20. Observational
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Thales De BritoInstitute of Tropical Medicine, São Paulo University Medical School, São Paulo, Brazil. thalesbr@usp.br
Vera Demarchi Aiello
Luis Fernando Ferraz da Silva
Ana Maria Gonçalves da Silva
Wellington Luiz Ferreira da Silva
Jussara Bianchi Castelli
Antonio Carlos Seguro
Universidade de São Paulo · BRBrazilian Society of Tropical Medicine · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLeptospirosis is a re-emerging zoonosis with protean clinical manifestations. Recently, the importance of pulmonary hemorrhage as a lethal complication of this disease has been recognized. In the present study, five human necropsies of leptospirosis (Weil's syndrome) with extensive pulmonary manifestations were analysed, and the antibodies expressed in blood vessels and cells involved in ion and water transport were used, seeking to better understand the pathophysiology of the lung injury associated with this disease. PRINCIPAL

findingsProminent vascular damage was present in the lung microcirculation, with decreased CD34 and preserved aquaporin 1 expression. At the periphery and even inside the extensive areas of edema and intraalveolar hemorrhage, enlarged, apparently hypertrophic type I pneumocytes (PI) were detected and interpreted as a non-specific attempt of clearence of the intraalveolar fluid, in which ionic transport, particularly of sodium, plays a predominant role, as suggested by the apparently increased ENaC and aquaporin 5 expression. Connexin 43 was present in most pneumocytes, and in the cytoplasm of the more preserved endothelial cells. The number of type II pneumocytes (PII) was slightly decreased when compared to normal lungs and those of patients with septicemia from other causes, a fact that may contribute to the progressively low PI count, resulting in deficient restoration after damage to the alveolar epithelial integrity and, consequently, a poor outcome of the pulmonary edema and hemorrhage.

conclusionsPathogenesis of lung injury in human leptospirosis was discussed, and the possibility of primary non-inflammatory vascular damage was considered, so far of undefinite etiopathogenesis, as the initial pathological manifestation of the disease.

Indexed as

AdultAgedAged, 80 and overAlveolar Epithelial CellsBlood VesselsCase-Control StudiesConnexin 43Epithelial Sodium ChannelsFemaleHumansImmunohistochemistryLungLung DiseasesMaleMicrocirculationMicroscopy, ConfocalConnexin 43Epithelial Sodium Channels

Identifiers

PMID23951234
PMCPMC3741125
OpenAlexW2135900330

What OpenQuestion holds

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LicenceCC BY
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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.