Evidence map›Paper›PMID 16478847›Full record

ArticleChest2006

Effect of interactions between lower airway bacterial and rhinoviral infection in exacerbations of COPD.

Tom M A Wilkinson, John R Hurst, Wayomi R Perera, Mark Wilks, Gavin C Donaldson, Jadwiga A Wedzicha

Open access · bronzeAbstract read
In one paragraph

Article in Chest, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 5 pooled it
22.7field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 5 syntheses or guidelines pooled it, 315 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Tom M A WilkinsonAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
John R HurstAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Wayomi R PereraAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Mark WilksAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Gavin C DonaldsonAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK.
Jadwiga A WedzichaAcademic Unit of Respiratory Medicine, St. Bartholomew's and the Royal London School of Medicine, St. Bartholomew's Hospital, London, UK. Electronic address: j.a.wedzicha@medsch.ucl.ac.uk.
St Bartholomew's Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STUDY

objectivesThe inflammatory responses and associated clinical severity of COPD exacerbations are greatly variable, and the determinants of these factors are poorly understood. We examined the hypothesis that bacteria and viruses may modulate this heterogeneity and that interactions between bacterial and viral infection may affect changes in airway bacterial load and the clinical features and inflammatory responses of exacerbations in patients with COPD.

designProspective cohort study.

settingOutpatient Department, London Chest Hospital, London, UK. PATIENTS: Thirty-nine patients with COPD. MEASUREMENTS: We prospectively studied 56 COPD exacerbations, obtaining clinical data and paired sputum and serum samples at baseline and exacerbation. Qualitative and quantitative microbiology, polymerase chain reaction detection for rhinovirus, and estimation of cytokine levels by enzyme-linked immunosorbent assay were performed.

resultsA total of 69.6% of exacerbations were associated with a bacterial pathogen, most commonly Haemophilus influenzae. Rhinovirus was identified in 19.6% of exacerbations. The rise in bacterial load at exacerbation correlated with the rise in sputum interleukin (IL)-8 (r = 0.37, p = 0.022) and fall in FEV1 (r = 0.35, p = 0.048). Exacerbations with both rhinovirus and H. influenzae had higher bacterial loads (10(8.56) cfu/mL vs 10(8.05)cfu/mL, p = 0.018) and serum IL-6 (13.75 pg/mL vs 6.29 pg/mL, p = 0.028) than exacerbations without both pathogens. In exacerbations with both cold symptoms (a marker of putative viral infection) and a bacterial pathogen, the FEV1 fall was greater (20.3% vs 3.6%, p = 0.026) and symptom count was higher (p = 0.019) than those with a bacterial pathogen alone.

conclusionsThe clinical severity and inflammatory responses in COPD exacerbations are modulated by the nature of the infecting organism: bacterial and viral pathogens interact to cause additional rises in inflammatory markers and greater exacerbation severity.

Indexed as

AgedBacterial InfectionsCommon ColdFemaleForced Expiratory VolumeHaemophilus InfectionsHaemophilus influenzaeHumansInterleukin-6Interleukin-8MalePicornaviridae InfectionsPulmonary Disease, Chronic ObstructiveRespiratory SystemRespiratory Tract InfectionsRhinovirusInterleukin-6Interleukin-8

Identifiers

PMID16478847
PMCPMC7094441
OpenAlexW2144792692

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.