Evidence map›Paper›PMID 20534161›Full record

ArticleJournal of inflammation (London, England)2010

Smoking status and tumor necrosis factor-alpha mediated systemic inflammation in COPD patients.

Suzana E Tanni, Nilva Rg Pelegrino, Aparecida Yo Angeleli, Camila Correa, Irma Godoy

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 3 pooled it
7.2field-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

51 citing papers in PubMed, 3 syntheses or guidelines pooled it, 122 citations in OpenAlex.

  1. Pooled it
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  3. Association between TNF-α -308 G/A polymorphism and COPD susceptibility: a meta-analysis update.International journal of chronic obstructive pulmonary disease · 2016
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  20. What are the factors associated with sarcopenia-related variables in adult women with severe obesity?Archives of public health = Archives belges de sante publique · 2020
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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.

Suzana E Tanni *Department of Internal Medicine, Pulmonology Division, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Nilva Rg Pelegrino *Department of Internal Medicine, Pulmonology Division, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Aparecida Yo Angeleli *Department of Internal Medicine, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Camila Correa *Department of Internal Medicine, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Irma Godoy *Department of Internal Medicine, Pulmonology Division, Botucatu Medical School. UNESP (Paulista State University). Distrito de Rubião Júnior, s/n. Botucatu, 18618-000, SP, Brazil.
Universidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmoking cause airway and systemic inflammation and COPD patients present low grade inflammation in peripheral blood. However, data on the influence of smoking itself on systemic inflammation in COPD patients are scarce. This study investigated the association between inflammation, smoking status, and disease.

methodsA cross-sectional analysis comparing 53 COPD ex-smokers, 24 COPD current smokers, 24 current smoker controls and 34 never-smoker controls was performed. Assessments included medical history, body composition, spirometry, and plasma concentration of tumor necrosis factor-alpha (TNF-alpha), interleukins (IL)-6, IL-8, and C-reactive protein (CRP).

resultsOur exploratory analysis showed that serum TNF-alpha was higher in COPD current smokers [4.8(4.2-5.8)pg/mL] and in current smoker controls [4.8 (4.2-6.1) pg/mL] when compared to COPD ex-smokers [4.3 (3.9-4.9)pg/mL; p = 0.02] and to never-smoker controls [3.7 (3.4-4.0)pg/mL; p < 0.001]. Multiple regression results with and without adjustment for covariates were consistent with the hypothesis that TNF-alpha levels were associated with smoking status in both models (p < 0.001 and p < 0.001). IL-6 and CRP were significantly higher in COPD patients when compared to smoker and never-smoker controls and the multiple regression analysis confirmed the association of these mediators with disease, but not with smoking status (p < 0.001 and p < 0.001). IL-8 had only a borderline association with disease in both models (p = 0.069 and p = 0.053). No influence of disease severity, inhaled corticosteroid, fat-free mass (FFM) depletion and long term oxygen therapy (LTOT) use on systemic inflammation was found.

conclusionSmoking may influence TNF-alpha mediated systemic inflammation, which, in turn, may account for some of the benefits observed in patients with COPD who stop smoking.

Identifiers

PMID20534161
PMCPMC2891738
OpenAlexW2110146694

What OpenQuestion holds

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Registered trials

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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.