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Vol. 44. Issue 1.
Pages 8-14 (January 2008)
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Vol. 44. Issue 1.
Pages 8-14 (January 2008)
Original Articles
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Association Between Bronchiectasis, Systemic Inflammation, and Tumor Necrosis Factor α
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Miguel Ángel Martínez-Garcíaa,
Corresponding author
miangel@comv.es

Correspondence: Dr. M.A. Martínez-García Unidad de Neumología, Hospital General de Requena Paraje Casa Blanca, s/n. 43230 Requena, Valencia, España
, Miquel Perpiñá-Torderab, Pilar Román-Sánchezc, Juan José Soler-Cataluñaa, Arturo Carratalád, Martín Yagod, María José Pastord
a Unidad de Neumología, Hospital General de Requena, Requena, Valencia, Spain
b Servicio de Neumología, Hospital Universitario La Fe, Valencia, Spain
c Servicio de Medicina Interna, Hospital General de Requena, Requena, Valencia, Spain
d Servicio de Laboratorio, Hospital General de Requena, Requena, Valencia, Spain
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Objective

The relationship between systemic inflammation and different measures of bronchiectasis severity has not been described. The objective of this study was to analyze the relationship between plasma concentrations of tumor necrosis factorα (TNF-α), as a marker of systemic inflammation, and some commonly used criteria for quantifying bronchiectasis severity in clinically stable patients whose disease was not caused by cystic fibrosis.

Patients and methods

Sixty-eight clinically stable patients with bronchiectasis and 19 age- and sex-matched healthy control subjects were included in the study. Data on disease history, symptoms, severity, functional variables, sputum volume, and microbiological cultures, laboratory findings, and other indicators of disease course were collected. Plasma concentrations of TNF-α were measured using high-resolution enzyme-linked immunosorbent assay.

Results

Plasma concentrations of TNF-α were higher in patients than controls (8.28 vs 5.67 pg/mL; P=.001). This observation correlated with other markers of systemic inflammation such as erythrocyte sedimentation rate (r=0.42; P=.001), C-reactive protein (r=0.45; P=.001), and percentage of peripheral blood neutrophils (r=0.45; P=.001). Patients with high plasma concentrations of TNF-α (>8.1 pg/dL) had more severe disease (5.19 vs 3.21; P=.001), were more likely to have respiratory failure (37.5% vs 8.3%; P=.003), and a higher rate of Pseudomonas aeruginosa colonization (34.3% vs 8.3%; P=.008).

Conclusions

High plasma concentrations of TNF-α were associated with several criteria usually used to assess severity of bronchiectasis in clinically stable patients with disease not caused by cystic fibrosis.

Key words:
Bronchiectasis
Tumor necrosis factorα
Pseudomonas aeruginosa
Objetivo

La relación existente entre la presencia de inflamación sistémica y los diferentes parámetros de gravedad en pacientes con bronquiectasias no ha sido descrita. El objetivo del estudio ha sido analizar la relación entre las concentraciones plasmáticas de factor de necrosis tumoral alfa (pTNF-α), como marcador de inflamación sistémica, y algunos criterios de gravedad comúnmente utilizados en pacientes con bronquiectasias, en fase de estabilidad clínica, no debidas a fibrosis quística.

Pacientes y métodos

Se incluyó en el estudio a 68 pacientes con bronquiectasias clínicamente estables y 19 controles sanos ajustados según edad y sexo. Se recogieron datos referentes a antecedentes patológicos, síntomas, extensión, variables funcionales, volumen de esputo y aspectos micro-biológicos, analíticos y evolutivos. Las concentraciones de pTNF-α se analizaron utilizando un método de enzimoinmunoanálisis de alta resolución.

Resultados

Se observó una mayor concentración de pTNF-α en los pacientes que en los controles (8,28 frente a 5,67 pg/ml; p = 0,001), que se correlacionó con otros parámetros de inflamación sistémica como la velocidad de sedimentación globular (r = 0,42; p = 0,001), la proteína C reactiva (r = 0,45; p = 0,001) y el porcentaje de neutrófilos periféricos (r = 0,45; p = 0,001). Los pacientes con concentraciones elevadas de pTNF-α (> 8,1 pg/dl) presentaron mayor extensión de la enfermedad (5,19 frente a 3,21; p = 0,001), mayor probabilidad de presentar insuficiencia respiratoria (el 37,5 frente al 8,3%; p = 0,003) y mayor porcentaje de colonizaciones por Pseudomonas aeruginosa (el 34,3 frente al 8,3%; p = 0,008).

Conclusiones

Las concentraciones elevadas de pTNF-α se asocian a varios parámetros comúnmente utilizados para valorar la gravedad en pacientes con bronquiectasias clínicamente estables y no debidas a fibrosis quística.

Palabras clave:
Bronquiectasias
Factor de necrosis tumoral alfa
Inflamación sistémica
Pseudomonas aeruginosa
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References
[1]
AF Barker.
Bronchiectasis.
N Engl J Med, 346 (2002), pp. 1383-1393
[2]
MA Martínez-García, M Perpiñá Tordera, P Román, JJ Soler.
Quality-of-life determinants in patients with clinically stable bronchiectasis.
Chest, 128 (2005), pp. 739-745
[3]
MA Martínez-García, M Perpiñá Tordera, P Román, JJ Soler.
Consistencia interna y validez de la versión española del St. George's Respiratory Questionnaire para su uso en pacientes afectados de bronquiectasias clínicamente estables.
Arch Bronconeumol, 41 (2005), pp. 110-117
[4]
AP Watt, V Brown, J Courtney, et al.
Neutrophil apoptosis, proinflammatory mediators and cell counts in bronchiectasis.
Thorax, 59 (2004), pp. 231-236
[5]
M Gaga, AM Bentley, M Humbert, et al.
Increases in CD4+ T lymphocytes. Macrophages, neutrophils and interleukin 8 positive cells in the airways of patients with bronchiectasis.
Thorax, 53 (1998), pp. 685-691
[6]
KW Tsang, K Chan, P Ho, et al.
Sputum elastase in steady-state bronchiectasis.
Chest, 117 (2000), pp. 420-426
[7]
IS Patel, I Vlahos, TMA Wilkinson, et al.
Bronchiectasis, exacerbations indices, and inflammation in chronic obstructive pulmonary disease.
Am J Respir Crit Care Med, 170 (2004), pp. 400-407
[8]
J Angrill, C Agustí, R De Celis, et al.
Bronchial inflammation and colonization in patients with clinically stable bronchiectasis.
Am J Respir Crit Care Med, 164 (2001), pp. 1628-1632
[9]
TL Bonfield, JR Panuska, MW Konstan, et al.
Inflammatory cytokines in cystic fibrosis lungs.
Am J Respir Crit Care Med, 152 (1995), pp. 2111-2118
[10]
CB Wilson, PW Jones, CJ O'Leary, et al.
Systemic markers of inflammation in stable bronchiectasis.
Eur Respir J, 12 (1998), pp. 820-824
[11]
AJ Puren, C Feldman, N Savage, PJ Becker, C Smith.
Patterns of cytokine expression in community-acquired pneumonia.
Chest, 107 (1995), pp. 1342-1349
[12]
AA Igonin, VW Armstrong, M Shipkova, NB Lazareva, VG Kukes, M Oellerich.
Circulating cytokines as markers of systemic inflammatory response in severe community-acquired pneumonia.
Clin Biochem, 37 (2004), pp. 204-209
[13]
D Norman, JS Elborn, SM Cordon, et al.
Plasma tumour necrosis factor alpha in cystic fibrosis.
Thorax, 46 (1991), pp. 91-95
[14]
J Kelley.
Cytokines of the lung.
Am Rev Respir Dis, 141 (1990), pp. 765-788
[15]
Y Sibille, HY Reynolds.
Macrophages and polymorphonuclear neutrophils in lung defense and injury.
Am Rev Respir Dis, 141 (1990), pp. 471-501
[16]
C Delclaux, E Azoulay.
Inflammatory response to infectious pulmonary injury.
Eur Respir J, 22 (2003), pp. 10-14
[17]
RE Sheehan, AU Wells, SJ Copley, et al.
A comparison of serial computed tomography and functional change in bronchiectasis.
Eur Respir J, 20 (2002), pp. 581-587
[18]
EY Kang, RR Miller, NL Müller.
Bronchiectasis: comparison of preoperative thin-section CT and pathologic findings in resected specimens.
Radiology, 195 (1995), pp. 649-654
[19]
Global Initiative for Asthma. Global strategy for asthma management and prevention. NHLBI/WHO Workshop Report 2002. Available at: http://www.ginasthma.com
[20]
DP Naidich, DI McCauley, NF Khouri, PP Stitik, SS Siegelman.
Computed tomography of bronchiectasis.
J Comput Assist Tomogr, 6 (1982), pp. 437-444
[21]
M Bhalla, N Turcios, V Aponte, et al.
Cystic fibrosis: scoring system with thin-section CT.
Radiology, 179 (1991), pp. 783-788
[22]
SM Brooks.
Surveillance for respiratory hazards.
ATS News, 8 (1982), pp. 12-16
[23]
TT Bauer, C Montón, A Torres, et al.
Comparison of systemic cytokine levels in patients with ARDS, severe pneumonia, and controls.
Eur Respir J, 14 (1999), pp. 324
[24]
C Montón, S Ewig, A Torres, et al.
Role of glucocorticoids on inflammatory response in nonimmunosuppressed patients with pneumonia: a pilot study.
Eur Respir J, 14 (1999), pp. 218-220
[25]
L Zheng, G Tipoe, W-K Lam, et al.
Endothelin-1 in stable bronchiectasis.
Eur Respir J, 16 (2000), pp. 146-149
[26]
L Zheng, G Tipoe, W-K Lam, et al.
Up-regulation of circulating adhesion molecules in bronchiectasis.
Eur Respir J, 16 (2000), pp. 691-696
[27]
N Takabatake, H Nakamura, S Abe, et al.
The relationship between chronic hypoxemia and activation of the tumor necrosis factor-α system in patients with chronic obstructive pulmonary disease.
Am J Respir Crit Care Med, 161 (2000), pp. 1179-1184
[28]
LS Nixon, B Yung, SC Bell, S Elborn, DJ Shale.
Circulating immunoreactive interleukin-6 in cystic fibrosis.
Am J Respir Crit Care Med, 157 (1998), pp. 1764-1769
[29]
MA Berry, B Hargadon, M Shelley, et al.
Evidence of a role of tumour necrosis factor-α in refractory asthma.
N Engl J Med, 354 (2006), pp. 697-708

Study performed in part with financial support from the Red Respira (ISCIII-TRIC-03/11) and from the company Glaxo SmithKline for purchase of tumor necrosis factor α and interleukin-8 reagents.

Copyright © 2008. Sociedad Española de Neumología y Cirugía Torácica (SEPAR)
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