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Vol. 44. Issue 4.
Pages 180-184 (January 2008)
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Vol. 44. Issue 4.
Pages 180-184 (January 2008)
Original Articles
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Association Between Chronic Colonization or Infection With Pseudomonas aeruginosa and Bronchial Hyperreactivity in Patients With Cystic Fibrosis
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José Valverde-Molinaa,
Corresponding author
jose.valverde@carm.es

Correspondence: Dr J. Valverde-Molina Servicio de Neumología Pediátrica, Hospital Los Arcos P.° de Colón, 54 30720 Santiago de la Ribera, Murcia, Spain
, Manuel Sánchez-Solísb,c, María Dolores Pastor-Viverob, Luis García-Marcosc
a Unidad de Neumología Pediátrica, Hospital Los Arcos, Santiago de la Ribera, Murcia, Spain
b Unidad de Neumología Pediátrica, Hospital Virgen de la Arrixaca, El Palmar, Murcia, Spain
c Instituto de Salud Respiratoria, Universidad de Murcia, Murcia, Spain
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Objective

In patients with cystic fibrosis, bronchial hyperreactivity is a common finding that has not been conclusively associated with atopy. The objective of the present study was to determine the relationship between chronic colonization or infection with Pseudomonas aeruginosa and bronchial hyperreactivity in a group of patients with cystic fibrosis.

Patients and methods

A nonspecific histamine bronchial provocation test was administered to a group of 32 cystic fibrosis patients with a mean (SD) age of 11.25 (3.7) years. The presence of atopy and of chronic colonization or infection with P aeruginosa was also studied.

Results

Nine of the 32 patients (28.1%) studied showed bronchial hyperreactivity. The clinical status of these 9 patients was significantly worse and all were colonized or infected with P aeruginosa. Atopy was present in 17 of the 32 patients (53.1%) in the study group, but in only 3 of the 9 patients (33.3%) with bronchial hyperreactivity. Bronchial hyperreactivity was significantly associated with colonization or infection with P aeruginosa (P<.001), but not with atopy (P=.12). In the patients without atopy, colonization was significantly associated with bronchial hyperreactivity (P=.017). In the group with normal lung function (forced expiratory volume in 1 second ≥80%) this association was also significant (P=.044), while the association between bronchial hyperreactivity and atopy was not (P=.11).

Conclusions

The results of the present study suggest that in patients with cystic fibrosis, bronchial hyperreactivity may be associated with colonization or infection with P aeruginosa, and that this may be a more important risk factor for bronchial hyperreactivity than atopy.

Key words:
Atopy
Cystic fibrosis
Bronchial hyperreactivity
Pseudomonas aeruginosa
Objetivo

La hiperreactividad bronquial (HRB) es un hallazgo común en la fibrosis quística (FQ), que no se ha relacionado de forma concluyente con la atopia. El objetivo del estudio ha sido investigar la relación existente entre la colonización-infección crónica por Pseudomonas aeruginosa y la HRB en un grupo de pacientes con FQ.

Pacientes y métodos

Se realizó la prueba de broncoprovocación inespecífica con histamina a un grupo de 32 pacientes con FQ cuya edad media ± desviación estándar era de 11,25 ± 3,7 años. Además se investigó en estos pacientes la existencia de atopia y colonización-infección crónica por P. aeruginosa.

Resultados

De los 32 pacientes estudiados, se encontró HRB en 9 (28,1%), cuya situación clínica era significativamente peor. Estos 9 pacientes con HRB presentaron todos colonización-infección crónica por P. aeruginosa. Tenían atopia 17 pacientes (53,1%) de la muestra estudiada, pero sólo 3 (33,3%) de los 9 con HRB. La HRB se asoció significativamente con la colonización-infección crónica por P. aeruginosa (p < 0,001), pero no con la atopia (p = 0,12). Entre los pacientes sin atopia, la colonización se asoció significativamente con HRB (p = 0,017). Además, en el grupo de pacientes con función pulmonar normal (volumen espiratorio forzado en el primer segundo ≥ 80%) esta asociación fue también significativa (p = 0,044), mientras que la asociación entre HRB y atopia no lo fue (p = 0,11).

Conclusiones

Los resultados del presente estudio indi-can que en pacientes con FQ la HRB podría estar relacionada con la colonización-infección crónica por P. aeruginosa, que podría ser un factor de riesgo de HRB más importante que la atopia.

Palabras clave:
Atopia
Fibrosis quística
Hiperreactividad bronquial
Pseudomonas aeruginosa
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References
[1]
R Dinwiddie.
Pathogenesis of lung disease in cystic fibrosis.
Respiration, 67 (2000), pp. 3-8
[2]
J Navarro, M Rainisio, HK Harms, ME Hodson, C Koch, G Mastella, et al.
Factors associated with poor pulmonary function: cross-sectional analysis of data from the ERCF. European Epidemiologic Registry of Cystic Fibrosis.
Eur Respir J, 18 (2001), pp. 298-305
[3]
C Halfhide, H Evans, J Couriel.
Inhaled bronchodilators for cystic fibrosis.
Cochrane Database Syst Rev, 4 (2005),
[4]
C Koch, SG McKenzie, H Kaplowitz, ME Hodson, HK Harms, J Navarro, et al.
International practice patterns by age and severity of lung disease in cystic fibrosis: data from the Epidemiologic Registry of Cystic Fibrosis (ERCF).
Pediatr Pulmonol, 24 (1997), pp. 147-154
[5]
IM Balfour-Lynn, JS Elborn.
“CF asthma”: what is it and what do we do about it?.
Thorax, 57 (2002), pp. 742-748
[6]
V de Rose.
Mechanisms and markers of airway inflammation in cystic fibrosis.
Eur Respir J, 19 (2002), pp. 333-340
[7]
TZ Khan, JS Wagener, T Bost, J Martínez, FJ Accurso, DW Riches.
Early pulmonary inflammation in infants with cystic fibrosis.
Am J Respir Crit Care Med, 151 (1995), pp. 1075-1082
[8]
DS Armstrong, K Grimwood, R Carzino, JB Carlin, A Olinsky, PD Phelan.
Lower respiratory infection and inflammation in infants with newly diagnosed cystic fibrosis.
BMJ, 310 (1995), pp. 1571-1572
[9]
K Balough, M McCubbin, M Weinberger, W Smits, R Ahrens, R Fick.
The relationship between infection and inflammation in the early stages of lung disease from cystic fibrosis.
Pediatr Pulmonol, 20 (1995), pp. 63-70
[10]
LP Ho, JA Innes, AP Greening.
Exhaled nitric oxide is not elevated in the inflammatory airways diseases of cystic fibrosis and bronchiectasis.
Eur Respir J, 12 (1998), pp. 1290-1294
[11]
C Marguet, F Jouen-Boedes, TP Dean, JO Warner.
Bronchoalveolar cell profiles in children with asthma, infantile wheeze, chronic cough, or cystic fibrosis.
Am J Respir Crit Care Med, 159 (1999), pp. 1533-1540
[12]
R Louis, LC Lau, AO Bron, AC Roldaan, M Radermecker, R Djukanovic.
The relationship between airways inflammation and asthma severity.
Am J Respir Crit Care Med, 161 (2000), pp. 9-16
[13]
C Moser, S Kjaergaard, T Pressler, A Kharazmi, C Koch, N Hoiby.
The immune response to chronic Pseudomonas aeruginosa lung infection in cystic fibrosis patients is predominantly of the Th2 type.
APMIS, 108 (2000), pp. 329-335
[14]
M Weinberger.
Airways reactivity in patients with CF.
Clin Rev Allergy Immunol, 23 (2002), pp. 77-85
[15]
DW Cockcroft, DN Killian, JJ Mellon, FE Hargreave.
Bronchial reactivity to inhaled histamine: a method and clinical survey.
Clin Allergy, 7 (1977), pp. 235-243
[16]
R Cantón, N Cobos, J De Gracia, F Baquero, J Honorato, S Gartner, en representación del Grupo Español de Consenso del Tratamiento Antimicrobiano en el Paciente con Fibrosis Quística, et al.
Tratamiento antimicrobiano frente a la colonización pulmonar por Pseudomonas aeruginosa en el paciente con fibrosis quística.
Arch Bronconeumol, 41 (2005), pp. 1-25
[17]
CM Mellis, H Levison.
Bronchial reactivity in cystic fibrosis.
Pediatrics, 61 (1978), pp. 446-450
[18]
MJ Tobin, O Maguire, D Reen, E Tempany, MX Fitzgerald.
Atopy and bronchial reactivity in older patients with cystic fibrosis.
Thorax, 35 (1980), pp. 807-813
[19]
I Mitchell, M Corey, R Woenne, IR Krastins, H Levison.
Bronchial hyperreactivity in cystic fibrosis and asthma.
J Pediatr, 93 (1978), pp. 744-748
[20]
PA Eggleston, BJ Rosenstein, CM Stackhouse, MF Alexander.
Airway hyperreactivity in cystic fibrosis. Clinical correlates and possible effects on the course of the disease.
Chest, 94 (1988), pp. 360-365
[21]
I Sánchez, RE Powell, V Chernick.
Response to inhaled bronchodilators and nonspecific airway hyperreactivity in children with cystic fibrosis.
Pediatr Pulmonol, 14 (1992), pp. 52-57
[22]
P van Asperen, CM Mellis, RT South, SJ Simpson.
Bronchial reactivity in cystic fibrosis with normal pulmonary function.
Am J Dis Child, 135 (1981), pp. 815-819
[23]
PI Macfarlane, D Heaf.
Changes in airflow obstruction and oxygen saturation in response to exercise and bronchodilators in cystic fibrosis.
Pediatr Pulmonol, 8 (1990), pp. 4-11
[24]
LT Rodwell, SD Anderson.
Airway responsiveness to hyperosmolar saline challenge in cystic fibrosis: a pilot study.
[25]
MS Zach, B Oberwaldner, G Forche, G Polgar.
Bronchodilators increase airway instability in cystic fibrosis.
Am Rev Respir Dis, 131 (1985), pp. 537-543
[26]
L García-Marcos, JA Castro-Rodríguez, MM Suárez-Varela, JB Garrido, GG Hernández, AM Gimeno, et al.
A different pattern of risk factors for atopic and non-atopic wheezing in 9-12-year-old children.
Pediatr Allergy Immunol, 16 (2005), pp. 471-477
[27]
JO Warner, SA Kilburn.
Cystic fibrosis and allergy.
Pediatr Allergy Immunol, 7 (1996), pp. 67-69
[28]
M Dahl, A Tybjaerg-Hansen, P Lange, BG Nordestgaard.
δF508 heterozygosity in cystic fibrosis and susceptibility to asthma.
Lancet, 351 (1998), pp. 1911-1913
[29]
C Lázaro, R De Cid, J Sunyer, J Soriano, J Giménez, M Álvarez, et al.
Missense mutations in the cystic fibrosis gene in adult patients with asthma.
[30]
A Bush, H Tiddens, M Silverman.
Clinical implications of inflammation in young children.
Am J Respir Crit Care Med, 162 (2000), pp. S11-S14
[31]
N Najafi, C Demanet, I Dab, M de Waele, A Malfroot.
Differential cytology of bronchoalveolar lavage fluid in asthmatic children.
Pediatr Pulmonol, 35 (2003), pp. 302-308
[32]
JL Simpson, R Scott, MJ Boyle, PG Gibson.
Inflammatory subtypes in asthma: assessment and identification using induced sputum.
[33]
A Sala, G Folco.
Neutrophils, endothelial cells, and cysteinyl leukotrienes: a new approach to neutrophil-dependent inflammation?.
Biochem Biophys Res Commun, 283 (2001), pp. 1003-1006
[34]
SR Hays, RE Ferrando, R Carter, HH Wong, PG Woodruff.
Structural changes to airway smooth muscle in cystic fibrosis.
Thorax, 60 (2005), pp. 226-228
[35]
FR Coulson, AD Fryer.
Muscarinic acetylcholine receptors and airway diseases.
Pharmacol Ther, 98 (2003), pp. 59-69
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