Relationship between airway inflammation and the frequency of exacerbations in patients with smoking related COPD.
BACKGROUND
Patients with more frequent exacerbations of chronic obstructive pulmonary disease (COPD) may have increased bronchial inflammation. Airway inflammation was measured in patients who had been thoroughly investigated with full pulmonary function testing, thoracic HRCT scanning, and sputum microbiology to examine further the relationship between exacerbation frequency and bronchial inflammation.


METHODS
Airway inflammation (spontaneous sputum sol phase myeloperoxidase (MPO), elastase, leukotriene (LT)B(4), interleukin (IL)-8, secretory leukoprotenase inhibitor (SLPI), protein leakage) and serum levels of C reactive protein (CRP) were compared in 40 patients with stable, smoking related COPD, divided into those with frequent (> or =3/year) or infrequent (< or =2/year) exacerbations according to the number of primary care consultations during the preceding year. The comparisons were repeated after excluding eight otherwise clinically indistinguishable patients who had tubular bronchiectasis on the HRCT scan.


RESULTS
Patients with frequent (n=12) and infrequent (n=28) exacerbations were indistinguishable in terms of their clinical, pulmonary function, and sputum characteristics, CRP concentrations, and all of their bronchial inflammatory parameters (p>0.05). The patients without evidence of tubular bronchiectasis (n=32) were equally well matched but the sputum concentrations of SLPI were significantly lower in the frequent exacerbators (n=8) in this subset analysis (p<0.05).


CONCLUSIONS
There are several clinical features that directly influence bronchial inflammation in COPD. When these were carefully controlled for, patients with more frequent reported exacerbations had lower sputum concentrations of SLPI. This important antiproteinase is also known to possess antibacterial and antiviral activity. Further studies are required into the nature of recurrent exacerbations and, in particular, the regulation and role of SLPI in affected individuals.
Gompertz
S
S
Department of Respiratory Medicine, Queen Elizabeth Hospital, Birmingham B15 2TH, UK. sgompertz@doctors.net
Bayley
D L
DL
Hill
S L
SL
Stockley
R A
RA
D000368:Aged; D015415:Biomarkers; D001987:Bronchiectasis / Q000150:complications / Q000000981:diagnostic imaging; D001991:Bronchitis / Q000473:pathology* / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism*; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D008173:Lung Diseases, Obstructive / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D008176:Lung Volume Measurements / Q000379:methods; D008297:Male; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins / Q000378:metabolism; D011859:Radiography; D053481:Secretory Leukocyte Peptidase Inhibitor; D012907:Smoking / Q000009:adverse effects*; D013183:Sputum / Q000737:chemistry / Q000382:microbiology; D014797:Vital Capacity / Q000502:physiology
D015415:Biomarkers; D053491:Proteinase Inhibitory Proteins, Secretory; D011506:Proteins; C506814:SLPI protein, human; D053481:Secretory Leukocyte Peptidase Inhibitor; D002097:C-Reactive Protein