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COPD exacerbations · 2: Aetiology

E Sapey, R A Stockley

Lung Investigation Unit, Queen Elizabeth Hospital, Birmingham B15 2TH, UK

Correspondence to:
Correspondence to:
Professor R A Stockley
Lung Investigation Unit, Nuffield House, Queen Elizabeth Hospital, Birmingham B15 2TH, UK; r.a.stockley{at}bham.ac.uk

Exacerbations of COPD are thought to be caused by complex interactions between the host, bacteria, viruses, and environmental pollution. These factors increase the inflammatory burden in the lower airways, overwhelming the protective anti-inflammatory defences leading to tissue damage. Frequent exacerbations are associated with increased morbidity and mortality, a faster decline in lung function, and poorer health status, so prevention or optimal treatment of exacerbations is a global priority. In order to evolve new treatment strategies there has been great interest in the aetiology and pathophysiology of exacerbations, but progress has been hindered by the heterogeneous nature of these episodes, vague definitions of an exacerbation, and poor stratification of known confounding factors when interpreting results. We review how an exacerbation should be defined, its inflammatory basis, and the importance of exacerbations on disease progression. Important aetiologies, with their potential underlying mechanisms, are discussed and the significance of each aetiology is considered.

Abbreviations: AECOPD, acute exacerbation of chronic obstructive pulmonary disease; CRP, C-reactive protein; CXCL8, interleukin 8; E selectin, endothelial selectin; FEV₁, forced expiratory volume in 1 second; FVC, forced vital capacity; GRO, growth-related oncogene ; IL, interleukin; LTB4, leukotriene B4; NE, neutrophil elastase; PEF, peak expiratory flow; sICAM-1, soluble intracellular adhesion molecule 1; SLPI, secretory leukoproteinase inhibitor; TNF, tumour necrosis factor

Keywords: chronic obstructive pulmonary disease; exacerbations; aetiology

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