Abstract

Bronchiectasis, first described by Rene Laennec in 1819, is a common long-term respiratory condition caused by permanently damaged airways. Over 1 in 1000 people in the United Kingdom now has this disease. Although there are a variety of aetiologies, there is a common end point that permanently damaged the airways with impaired mucociliary clearance and neutrophilic airways inflammation. Despite the abundance of neutrophils, over two thirds of the patients are chronically colonised with bacteria. There has been a long debate whether bronchiectasis remains a local problem in the airway or that advanced local inflammation in the airways can lead to systemic inflammation. The study by Gale and colleagues demonstrated that although patients with bronchiectasis are clinically stable (n 1⁄4 20) compared with age-matched controls (n 1⁄4 20), they had increased concentrations of interleukin-6 in peripheral blood, reduced albumin concentrations and increased arterial stiffness using aortic pulse wave velocity. Patients also had reduced exercise tolerance and reduced physical activity score, and only 20% had normal bone mineral density. This study revealed increased systemic inflammation with increased arterial stiffness, the latter thought consequent on the systemic inflammation. Wilson and colleagues also showed that the patients with bronchiectasis in a stable phase (n 1⁄4 87) have raised systemic markers of inflammation and some markers, particularly the neutrophil count, which is correlated with disease severity. Martinez-Garcia and colleagues, in a study of 76 stable adult patients with bronchiectasis, showed that the independent factors associated with an accelerated decline in lung function were due to chronic colonization with Pseudomonas aeruginosa, more frequent severe exacerbations and more systemic inflammation. Similarly, our group investigated 385 patients with stable bronchiectasis and patients with sputum bacterial loads of 10 colony forming units/ml, showing an evidence of increased concentration of the vascular endothelial adhesion markers, in particular increased serum intercellular adhesion molecule-1 (ICAM-1), which was reduced with both shortand long-term antibiotic treatments. Therefore, it is important to consider bronchiectasis as not only a localised disease but also as a systemic disease. Further studies are needed to see whether bronchiectasis impacts on vascular morbidity and mortality and whether long term interventions impact on this. It is refreshing that there has been a resurgence of interest in bronchiectasis. The British Thoracic Society (BTS) have published national guidelines in bronchiectasis and more recently have published quality standards in bronchiectasis. There are 11 quality standards focussed on the following:

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