LAUSR

could play a crucial role, 6 while Huang et al. observed that an increased serum concentration of desmosine (as part of systemic inflammation in bronchiectasis) was associated with an increased adjusted cardiovascular mortality in bronchiectasis patients. 10 The future therapeutic implications of this situation could be highly significant. Some authors have observed that both non-pharmacological treatments (such as muscle reha-bilitation and nutritional programs) and pharmacological treatments (such as statins, neutrophil elastase inhibitors, CXCR2 inhibitors, antibiotics and other immunomodula-tory treatments) 11 can reduce the level of some systemic proinflammatory molecules. However, no beneficial effect on bronchiectasis has been demonstrated from treatment of systemic inflammation, and, consequently, international guidelines do not recommend such interventions. Finally, some markers of systemic inflammation could also be used to predict treatment response. For example, the number or percentage of peripheral eosinophils could predict the response to biological or inhaled steroid treatments in bronchiectasis (as in the case of COPD), as already sug-gested by various authors. 12 In conclusion, systemic inflammation in bronchiectasis patients has been demonstrated in the past decade, and it could cause extrapulmonary damage, especially in terms of an increased risk of cardiovascular and metabolic/nutritional diseases. As highlighted by the EMBARC ( European Multi-centre Bronchiectasis Audit and Research Collaboration ) taskforce on research priorities, further studies are needed to identify biomarkers that can assist in risk stratification, tar-geted interventions and monitoring strategies, as well as the confirmation of a causal relationship between the presence of systemic inflammation (directly or through an increase in exacerbations of bronchial infection) and damage to several target organs.