The systemic effects of chronic obstructive pulmonary disease (COPD) are becoming increasingly apparent. Systemic inflammatory markers are of interest in mediating these systemic effects, and studies have shown that increased levels of inflammatory markers such as fibrinogen and C-reactive protein are associated not only with COPD severity, but also with the risk of cardiovascular morbidity and mortality. In addition, higher levels of fibrinogen and C-reactive protein are associated with lower lung function in individuals with no evidence of lung disease. Cigarette smoke is traditionally considered to be a risk factor for COPD and a potential stimulus for systemic inflammation, but COPD does not develop in all smokers. As such, other mechanisms are likely involved. Certain individuals may exhibit an “inflammatory phenotype” and have a greater predisposition to mounting an excessive inflammatory response to a certain stimulus. Therapy with inhaled corticosteroids has shown a decrease in systemic markers of inflammation and a trend towards improving lung function and mortality.