Metabolic syndrome and impaired lung function.

We read with great interest the recent article in CHEST (October 2009) 1 by Watz and colleagues showing an independent association between metabolic syndrome and systemic infl ammatory markers in chronic bronchitis and patients with COPD. The authors also demonstrate that the prevalence of metabolic syndrome does not increase for increasing COPD severity, as expressed by the Global Initiative for Chronic Obstructive Lung Disease stage. Interestingly, metabolic syndrome is also associated with a restrictive ventilatory pattern at spirometry, especially in patients with the highest waist circumference. 2 In this population, visceral fat is known to produce prothrombotic and infl ammatory mediators, including C-reactive protein, fi brinogen, interleukin-6, and tumor necrosis factora . Since lung restriction is frequently associated with systemic infl ammation independent of obesity, the infl ammatory burden due to restriction may add to that related to visceral obesity in patients having both diseases. 3 For this reason we believe that the authors should have provided information on the prevalence of a mixed ventilatory pattern in their population instead of classifying patients only on the basis of the FEV 1 FVC ratio and FEV 1 %. This would have required the measurement of total lung capacity. Nonetheless, based on the available data, it would be of interest at least to know how prevalent was a spirometric pattern suggesting a restrictive component, which is known to be associated with systemic infl ammation. 4 Indeed, recent evidence is consistent with an FVC based on presumptive diagnosis of lung restriction being comparably accurate in people with and without obstruction. 5 Finally, the authors provide the Charlson index of comorbidity, but they do not list individual comorbidities and their prevalences; selected conditions, such as renal failure, could per se promote systemic infl ammation. Providing such information would allow the authors and the readers to verify whether the infl ammatory pattern changes for different combinations of COPD, a restrictive component and visceral obesity. Otherwise, the authors might ascribe to COPD an infl ammatory status, which in a relevant proportion of patients likely is multifactorial in origin.