RT Journal Article
SR Electronic
T1 The EvA study: aims and strategy
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 823
OP 829
DO 10.1183/09031936.00142811
VO 40
IS 4
A1 Loems Ziegler-Heitbrock
A1 Marion Frankenberger
A1 Irene Heimbeck
A1 Dorothe Burggraf
A1 Matthias Wjst
A1 Karl Häussinger
A1 Chris Brightling
A1 Sumit Gupta
A1 David Parr
A1 Deepak Subramanian
A1 Dave Singh
A1 Umme Kolsum
A1 Piera Boschetto
A1 Alfredo Potena
A1 Dorota Gorecka
A1 Adam Nowinski
A1 Imre Barta
A1 Balazs Döme
A1 Janos Strausz
A1 Timm Greulich
A1 Claus Vogelmeier
A1 Robert Bals
A1 Jens M. Hohlfeld
A1 Tobias Welte
A1 Per Venge
A1 Ivo Gut
A1 Anne Boland
A1 Robert Olaso
A1 Jörg Hager
A1 Pieter Hiemstra
A1 Klaus F. Rabe
A1 Martina Unmüßig
A1 Joachim Müller-Quernheim
A1 Antje Prasse
YR 2012
UL http://erj.ersjournals.com/content/40/4/823.abstract
AB The EvA study is a European Union-funded project under the Seventh Framework Programme (FP7), which aims at defining new markers for chronic obstructive pulmonary disease (COPD) and its subtypes. The acronym is derived from emphysema versus airway disease, indicating that the project targets these two main phenotypes of the disease. The EvA study is based on the concept that emphysema and airway disease are governed by different pathophysiological processes, are driven by different genes and have differential gene expression in the lung. To define these genes, patients and non-COPD controls are recruited for clinical examination, lung function analysis and computed tomography (CT) of the lung. CT scans are used to define the phenotypes based on lung density and airway wall thickness. This is followed by bronchoscopy in order to obtain samples from the airways and the alveoli. These tissue samples, along with blood samples, are then subjected to genome-wide expression and association analysis and markers linked to the phenotypes are identified. The population of the EvA study is different from other COPD study populations, since patients with current oral glucocorticoids, antibiotics and exacerbations or current smokers are excluded, such that the signals detected in the molecular analysis are due to the distinct inflammatory process of emphysema and airway disease in COPD.