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Ian D. Pavord
Researcher at University of Oxford
Publications - 654
Citations - 55329
Ian D. Pavord is an academic researcher from University of Oxford. The author has contributed to research in topics: Asthma & Sputum. The author has an hindex of 108, co-authored 575 publications receiving 47691 citations. Previous affiliations of Ian D. Pavord include John Radcliffe Hospital & University of Warwick.
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Mepolizumab reduces exacerbations in patients with severe eosinophilic asthma irrespective of baseline maintenance ocs use: meta-analysis from two ph3 trials
Steven G. Smith,Njira L Lugogo,Ian D. Pavord,Elisabeth H. Bel,Jean-Pierre Llanos-Ackert,Stephen Mallett,Eric S. Bradford,Steven W. Yancey,Frank C. Albers +8 more
Journal Article
Current Controversies in Chronic Obstructive Pulmonary Disease: A Report from the GOLD Scientific Committee.
G.J. Criner,Fernando J. Martinez,Shawn D. Aaron,A Agusti,Antonio Anzueto,Mona Bafadhel,Peter J. Barnes,Jean Bourbeau,Ruchong Chen,J Ewig,Leonardo M. Fabbri,Peter Frith,Halpin Dmg.,MeiLan K. Han,M. Montes de Oca,Masaharu Nishimura,Denis E. O'Donnell,Alberto Papi,Ian D. Pavord,Nicolas Roche,Roberto Rodriguez-Roisin,Sundeep Salvi,Dave Singh,Don D. Sin,Robert A. Stockley,M.V. Lopez Varela,Jørgen Vestbo,Claus Vogelmeier,George R. Washko,Jadwiga A. Wedzicha,Bartolomei Celli +30 more
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Th2 cytokine expression by bronchoalveolar lavage T-lymphocytes in asthma and eosinophilic bronchitis without asthma
TL;DR: Increased Th2 Cytokine expression by BAL T-cells is a feature of EB and asthma suggesting that they play a role in the airway inflammation observed in EB but that release of Th2 cytokines is not important in the development of disordered airway physiology in asthma.
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Reply to Boulet and Nair: Inhaled Corticosteroids and Adult Asthma.
TL;DR: There is a significant care gap in asthma management with an underutilization of noninvasive measurements of airway inflammation, particularly in moderate to severe asthma, and the need for rigorous dose–response studies of ICS to be conducted in patients who are well characterized on the basis of their inflammatory endotypes is endorsed.