Vincent Cottin

Publications (203) View all

• Article: The pathogenesis of pulmonary fibrosis: a moving target.

  Wim A Wuyts, C Agostini, Km Antoniou, D Bouros, Rc Chambers, V Cottin, Jj Egan, Bn Lambrecht, R Lories, H Parfrey, A Prasse, C Robalo-Cordeiro, E Verbeken, Ja Verschakelen, Au Wells, Gm Verleden
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  ABSTRACT: Pulmonary fibrosis is the end stage of many diffuse parenchymal lung diseases. It is characterised by excessive matrix formation leading to destruction of the normal lung architecture and finally death. Despite an exponential increase in our understanding of potentially important mediators and mechanisms, the delineation of primary pathways has proven to be elusive.In this paper susceptibility and injurious agents such as viruses and gastroesophageal reflux and their likely role in initiating disease are discussed. Further topics that are elaborated are candidate ancillary pathways, including immune mechanisms, oxidative and endoplasmic reticulum stress, activation of the coagulation cascade and the potential role of stem cells. The paper will try to provide the reader with an integrated view on the current knowledge and attempts to provide a road map for future research.It is important to explore robust models of overall pathogenesis, reconciling a large number of clinical and scientific observations. We believe that the integration of current data into a "big picture" overview of fibrogenesis is essential for the development of effective antifibrotic strategies. The latter will likely consist of a combination of agents targeting a number of key pathways.
  European Respiratory Journal 05/2013; 41(5):1207-18. · 5.89 Impact Factor
• Article: [Syndrome of combined pulmonary fibrosis and emphysema: Understanding the functional profile].

  V Cottin
  Revue des Maladies Respiratoires 03/2013; 30(3):173-5. · 0.59 Impact Factor
• Article: Hypereosinophilic obliterative bronchiolitis: a distinct, unrecognised syndrome.

  J F Cordier, V Cottin, C Khouatra, D Revel, C Proust, N Freymond, F Thivolet-Béjui, J C Glérant
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  ABSTRACT: Background: Only isolated biopsy-proven cases of eosinophilic bronchiolitis have been reported, all from Japan.Methods: We present 6 patients with hypereosinophilic obliterative bronchiolitis (HOB), defined by the following criteria: 1-blood eosinophil cell count>1 G·L(-1) and/or BAL eosinophil count>25%, 2-persistent airflow obstruction despite high-dose inhaled bronchodilators and corticosteroids, 3-eosinophilic bronchiolitis at lung biopsy (n=2) and/or direct signs of bronchiolitis (centrilobular nodules, branching opacities) on computed tomography (n=6).Results: Chronic dyspnoea and cough often severe, without the characteristic features of asthma, were the main clinical manifestations. Atopy and asthma were present in the history of 3 and 2 patients, respectively. One patient met biological criteria of the lymphoid variant of idiopathic hypereosinophilic syndrome. Mean blood eosinophil cell count was 2.7 G·L(-1) and mean eosinophil differential percentage at bronchoalveolar lavage was 63%. Mean initial FEV1/FVC ratio was 50%, normalising with oral corticosteroid therapy in all patients. HOB manifestations recurred when oral prednisone was decreased to 10-20 mg·day(-1), but higher doses controlled the disease.Conclusion: HOB is a characteristic entity deserving to be individualised among the eosinophilic respiratory disorders. Thorough analysis is needed to determine whether unrecognised and/or smouldering HOB may further be a cause of irreversible airflow obstruction in chronic eosinophilic respiratory diseases.
  European Respiratory Journal 12/2012; · 5.89 Impact Factor
• Source

  Available from: Vincent Cottin

  Dataset: 1999 cottin tnfR JBC

  A Van Linden, D W Riches, V Cottin
• Source

  Available from: Vincent Cottin

  Dataset: 2011 Robalo Cordeiro ILD Interventional pneumology LAM PF PH Rehabilitation ERJ

  S Ley, N H Chavannes, C Robalo Cordeiro, E Clini, V Cottin, S Singh, F J F Herth