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Mechanisms of Pulmonary Fibrosis*: Conference Summary

Robert M. Strieter, MD, FCCP
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*From the University of California, Los Angeles School of Medicine, Department of Medicine, Division of Pulmonary and Critical Care Medicine, Los Angeles, CA.

Correspondence to: Robert M. Strieter, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Department of Medicine, UCLA School of Medicine, 900 Veteran Ave, 14–154 Warren Hall, Box 711922, Los Angeles, CA 90095-1922; e-mail: rstrieter@mednet.ucla.edu



Chest. 2001;120(1_suppl):S77-S85. doi:10.1378/chest.120.1_suppl.S77-a
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I would first like to thank David Riches and Scott Worthen for organizing an outstanding meeting and for inviting me as conference summarizer. The presentations and discussions of mechanisms of pulmonary fibrosis at this meeting have reinforced five major issues. First, there have been and presently are outstanding investigations in the field of pulmonary fibrosis as exemplified by this conference. Second, although these studies have made outstanding contributions to further our understanding of the mechanisms related to pulmonary fibrosis, it is clear that we have the need to further our basic and clinical science knowledge of this complex process. Third, the missing link between basic science research and clinical research is that we lack information regarding the natural history of human pulmonary fibrosis, and we are left with only descriptive “snapshots” of the histopathology of human pulmonary fibrosis. This situation directly impacts on our understanding of the actual pathogenesis of these disorders. Fourth, as Dr. King points out, idiopathic pulmonary fibrosis (IPF) is a devastating disease with a 5-year survival of only 30%. This is potentially related to the fact that fibroblastic foci of granulation tissue and its potential relationship to survival highlight why our current immunosuppressive therapy is ineffective in the treatment of IPF. Fifth, based on the severity of the prognosis and the relative lack of response to currently approved medications, we need an infrastructure to support a multicenter group of investigators to facilitate the clinical study of patients with IPF. This organizational scheme would create the opportunity to study the response of these patients to novel therapeutic intervention and to establish the potential of genetic predisposition of this disorder.

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