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Acute Exacerbations of Fibrotic Hypersensitivity Pneumonitis: A Case Series

Amy L. Olson, MD, MSPH; Tristan J. Huie, MD; Steve D. Groshong, MD, PhD; Gregory P. Cosgrove, MD, FCCP; William J. Janssen, MD, FCCP; Marvin I. Schwarz, MD, FCCP; Kevin K. Brown, MD, FCCP; Stephen K. Frankel, MD, FCCP
Author and Funding Information

*From the Division of Pulmonary Sciences and Critical Care Medicine (Drs. Olson, Huie, and Schwarz), University of Colorado Health Sciences Center; and Interstitial Lung Disease Program (Drs. Groshong, Cosgrove, Janssen, Brown, and Frankel), Section of Critical Care and Hospital Medicine, National Jewish Medical and Research Center, Denver, CO.

Correspondence to: Amy L. Olson, MD, MSPH, University of Colorado Health Sciences Center, Division of Pulmonary Sciences and Critical Care Medicine, 4200 East Ninth Ave, C272, Denver, CO 80262; e-mail: amy.olson@uchsc.edu


This work was performed at National Jewish Medical and Research Center, Denver, CO.

The authors have no conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(4):844-850. doi:10.1378/chest.08-0428
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Background:  It is now recognized that a significant portion of patients with idiopathic pulmonary fibrosis (IPF) can have sudden and rapid deteriorations in disease course that cannot be explained by infection, heart failure, or thromboembolic disease. These events are often fatal and have been termed acute exacerbations (AEs) of underlying disease. While best described in patients with IPF, they have also been reported in patients with other forms of interstitial lung disease. We sought to determine if this same phenomenon occurs in patients with hypersensitivity pneumonitis (HP).

Methods:  We retrospectively reviewed our clinical experience at National Jewish Medical and Research Center for patients with surgical lung biopsy-proven fibrotic HP who had an acute decline in respiratory status and met criteria similar to those proposed for the diagnosis of an AE of IPF.

Results:  Over a 2-year period, we identified four patients with an AE of fibrotic HP. All patients had a clinical course similar to that most frequently described in AEs of IPF: respiratory failure requiring assisted ventilation, lack of clinical response to high-dose corticosteroid therapy, and a poor prognosis (all cases resulted in death or emergent lung transplantation). Lung biopsy at the time of the AE, explant, or autopsy revealed organizing diffuse alveolar damage superimposed on fibrotic lung disease.

Conclusions:  Fibrotic HP, like other forms of fibrotic lung disease, can be associated with AEs of disease. Further investigation into similarities and pathways common in AEs of various fibrotic lung diseases may yield additional insight into this recently recognized syndrome.

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