Kevin K Brown

National Jewish Health, Denver, Colorado, United States

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Publications (234)1573.97 Total impact

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    ABSTRACT: and purpose: The Phase II TOMORROW trial and two Phase III INPULSIS® trials investigated the efficacy and safety of nintedanib versus placebo in patients with idiopathic pulmonary fibrosis (IPF). To obtain an overall estimate of the treatment effect of nintedanib 150 mg twice daily (bid), pooled and meta-analyses of data from these three trials were conducted.
    No preview · Article · Feb 2016
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    ABSTRACT: Rationale: Sequence variation, methylation differences, and transcriptional changes in Desmoplakin (DSP) have been observed in patients with idiopathic pulmonary fibrosis (IPF). Objectives: To identify novel variants in DSP associated with IPF and to characterize the relationship of these IPF sequence variants with DSP gene expression in human lung. Methods: A chromosome 6 locus (Chr6:7,370,061-7,606,946) was sequenced in 230 IPF cases and 228 controls. Validation genotyping of disease-associated variants was conducted in 936 IPF cases and 936 controls. DSP gene expression was measured in lung tissue from 334 IPF and 201 control subjects. Measurements and main results: We identified 23 sequence variants in the Chr6 locus associated with IPF. Genotyping of selected variants in our validation cohort revealed that non-coding intron 1 variant rs2744371 (OR=0.77, 95% CI 0.66-0.91, p=0.002) is protective for IPF and a previously described IPF-associated intron 5 variant (rs2076295) is associated with increased risk of IPF (OR=1.36, 95% CI 1.19-1.56, p<0.001) after controlling for sex and age. DSP expression is 2.3 fold-increased (95% CI 1.91 - 2.71) in IPF lung tissue (p<0.0001). Only the minor allele at rs2076295 is associated with decreased DSP expression (p=0.001). Staining of fibrotic and normal human lung tissue localized DSP to airway epithelia. Conclusions: Sequence variants in DSP are associated with IPF, and rs2076295 genotype is associated with differential expression of DSP in the lung. DSP expression is increased in IPF lung and concentrated in the airway epithelia, suggesting a potential role for DSP in the pathogenesis of IPF.
    No preview · Article · Dec 2015 · American Journal of Respiratory and Critical Care Medicine
  • Amen Sergew · Kevin K Brown
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    ABSTRACT: Introduction: Idiopathic pulmonary fibrosis (IPF) is a lung limited, progressive fibrotic disease with a poor prognosis. The cause is unknown, and currently there is no treatment that reverses the disease or stops progression. This combination of a poor prognosis and the absence of curative therapy has prompted a sustained investigative effort to identify beneficial treatments. Recently released trial results suggest progress. Areas covered: Although the mechanism of disease is poorly understood, a number of compounds that influence pathways thought to play a mechanistic role have been studied for use in IPF. This article discusses a number of these landmark trials. Expert opinion: From these studies we conclude that the future treatment of IPF will include expanding pharmacological options. Recent studies have identified two agents that appear to slow disease progression and may offer a window into pathogenesis and future drug targets.
    No preview · Article · Dec 2015 · Expert Opinion on Emerging Drugs
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    ABSTRACT: Idiopathic interstitial pneumonias (IIPs) are a group of heterogeneous, somewhat unpredictable diseases characterized by progressive scarring of the interstitium. Since lung function is a key determinant of survival, we reasoned that the transcriptional profile in IIP lung tissue would be associated with measures of lung function, and could enhance prognostic approaches to IIPs. Using gene expression profiling of 167 lung tissue specimens with IIP diagnosis and 50 control lungs, we identified genes whose expression is associated with changes in lung function (% predicted FVC and % predicted D L CO) modeled as categorical (severe vs mild disease) or continuous variables while adjusting for smoking status and IIP subtype; false discovery rate (FDR) approach was used to correct for multiple comparisons. This analysis identified 58 transcripts that are associated with mild vs severe disease (categorical analysis), including those with established role in fibrosis (ADAMTS4, ADAMTS9, AGER, HIF-1α, SERPINA3, SERPINE2, and SELE) as well as novel IIP candidate genes such as rhotekin 2 (RTKN2) and peptidase inhibitor 15 (PI15). Protein-protein interactome analysis of 553 genes whose expression is significantly associated with lung function when modeled as continuous variables demonstrates that more severe presentation of IIPs is characterized by an increase in cell cycle progression and apoptosis, increased hypoxia, and dampened innate immune response. Our findings were validated in an independent cohort of 131 IIPs and 40 controls at the mRNA level and for one gene (RTKN2) at the protein level by immunohistochemistry in a subset of samples. We identified commonalities and differences in gene expression among different subtypes of IIPs. Disease progression, as characterized by lower measures of FVC and D L CO, results in marked changes in expression of novel and established genes and pathways involved in IIPs. These genes and pathways represent strong candidates for biomarker studies and potential therapeutic targets for IIP severity.
    Preview · Article · Dec 2015 · BMC Genomics
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    ABSTRACT: Background: Exertional dyspnea is a hallmark symptom of fibrosing interstitial lung disease (fILD), and oxygen (O2) desaturation is common among patients with fILD. Supplemental O2 is prescribed to maintain normoxia and alleviate dyspnea. We sought to better understand the associations between O2 and dyspnea in fILD during the 6-min walk test (6MWT). Methods: 1326 fILD patients compose the sample group. Borg dyspnea and other 6MWT variables were compared between subjects who performed the test without (non-users) versus with O2 (users). Results: There were 812 users and 514 non-users; users were older, more likely to have smoked, had greater body mass index, and had more severe fILD. Despite a similar 6-min SpO2, users perceived greater dyspnea than non-users (Borg 3.9 ± 2.0 vs 2.9 ± 1.7, p < 0.0001). Whether subjects became hypoxemic (6-min SpO2 < 89 %) or not during the walk, the results were the same: users perceived greater dyspnea than non-users (hypoxemic: users 3.5 ± 2.1 vs non-users 2.7 ± 1.8, p < 0.0001; non-hypoxemic: users 3.4 ± 1.9 vs non-users 2.4 ± 1.6, p < 0.0001). Among subjects who did not desaturate (SpO2 drop < 4 %), users walked a shorter distance (944.9 ± 367.0 vs 1385.3 ± 322.4 feet, p < 0.0001) but perceived greater dyspnea than non-users (3.3 ± 1.6 vs 2.3 ± 1.7, p = 0.005). No combination of potentially influential predictor variables entered in multivariate models explained more than 11 % of the variance in dyspnea ratings. Conclusion: Dyspnea is a complex perception, and in patients with fILD, O2 may lessen, but does not resolve, it. Further research is needed to clarify why fILD patients who use O2 perceive greater levels of dyspnea with activity than O2 non-users.
    Full-text · Article · Dec 2015
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    ABSTRACT: Interstitial lung disease (ILD) is a common pulmonary manifestation of rheumatoid arthritis. There is lack of clarity around predictors of mortality and disease behaviour over time in these patients.We identified rheumatoid arthritis-related interstitial lung disease (RA-ILD) patients evaluated at National Jewish Health (Denver, CO, USA) from 1995 to 2013 whose baseline high-resolution computed tomography (HRCT) scans showed either a nonspecific interstitial pneumonia (NSIP) or a "definite" or "possible" usual interstitial pneumonia (UIP) pattern. We used univariate, multivariate and longitudinal analytical methods to identify clinical predictors of mortality and to model disease behaviour over time.The cohort included 137 subjects; 108 had UIP on HRCT (RA-UIP) and 29 had NSIP on HRCT (RA-NSIP). Those with RA-UIP had a shorter survival time than those with RA-NSIP (log rank p=0.02). In a model controlling for age, sex, smoking and HRCT pattern, a lower baseline % predicted forced vital capacity (FVC % pred) (HR=1.46; p<0.0001) and a 10% decline in FVC % pred from baseline to any time during follow up (HR=2.57; p<0.0001) were independently associated with an increased risk of death.Data from this study suggest that in RA-ILD, disease progression and survival differ between subgroups defined by HRCT pattern; however, when controlling for potentially influential variables, pulmonary physiology, but not HRCT pattern, independently predicts mortality.
    No preview · Article · Nov 2015 · European Respiratory Journal
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    ABSTRACT: The objective of this study was to determine the safety and efficacy of carlumab in the treatment of idiopathic pulmonary fibrosis (IPF).A phase 2, randomised, double-blind placebo-controlled dose-ranging study was conducted in patients with IPF (n=126). Patients were randomised to carlumab (1 mg·kg(-1), 5 mg·kg(-1), or 15 mg·kg(-1)) or placebo every 4 weeks. The primary endpoint was the rate of percentage change in forced vital capacity (FVC). Secondary endpoints were time to disease progression, absolute change in FVC, relative change in diffusing capacity of the lung for carbon monoxide (DLCO), and St George's Respiratory Questionnaire (SGRQ) total score.Due to a pre-planned, unfavourable interim benefit-risk analysis, dosing was suspended. The rate of percentage change in FVC showed no treatment effect (placebo -0.582%, 1 mg·kg(-1) -0.533%, 5 mg·kg(-1) -0.799% and 15 mg·kg(-1) -0.470%; p=0.261). All active treatment groups showed a greater decline in FVC (1 mg·kg(-1) -290 mL, 5 mg·kg(-1) -370 mL and 15 mg·kg(-1) -320 mL) compared with placebo (-130 mL). No effect on disease progression, DLCO, infection rates or mortality was observed. SGRQ scores showed a nonsignificant trend toward worsening with active treatment. Unexpectedly, free CC-chemokine ligand 2 levels were elevated above baseline at both 24 and 52 weeks. A higher proportion of patients with one or more serious adverse events was observed in the 5 mg·kg(-1) group (53.1%) compared with 1 mg·kg(-1) (15.2%), 15 mg·kg(-1) (21.9%) and placebo (46.4%), although no unexpected serious adverse events were noted.Although dosing was stopped prematurely, it is unlikely that carlumab provides benefit to IPF patients.
    No preview · Article · Oct 2015 · European Respiratory Journal
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    ABSTRACT: Background: Idiopathic pulmonary fibrosis is a progressive lung disease with variable course in individuals. The Gender-Age-Physiology (GAP) Index stage uses clinical variables to stage mortality risk. It is unknown whether clinical staging predicts future pulmonary function decline. We assess whether the GAP stage predicts future pulmonary function decline, and whether interval pulmonary function change predicts mortality after accounting for stage. Methods: Patients with Idiopathic Pulmonary Fibrosis (n=657) were identified retrospectively at three tertiary referral centers and baseline GAP stage assessed. Mixed models describe average trajectories of forced vital capacity (FVC) and diffusion capacity (DLCO). Multivariable Cox proportional hazards models assess whether pulmonary function declines of 10% or more in 6 months predict mortality after accounting for stage. Results: Over 2 years, GAP stage was not associated with differences in yearly lung function decline. After accounting for stage, a 10% decrease in FVC or DLCO over 6 months independently predicted death or transplant (FVC HR=1.37, DLCO HR 1.30, both p≤0.03). GAP stage 2 patients with declining pulmonary function experienced a survival profile similar to GAP 3 patients with 1-year event-free survival of 59.3% (CI95% 49.4-67.8) versus 56.9% (CI95% 42.2-69.1). Conclusions: Baseline GAP stage predicts death or lung transplantation, but not the rate of future pulmonary function decline. After accounting for GAP stage, a decline of 10% or more over 6 months independently predicts death or lung transplant.
    No preview · Article · Oct 2015 · Chest
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    ABSTRACT: The clinical course of pulmonary hypertension (PH) in idiopathic pulmonary fibrosis (IPF) is not known except in advanced disease.488 subjects in a placebo-controlled study of ambrisentan in IPF with mild-moderate restriction in lung volume, underwent right heart catheterisation (RHC) at baseline and 117 subjects (24%) had repeated haemodynamic measurements at 48 weeks.The subjects were categorised into a) World Health Organization (WHO) Group 3 PH (PH associated with pulmonary disease), n=68 (14%); b) WHO Group 2 PH (PH associated with left-sided cardiac disease), n=25 (5%); c) no PH but elevated pulmonary artery wedge pressure (PAWP), n=21 (4%); and d) no PH but without elevation of PAWP, n=374 (77%). The WHO Group 3 PH subjects had a lower diffusion capacity, 6MWD and oxygen saturation compared to the subjects with no PH. There was no significant change in mean pulmonary arterial pressure with ambrisenten or placebo after 12 months.Subjects with IPF associated with WHO Group 3 PH had impaired gas exchange and exercise capacity compared to patients without PH. An additional 9% of the subjects had haemodynamic evidence of subclinical left-ventricular dysfunction. Pulmonary artery pressures remained stable over 1 year in the majority of the cohort. Copyright ©ERS 2015.
    No preview · Article · Aug 2015 · European Respiratory Journal
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    ABSTRACT: The goal of this review is to summarise the clinical features, management, and prognosis of acute exacerbations of idiopathic pulmonary fibrosis (AE-IPF). AE-IPF has previously been defined based on clinical and radiological features that include the subacute onset of dyspnoea, bilateral ground glass changes on chest high-resolution computed tomography, and the absence of an identifiable aetiology. The annual incidence of AE-IPF is typically reported at 5-15%, but is less common in mild disease. Features of diffuse alveolar damage are present when a biopsy is performed. Idiopathic pulmonary fibrosis (IPF) patients with acute respiratory worsening are often initially treated with high dose corticosteroids and antimicrobials; however, there are no clear data to support these therapies, and the short-term mortality of AE-IPF is ∼50%. Recent studies have shown that the features and prognosis of AE-IPF are similar to other causes of acute respiratory worsening, including infection, aspiration, air pollution and mechanical injury to the alveolar epithelium. Based on this emerging evidence, we propose a novel approach to the classification of acute respiratory worsening events in patients with IPF that focuses on clinical and radiological findings consistent with an underlying pathobiology of diffuse alveolar damage. Copyright ©ERS 2015.
    No preview · Article · Aug 2015 · European Respiratory Journal
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    ABSTRACT: Many patients with an idiopathic interstitial pneumonia (IIP) have clinical features that suggest an underlying autoimmune process but do not meet established criteria for a connective tissue disease (CTD). Researchers have proposed differing criteria and terms to describe these patients, and lack of consensus over nomenclature and classification limits the ability to conduct prospective studies of a uniform cohort.The "European Respiratory Society/American Thoracic Society Task Force on Undifferentiated Forms of Connective Tissue Disease-associated Interstitial Lung Disease" was formed to create consensus regarding the nomenclature and classification criteria for patients with IIP and features of autoimmunity.The task force proposes the term "interstitial pneumonia with autoimmune features" (IPAF) and offers classification criteria organised around the presence of a combination of features from three domains: a clinical domain consisting of specific extra-thoracic features, a serologic domain consisting of specific autoantibodies, and a morphologic domain consisting of specific chest imaging, histopathologic or pulmonary physiologic features.A designation of IPAF should be used to identify individuals with IIP and features suggestive of, but not definitive for, a CTD. With IPAF, a sound platform has been provided from which to launch the requisite future research investigations of a more uniform cohort. Copyright ©ERS 2015.
    Preview · Article · Jul 2015 · European Respiratory Journal
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    ABSTRACT: Idiopathic pulmonary fibrosis is a progressive fibrotic lung disease that distorts pulmonary architecture, leading to hypoxia, respiratory failure, and death. Diagnosis is difficult because other interstitial lung diseases have similar radiological and histopathological characteristics. A usual interstitial pneumonia pattern is a hallmark of idiopathic pulmonary fibrosis and is essential for its diagnosis. We aimed to develop a molecular test that distinguishes usual interstitial pneumonia from other interstitial lung diseases in surgical lung biopsy samples. The eventual goal of this research is to develop a method to diagnose idiopathic pulmonary fibrosis without the patient having to undergo surgery.
    Full-text · Article · May 2015
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    ABSTRACT: The response of the right ventricle (RV) to pulmonary arterial hypertension (PAH) involves changes in contractile function, chamber size, hypertrophy, and extracellular matrix (ECM). Galectin-3 (Gal-3) is a mediator of myocardial ECM metabolism and biomarker for left heart remodeling, yet its ability to reflect RV remodeling is unknown. We hypothesized that serum Gal-3 levels correlate with RV morphology and function in PAH, and that Gal-3 is associated with circulating markers of ECM. Fifteen subjects with PAH and 10 age-matched controls underwent same-day echocardiography, cardiac magnetic resonance (CMR) imaging, and phlebotomy for Gal-3 and ECM biomarkers including N-terminal propeptide of type III collagen type (PIIINP), tissue inhibitor of metalloproteinase-1 (TIMP-1), and hyaluronic acid (HA). RV ejection fraction, end diastolic volume index, end systolic volume index, and mass index were calculated using CMR. Echocardiography was used to estimate RV systolic pressure and measure RV strain. Serum Gal-3, TIMP-1, and HA levels were all significantly increased in PAH subjects when compared to controls. Gal-3 correlated with RV ejection fraction (ρ −0.44, p 0.03), end diastolic volume index (ρ 0.42, p 0.03), end systolic volume index (ρ 0.44, p 0.027), mass index (ρ 0.47, p 0.016), systolic pressure (ρ 0.55, p
    No preview · Article · May 2015 · Heart and Vessels
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    ABSTRACT: The past decade has seen substantial progress in understanding the pathobiology, natural history, and clinical significance of idiopathic pulmonary fibrosis (IPF), culminating in the establishment of two effective medical therapies. Now seems an important time to reconsider the design and conduct of future IPF clinical trials. Building on lessons learned over the past decade, we use this perspective to lay out four key considerations for moving forward effectively and efficiently with the next generation of clinical trials in IPF. These are: development of a coordinated IPF clinical trials network; establishment of expectations for early phase proof of concept studies; adaptation of late-phase efficacy trial designs to the emergence of approved therapies, and; agreement on primary end-points for late phase clinical trials. Continued progress in the field of IPF will require creativity and collaboration on the part of all stakeholders. We believe that addressing these four considerations will encourage and enable investment in this new era of drug development in IPF, and will lead to more rapid development of effective therapies. Copyright ©ERS 2015.
    No preview · Article · Apr 2015 · European Respiratory Journal
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    ABSTRACT: Mortality is an impractical primary endpoint for clinical trials in patients with idiopathic pulmonary fibrosis who have mild-to-moderate physiological impairment because event rates are low. Change in forced vital capacity (FVC) is widely accepted as a surrogate for mortality and is the most common primary endpoint in clinical trials for this disorder. Use of hospital admission as a predictor for mortality, independent of FVC decline, has not been well defined. We aimed to ascertain the independent and combined association of hospital admission and at least a 10% decrease in FVC with all-cause mortality.
    No preview · Article · Apr 2015
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    ABSTRACT: Physical functional capacity is impaired in idiopathic pulmonary fibrosis (IPF). There is no tool to measure this key clinical outcome. The continuous-scale physical function performance (CS-PFP) test is one that assesses activities of daily living, but it has never been used in IPF. We determined internal consistency of the CS-PFP. We used correlations to assess the strength of association between CS-PFP scores and various parameters of IPF severity, and compared the CS-PFP scores between patients with IPF and published values from a healthy control group. Sixteen subjects completed the test and retest. Test-retest reliability (0.84, p = 0.003) and internal consistency (Cronbach's α = 0.91) were excellent. Subjects with IPF had significantly worse CS-PFP scores than controls (46.0 ± 11.1 vs 58.7 ± 12.5, p = 0.001). In IPF, the CS-PFP scores correlated moderately to very strongly with several disease severity variables. The CS-PFP is a reliable and valid tool in IPF.
    No preview · Article · Apr 2015 · Expert Review of Respiratory Medicine
  • Tristan J. Huie · Kevin K. Brown
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    ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic, fibrosing interstitial lung disease of unknown etiology characterized by progressive lung scarring and a median survival of 3-5 years from the time of diagnosis. The most recent consensus guidelines adopt a diagnostic process that characterizes patients as having a final diagnosis of IPF, probable IPF, or possible IPF determined from a combination of the clinical context and specific chest imaging and histologic disease patterns. Based on currently available data, the enrollment criteria for treatment trials could be expanded to include not only patients with IPF but also those with probable and possible IPF without adversely affecting trial design or outcomes. Copyright © 2015 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.
    No preview · Article · Mar 2015
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    ABSTRACT: Background: Up to 20% of cases of idiopathic interstitial pneumonia (IIP) cluster in families, comprising the syndrome of Familial Interstitial Pneumonia (FIP); however, the genetic basis of FIP remains uncertain in a majority of families. We hypothesized that new disease-causing rare genetic variants could be identified using whole-exome sequencing of affected members from FIP families, providing additional insights into disease pathogenesis. Methods: Affected subjects from 25 kindreds were selected from an ongoing FIP registry for whole-exome sequencing (WES) from genomic DNA. Candidate rare variants were confirmed by Sanger sequencing and co-segregation analysis was performed in families, followed by additional sequencing of affected individuals from another163 kindreds. Results: We identified a potentially damaging rare variant in the gene encoding for regulator of telomere elongation helicase 1 (RTEL1) that segregated with disease and was associated with very short telomeres in peripheral blood mononuclear cells in one of 25 families in our original WES cohort. Evaluation of affected individuals in 163 additional kindreds revealed another 8 families (5%) with heterozygous rare variants in RTEL1 that segregated with clinical FIP. Probands and unaffected carriers of these rare variants had short telomeres (<10% for age) in peripheral blood mononuclear cells and increased T-circle formation, suggesting impaired RTEL1 function. Conclusions: Rare loss-of-function variants in RTEL1 represent a newly defined genetic predisposition for FIP, supporting the importance of telomere-related pathways in pulmonary fibrosis.
    Full-text · Article · Feb 2015 · American Journal of Respiratory and Critical Care Medicine
  • Aryeh Fischer · Kevin K Brown
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    ABSTRACT: The intersection of interstitial lung disease (ILD) and connective tissue disease (CTD) is complex and commonly includes the scenario whereby ILD is identified in patients with pre-existing CTD, is the presenting manifestation of an occult CTD, or arises within the context of a suggestive form of CTD. Determining that an ILD is CTD-associated is important because this knowledge often impacts management and prognosis. Identifying occult CTD in patients with presumed idiopathic ILD can be challenging and requires a comprehensive, often multidisciplinary, evaluation. There is much uncertainty and controversy surrounding the suggestive forms of CTD-associated ILD (CTD-ILD) and prospective studies are needed to provide a better understanding of the natural history of these cohorts, how to best manage them, and to determine whether they behave similar to classifiable forms of CTD-ILD. © 2014 American College of Rheumatology.
    No preview · Article · Jan 2015
  • Evans R. Fernández Pérez · Kevin K. Brown
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    ABSTRACT: Fibrotic hypersensitivity pneumonitis (FHP) is a specific form of HP defined by chest imaging evidence or pathologic evidence of fibrosis or scarring. Fibrotic HP appears to be irreversible, is often progressive and frequently indistinguishable from other forms of chronic fibrosing interstitial lung diseases (ILD), in particular idiopathic pulmonary fibrosis (IPF). Accurate diagnosis is a challenge given the diverse and often nonspecific clinicoradiologic patterns, heterogenous clinical course, and a frequent lack of a readily recognizable temporal relationship between exposure to an inciting antigen (IA) and symptoms in more than half of the patients. This chapter focuses on the clinical features, diagnostic evaluation and management of FHP.
    No preview · Article · Dec 2014

Publication Stats

12k Citations
1,573.97 Total Impact Points

Institutions

  • 2006-2015
    • National Jewish Health
      Denver, Colorado, United States
  • 2002-2015
    • University of Colorado
      • • Department of Medicine
      • • Division of Pulmonary Sciences and Critical Care Medicine
      Denver, Colorado, United States
    • Max Planck Institute for Mathematics in the Sciences
      Leipzig, Saxony, Germany
  • 2006-2009
    • National Research Center (CO, USA)
      Boulder, Colorado, United States
  • 2007
    • National Institute of Environmental Health Sciences
      • Laboratory of Respiratory Biology (LRB)
      Durham, North Carolina, United States
  • 2002-2006
    • Duke University
      Durham, North Carolina, United States
  • 2005
    • University of Michigan
      • Department of Internal Medicine
      Ann Arbor, Michigan, United States
  • 2004
    • Yamaguchi University
      • Division of Radiology
      Yamaguti, Yamaguchi, Japan
  • 2003
    • University of Colorado Hospital
      Denver, Colorado, United States
  • 2000
    • University of California, San Francisco
      • Department of Medicine
      San Francisco, California, United States