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• Prediction models for hypersensitivity pneumonitis
  Yves Lacasse
  Published on: 26 January 2017
• Authors' Response to: Prediction models for hypersensitivity pneumonitis
  Kerri A. Johannson
  Published on: 25 January 2017

• Published on: 26 January 2017

  Prediction models for hypersensitivity pneumonitis

  • Yves Lacasse, Pulmonologist

  To the Editor,

  The diagnosis of hypersensitivity pneumonitis (HP) is difficult and often relies on an array of clinical symptoms and signs developed in an appropriate setting, with the demonstration of radiographic and tomographic abnormalities, serum precipitating antibodies against offending antigens, a lymphocytic alveolitis on bronchoalveolar lavage, and/or a granulomatous reaction on lung biopsies. Taken...

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  To the Editor,

  The diagnosis of hypersensitivity pneumonitis (HP) is difficult and often relies on an array of clinical symptoms and signs developed in an appropriate setting, with the demonstration of radiographic and tomographic abnormalities, serum precipitating antibodies against offending antigens, a lymphocytic alveolitis on bronchoalveolar lavage, and/or a granulomatous reaction on lung biopsies. Taken separately, all these manifestations are nonspecific and only the combination of several of them may help clinicians to arrive at a correct diagnosis. By providing better estimates of the probability of a disease than clinical judgement, prediction rules (i.e., tools that quantifies the contribution that various components of the history, physical examination and basic laboratory results makes toward the diagnosis in an individual patient) may guide clinical practice.[1] In this regard, we read with much interest Johannson and colleagues' report of a multidimensional diagnostic model for chronic hypersensitivity pneumonitis (HP).[2] This research parallels the HP Study previously reported, the objective of which was to develop a clinical prediction rule for the diagnosis of active HP.[3]

  Johannson's study bears some resemblance to the HP study, especially in its statistical methods. However, similarities end here. The HP study was a prospective multicenter study of 661 patients presenting with an acute pulmonary syndrome for which HP was considered in the differential diagnosis. Johannson's study is a single-center retrospective analysis of 190 patients with biopsy-proven, chronic HP. The HP study specifically applied to active acute, subacute and chronic HP, and only excluded inactive residual HP. It included consecutive patients, chosen in an unbiased fashion and representing a wide spectrum of diseases from a variety of institutions, hence increasing generalizability. By including only patients who required surgical lung biopsy, Johannson and colleagues likely preselected difficult cases of HP and non-HP interstitial lung disease, with the consequence of underestimating the accuracy of their prediction models. The HP Study looked at simple and objective clinical criteria and used high resolution computed tomography (HRCT) in the gold standard definition of HP, whereas Johansson's study incorporated radiological features from HRCT and a radiologist's diagnostic impression in their prediction model. Bronchoalveolar lavage was obtained in all patients in the HP study but it was not considered in Johannson's study.

  Johannson's study and the HP Study are not competing studies; they are complementary and their results cannot be directly compared. Although the two studies had different patient populations and case selection, they may be useful in the appropriate setting. Both studies have another point in common: to be elevated in the hierarchy of evidence for clinical decision rules, they should be validated again in different populations.[1]

  Yves Lacasse MD, Institut universitaire de cardiologie et de pneumologie de Quebec, Universite Laval, Quebec, Canada

  Moises Selman MD, Instituto Nacional de Enfermedades Respiratorias, Mexico DF, Mexico

  Ulrich Costabel MD, Ruhrlandklinik, Essen, Germany

  Jean-Charles Dalphin MD, Centre Hospitalier Universitaire de Besancon, Besancon, France

  Thomas V. Colby MD, Mayo Clinic Scottsdale, Scottsdale, USA

  Riitta Erkinjuntti-Pekkanen MD, Social Insurance Institution, Helsinki, Finland

  Ferran Morell MD, Hospital Universitari Vall d'Hebron, Barcelona, Spain

  Yvon Cormier MD, Universite Laval, Quebec, Canada

  for the HP Study Group.

  References

  1 McGinn TG, Guyatt GH, Wyer PC, et al. Users' guides to the medical literature: XXII: how to use articles about clinical decision rules. Evidence-Based Medicine Working Group. JAMA 2000;284:79-84.

  2 Johannson KA, Elicker BM, Vittinghoff E, et al. A diagnostic model for chronic hypersensitivity pneumonitis. Thorax 2016;71:951-4.

  3 Lacasse Y, Selman M, Costabel U, et al. Clinical diagnosis of hypersensitivity pneumonitis. Am J Respir Crit Care Med 2003;168:952-8.

  Conflict of Interest:

  Yves Lacasse was the principal investigator of the HP Study. All co-authors of this letter were co-investigators of the HP Study.

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  Conflict of Interest:
  None declared.

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• Published on: 25 January 2017

  Authors' Response to: Prediction models for hypersensitivity pneumonitis

  • Kerri A. Johannson
  • Other Contributors:
    • Brett M. Elicker, Eric Vittinghoff, Deborah Assayag, Kaissa de Boer, Jeffrey A. Golden, Kirk D. Jones, Talmadge E. King Jr., Laura L. Koth, Joyce S. Lee, Brett Ley, Paul J. Wolters, Harold R. Collard.

  We thank Dr. Lacasse and the HP Study Group for their correspondence regarding 'A diagnostic model for chronic hypersensitivity pneumonitis', and appreciate their thoughtful consideration of our work.(1) We agree that these two studies are complementary, and hope that both will serve to improve diagnostic accuracy in the evaluation of patients with suspected HP. We further concur that much work remains to be done to advan...

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  We thank Dr. Lacasse and the HP Study Group for their correspondence regarding 'A diagnostic model for chronic hypersensitivity pneumonitis', and appreciate their thoughtful consideration of our work.(1) We agree that these two studies are complementary, and hope that both will serve to improve diagnostic accuracy in the evaluation of patients with suspected HP. We further concur that much work remains to be done to advance our understanding of HP.

  The HP Study was a pivotal paper in our field, the first to define a clinically applicable prediction model to diagnose acute, subacute and chronic HP.(2) However, the HP Study cohort included patients with 'active' disease, specifically excluding patients with fibrotic sequelae or 'residual inactive HP'. Notably, an inciting antigen was identified in 114/116 (97%) of patients with HP. Our focus was on a different clinical population and conundrum - the differentiation of chronic, commonly fibrotic HP from other fibrotic interstitial lung diseases, in particular idiopathic pulmonary fibrosis (IPF). These HP patients typically do not present with an acute pulmonary syndrome, and previous data from our center have demonstrated 60% to be antigen indeterminate, despite thorough investigation,(3) consistent with data from similar sub-specialty centers.(4) We required surgical lung biopsy as part of our gold standard multi-disciplinary discussion-based diagnosis of HP given the lack of universally accepted non-histopathological criteria in this clinical scenario.

  The study of HP is challenging, attributable to a lack of universally accepted diagnostic criteria, the conundrum of antigen indeterminate disease and controversies over the clinical utility of bronchoalveolar lavage fluid analysis, serum specific antibodies, and inhalational challenge. A recent review suggests focused areas for future research and we are enthused by the increasing interest in this area.(5) Along with the HP Study group, we remain hopeful that our complementary contributions to clinical prediction models will lead to an overall better diagnostic accuracy of HP in all its forms, and ultimately improved patient care.

  Kerri A. Johannson MD MPH, University of Calgary, Calgary AB Canada; Brett M. Elicker MD, University of California, San Francisco, San Francisco CA USA; Eric Vittinghoff PhD, University of California, San Francisco, San Francisco CA USA; Deborah Assayag MD, McGill University, Montreal QC Canada; Kaissa de Boer MD, University of Ottawa, Ottawa ON Canada; Jeffrey A. Golden MD, University of California, San Francisco, San Francisco CA USA; Kirk D. Jones MD, University of California, San Francisco, San Francisco CA USA; Talmadge E. King Jr. MD, University of California, San Francisco, San Francisco CA USA; Laura L. Koth MD, University of California, San Francisco, San Francisco CA USA; Joyce S. Lee MD, University of Colorado, Denver, Aurora CO USA; Brett Ley MD, University of California, San Francisco, San Francisco CA USA; Paul J. Wolters MD, University of California, San Francisco, San Francisco CA USA; Harold R. Collard MD, University of California, San Francisco, San Francisco CA USA.

  References

  1. Johannson KA, Elicker BM, Vittinghoff E, Assayag D, de Boer K, Golden JA, Jones KD, King TE, Koth LL, Lee JS, Ley B, Wolters PJ, Collard HR. A diagnostic model for chronic hypersensitivity pneumonitis. Thorax 2016.

  2. Lacasse Y, Selman M, Costabel U, Dalphin JC, Ando M, Morell F, Erkinjuntti-Pekkanen R, Muller N, Colby TV, Schuyler M, Cormier Y. Clinical diagnosis of hypersensitivity pneumonitis. Am J Respir Crit Care Med 2003; 168: 952-958.

  3. Mooney JJ, Elicker BM, Urbania TH, Agarwal MR, Ryerson CJ, Nguyen ML, Woodruff PG, Jones KD, Collard HR, King TE, Koth LL. Radiographic fibrosis score predicts survival in hypersensitivity pneumonitis. Chest 2013; 144: 586-592.

  4. Fernandez Perez ER, Swigris JJ, Forssen AV, Tourin O, Solomon JJ, Huie TJ, Olson AL, Brown KK. Identifying an inciting antigen is associated with improved survival in patients with chronic hypersensitivity pneumonitis. Chest 2013; 144: 1644-1651.

  5. Salisbury ML, Myers JL, Belloli EA, Kazerooni EA, Martinez FJ, Flaherty KR. Diagnosis and Treatment of Fibrotic Hypersensitivity Pneumonia. Where We Stand and Where We Need to Go. Am J Respir Crit Care Med 2016.

  Conflict of Interest:

  None declared

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  Conflict of Interest:
  None declared.

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