Hypersensitivity pneumonitis: A fibrosing alveolitis produced by inhalation of diverse antigens

Paul A. Greenberger*

*Corresponding author for this work

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Hypersensitivity pneumonitis (HP) is a T H 1 lymphocyte–biased fibrosing alveolitis caused by antigens ranging from avian excreta, fungi, thermophilic bacteria, and protozoa to reactive chemicals found in the workplace. Mimicking a viral syndrome, acute exposures to inciting antigens cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise usually from 4 to 8 hours later so that the temporal relationship between antigen exposure and symptoms might be unsuspected. The histology of HP reveals prominent lymphocyte infiltrates that thicken the alveolar septa with poorly formed granulomas or giant cells. Bronchoalveolar lavage fluid demonstrates greater than 20% lymphocytes in nearly all patients. Abnormalities on high-resolution computed tomographic examinations range from nodular centrilobular opacities in acute/subacute disease to increased reticular markings and honeycombing fibrosis, which typically are predominant in the upper lobes, in patients with advanced disease. Descriptors include “mosaic” attenuation and ground-glass opacities. Repeated episodes can result in nodular pulmonary infiltrates and suspected nonspecific interstitial pneumonia or idiopathic pulmonary fibrosis. Clinicians require a high level of suspicion to make an early diagnosis of HP before extensive pulmonary fibrosis or restrictive lung disease has occurred.

Original languageEnglish (US)
Pages (from-to)1295-1301
Number of pages7
JournalJournal of Allergy and Clinical Immunology
Volume143
Issue number4
DOIs
StatePublished - Apr 2019

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Extrinsic Allergic Alveolitis
Pulmonary Fibrosis
Inhalation
Antigens
Giant Cell Granuloma
Lymphocytes
Chills
Idiopathic Pulmonary Fibrosis
Interstitial Lung Diseases
Bronchoalveolar Lavage Fluid
Arthralgia
Acute Disease
Cough
Workplace
Dyspnea
Lung Diseases
Glass
Early Diagnosis
Histology
Fibrosis

Keywords

  • Hypersensitivity
  • avian
  • granulomas
  • lymphocytes
  • pneumonitis
  • precipitins
  • restrictive
  • thermophilic

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

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title = "Hypersensitivity pneumonitis: A fibrosing alveolitis produced by inhalation of diverse antigens",
abstract = "Hypersensitivity pneumonitis (HP) is a T H 1 lymphocyte–biased fibrosing alveolitis caused by antigens ranging from avian excreta, fungi, thermophilic bacteria, and protozoa to reactive chemicals found in the workplace. Mimicking a viral syndrome, acute exposures to inciting antigens cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise usually from 4 to 8 hours later so that the temporal relationship between antigen exposure and symptoms might be unsuspected. The histology of HP reveals prominent lymphocyte infiltrates that thicken the alveolar septa with poorly formed granulomas or giant cells. Bronchoalveolar lavage fluid demonstrates greater than 20{\%} lymphocytes in nearly all patients. Abnormalities on high-resolution computed tomographic examinations range from nodular centrilobular opacities in acute/subacute disease to increased reticular markings and honeycombing fibrosis, which typically are predominant in the upper lobes, in patients with advanced disease. Descriptors include “mosaic” attenuation and ground-glass opacities. Repeated episodes can result in nodular pulmonary infiltrates and suspected nonspecific interstitial pneumonia or idiopathic pulmonary fibrosis. Clinicians require a high level of suspicion to make an early diagnosis of HP before extensive pulmonary fibrosis or restrictive lung disease has occurred.",
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AB - Hypersensitivity pneumonitis (HP) is a T H 1 lymphocyte–biased fibrosing alveolitis caused by antigens ranging from avian excreta, fungi, thermophilic bacteria, and protozoa to reactive chemicals found in the workplace. Mimicking a viral syndrome, acute exposures to inciting antigens cause abrupt onset of nonproductive cough, dyspnea, and chills with arthralgias or malaise usually from 4 to 8 hours later so that the temporal relationship between antigen exposure and symptoms might be unsuspected. The histology of HP reveals prominent lymphocyte infiltrates that thicken the alveolar septa with poorly formed granulomas or giant cells. Bronchoalveolar lavage fluid demonstrates greater than 20% lymphocytes in nearly all patients. Abnormalities on high-resolution computed tomographic examinations range from nodular centrilobular opacities in acute/subacute disease to increased reticular markings and honeycombing fibrosis, which typically are predominant in the upper lobes, in patients with advanced disease. Descriptors include “mosaic” attenuation and ground-glass opacities. Repeated episodes can result in nodular pulmonary infiltrates and suspected nonspecific interstitial pneumonia or idiopathic pulmonary fibrosis. Clinicians require a high level of suspicion to make an early diagnosis of HP before extensive pulmonary fibrosis or restrictive lung disease has occurred.

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