J Korean Med Assoc.  2009 Jan;52(1):49-58. 10.5124/jkma.2009.52.1.49.

Diagnosis and Treatment of Hypersensitivity Pneumonitis

• Park MS

• KMID: 2137733
• DOI: http://doi.org/10.5124/jkma.2009.52.1.49

Abstract

Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is an immunologically mediated granulomatous, inflammatory disease of the lungs caused by repeated inhalation of various antigens. HP may occur in acute, subacute, or chronic forms. Chronic HP may be progressive, irreversible, and evolve to fibrotic interstitial lung disease. The diagnosis of HP can be made from a combination of clinical, laboratory, radiologic, and pathologic findings. A careful environmental and occupational history and establishment of exposure to a known inciting antigen are key factors in making the diagnosis of HP. Serum precipitating antibodies, bronchoalveolar lavage, and lung biopsy may be helpful in making the diagnosis. The pathology of HP is characterized by interstitial lymphocytic infiltration, poorlyformed noncaseating granulomas, cellular bronchiolitis, and fibrosis. In the pathogenesis of HP, recent studies showed that both type III and type IV hypersensitivity reactions are involved and are mediated by immune complexes and Th1 T cells, respectively. IFN-gamma is essential for the development of HP, and IL-10 appears to modulate the severity of the disease. TNF-alpha and TGF-beta have been implicated in development of the pulmonary fibrosis that is seen in chronic HP. Avoidance of organic antigen exposure is the most important factor for the management of HP. There is often an apparent beneficial response to corticosteroids in the cases of severe acute and subacute HP, and for chronic HP that is severe or progressive.

Keyword

Hypersensitivity pneumonitis; Extrinsic allergic alveolitis; Interstitial lung disease; Diagnosis; Treatment

MeSH Terms

Adrenal Cortex Hormones
Alveolitis, Extrinsic Allergic
Antibodies
Antigen-Antibody Complex
Biopsy
Bronchiolitis
Bronchoalveolar Lavage
Fibrosis
Granuloma
Hypersensitivity
Hypersensitivity, Delayed
Inhalation
Interleukin-10
Lung
Lung Diseases, Interstitial
Pulmonary Fibrosis
T-Lymphocytes
Transforming Growth Factor beta
Tumor Necrosis Factor-alpha
Adrenal Cortex Hormones
Antibodies
Antigen-Antibody Complex
Interleukin-10
Transforming Growth Factor beta
Tumor Necrosis Factor-alpha

Figure

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  Figure 1 Chest X-ray of acute hypersensitivity pneumonitis. Chest X-ray showed some reticulonodular densities in both upper lobes.

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  Figure 2 High-resolution computed tomography scans of acute hypersensitivity pneumonitis showed discrete ground glass attenuation and tiny, ill-defined centrilobular nodules on upper and lower lung field.

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  Figure 3 After recurrent exposure to antigen, chest X-ray showed diffuse poorly-defined small nodular densities and diffuse ground glass opacities in subacute patient with hypersensitivity pneumonitis.

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  Figure 4 High-resolution computed tomography scans of subacute hypersensitivity pneumonitis showed discrete ground glass attenuatiuon and tiny, ill-defined centrilobular nodules, predominant on upper lung field.

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  Figure 5 Chest X-ray of chronic hypersensitivity pneumonitis. Chest X-ray showed coarse rericular opacities with diffusely scattered patchy ground glass opacities in both lung fields.

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  Figure 6 (A) High-resolution computed tomography scans of chronic hypersensitivity pneumonitis showed patchy areas of lung fibrosis, mainly peribronchiolar regions, and traction bronchiectasis or bronchiolectasis, slightly dominant on the upper lung field. Lobular air trappings were also seen in multifocal areas. (B) End-stage chronic hypersensitivity pneumonitis.

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  Figure 7 Pathologic findings of subacute hypersensitivity pneumonitis. Lymphocyte infiltration of the respiratory bronchioles and alveolar walls with ill-defined granuloma (H & E × 100).

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  Figure 8 Pathologic findings of chronic hypersensitivity pneumonitis. Chronic interstitial pneumonia pattern with illdefined granuloma and focal fibroblastic proliferation (H & E × 100).

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