Hypersensitivity pneumonitis

• Published in: Allergy Vol. 64; no. 3; pp. 322 - 334
• Main Authors: Girard, M., Lacasse, Y., Cormier, Y.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.03.2009; Blackwell
• Subjects: Alveolitis, Extrinsic Allergic - diagnosis; Alveolitis, Extrinsic Allergic - epidemiology; Alveolitis, Extrinsic Allergic - therapy; Animals; Antigens; Biological and medical sciences; Chemical and industrial products toxicology. Toxic occupational diseases; Dermatology; environment; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Immune system; immunology; inflammation; Inflammatory diseases; Inorganic dusts (pneumoconiosises) and organic dusts (byssinosis etc.); interstitial lung disease; Lungs; Medical diagnosis; Medical sciences; Medical treatment; organic dust; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Toxicology; Lung disease; Allergy; Immunopathology; Occupational disease; Respiratory disease; Dermatology; Inflammation; organic dust; Dust; Immunology; Interstitial pneumonitis; Environment; Bird breeder lung; environment; immunology; inflammation; interstitial lung disease
• ISSN: 0105-4538; 1398-9995; 0108-1675
• DOI: 10.1111/j.1398-9995.2009.01949.x

The first few cases of hypersensitivity pneumonitis (HP) were described in the early 20th century in farmers exposed to moldy hay or straw. As then, HP has been ascribed to multiple inhaled antigens found in a large variety of environmental settings. Hypersensitivity pneumonitis results from an exaggerated immune response, which gives rise to acute infection‐like symptoms or to progressive, sometimes irreversible lung damage. The diagnosis is based on a combination of clinical characteristics of the disease. Clinical diagnostic criteria have recently been published. The immune mechanisms leading to HP are still incompletely understood. Initially, believed to be a classes III and IV immune response, we now have a clearer understanding of the complex inflammatory events involved. These include the release of pro inflammatory cytokines and a decrease in the immune control mechanisms via surfactant, dendritic and T‐regulatory cells. Despite the improved understanding, the treatment and outcome of HP have not changed. Oral corticosteroids remain the only effective drugs and contact withdrawal constitutes the ideal solution. If unchecked, HP can lead to irreversible lung damage in the form of fibrosis or emphysema, respiratory insufficiency and even death.