Chapter 19: Hypersensitivity pneumonitis

Allergy Asthma Proc. 2012 May-Jun:33 Suppl 1:64-66. doi: 10.2500/aap.2012.33.3552.


Hypersensitivity pneumonitis (HP), also referred to as extrinsic allergic alveolitis, is characterized by non-IgE-mediated inflammation of the parenchyma, alveoli, and terminal airways of the lung initiated by inhaled antigens in a susceptible host. Etiologic agents of HP are either organic high molecular weight compounds such as bacteria, fungi, amoebae, plant, and animal proteins or inorganic low molecular weight haptens such as isocyanate and drugs including amiodarone, nitrofurantoin, and minocycline. Six significant predictors have been identified that provide ∼95% diagnostic accuracy. These six predictors are (1) exposure to a known offending allergen, (2) positive precipitating antibodies to the offending antigen, (3) recurrent episodes of symptoms, (4) inspiratory crackles on lung auscultation, (5) symptoms occurring 4-8 hours after exposure, and (6) weight loss. HP is staged into acute, subacute, and chronic. In the acute stage after direct exposure to the antigen, there is fever, chills, nonproductive cough, dyspnea, malaise, and myalgias, all resembling influenza. However, if obtained, a chest radiograph shows nodular infiltrates, and pulmonary function testing is restrictive (unless the cause is avian in which obstruction or obstruction with restriction is present). In the chronic stage, fever and chills are absent, but weight loss can occur. The immunologic response includes activated macrophages and CD8(+) cytotoxic lymphocytes, and bronchoalveolar lavage fluid reveals marked lymphocytosis with a ratio of CD4(+) cells to CD8(+) cells <1. Activated macrophages have increased expression of CD80/CD86, and T cells have increased expression of its counter-ligand CD28, evidence for heightened antigen presentation.

Publication types

  • Review

MeSH terms

  • Alveolitis, Extrinsic Allergic / diagnosis*
  • Alveolitis, Extrinsic Allergic / drug therapy
  • Alveolitis, Extrinsic Allergic / etiology*
  • Humans