From the Guidelines
Extrinsic allergic alveolitis (EAA), also known as hypersensitivity pneumonitis, is an inflammatory lung disease caused by repeated inhalation of environmental antigens that trigger an immune response in susceptible individuals. This condition affects the small air sacs (alveoli) and surrounding lung tissue, leading to inflammation and potential scarring if left untreated. According to the most recent and highest quality study 1, HP is now understood as an immunologically mediated form of lung disease resulting from inhalational exposure to a large variety of environmental and/or occupational organic and nonorganic inciting antigens. Common triggers include organic dusts from moldy hay, bird proteins, fungi in humidifiers or air conditioners, and certain chemicals in the workplace. EAA typically presents in acute, subacute, or chronic forms with symptoms including shortness of breath, dry cough, fatigue, and flu-like symptoms such as fever and chills.
The primary treatment involves identifying and avoiding the triggering antigen, which often leads to symptom improvement. In more severe cases, corticosteroids like prednisone may be prescribed to reduce inflammation. The disease mechanism involves both type III (immune complex) and type IV (cell-mediated) hypersensitivity reactions, with the repeated antigen exposure causing lung damage through inflammatory processes. Early diagnosis and intervention are crucial to prevent progression to irreversible pulmonary fibrosis, as highlighted in the study 1. Key characteristics of HP include:
- The temporal relationship between exposure and symptoms
- Occupation
- The type of antigen
- The presence of radiographic or histopathological fibrosis, which is the primary determinant of prognosis, as noted in the study 1.
Overall, the most effective approach to managing EAA is to identify and avoid the triggering antigen, and to provide early treatment to prevent long-term lung damage 1.
From the Research
Definition of Extrinsic Allergic Alveolitis (EAA)
- Extrinsic allergic alveolitis (EAA), also known as hypersensitivity pneumonitis, is a disease caused by a hypersensitivity reaction after repeated inhalation of finely dispersed antigens, mainly organic particles or low molecular weight chemicals 2.
- It 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 3.
Causes and Risk Factors
- The disease is caused by the inhalation of small organic allergen particles by non-atopic subjects, which provoke an allergic reaction, thought to be chiefly due to a type III mechanism, in the peripheral respiratory tissues 4.
- Etiologic agents of EAA 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 3.
Clinical Features
- The clinical features of EAA are determined by the nature of exposure, the immunopathological mechanism(s) involved, and the site of reaction in the lung 4.
- The disease has been defined as acute, subacute, and chronic, with symptoms ranging from flu-like symptoms, dyspnea, and cough in the acute form to progressive dyspnea in the chronic form 5.
- Six significant predictors have been identified that provide ∼95% diagnostic accuracy, including exposure to a known offending allergen, positive precipitating antibodies to the offending antigen, recurrent episodes of symptoms, inspiratory crackles on lung auscultation, symptoms occurring 4-8 hours after exposure, and weight loss 3.
Diagnosis and Management
- The diagnosis of EAA is made by recognizing the clinical presentation, identifying the source of allergen exposure, and obtaining supportive evidence from precipitin and skin tests, or from allergen inhalation tests or lung biopsy 4.
- The clinic, radiographic, laboratory, and histologic abnormalities are results of inhaled antigen contact and support the diagnosis of EAA 5.
- Antigen avoidance is the key element in the treatment of EAA, and there is often an apparent beneficial response to corticosteroids 2.