Hypersensitivity pneumonitis
(Redirected from Extrinsic allergic alveolitis)
Hypersensitivity pneumonitis | |
---|---|
Synonyms | Extrinsic allergic alveolitis |
Pronounce | N/A |
Specialty | Pulmonology |
Symptoms | Cough, dyspnea, fever, fatigue |
Complications | Pulmonary fibrosis, respiratory failure |
Onset | Hours to years after exposure |
Duration | Variable |
Types | N/A |
Causes | Inhalation of organic dusts |
Risks | Occupational exposure, farming, bird keeping |
Diagnosis | Clinical history, imaging, lung biopsy |
Differential diagnosis | N/A |
Prevention | N/A |
Treatment | Avoidance of antigen, corticosteroids |
Medication | N/A |
Prognosis | Variable, depends on chronicity and management |
Frequency | N/A |
Deaths | N/A |
Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is an inflammatory syndrome affecting the lungs, caused by the inhalation of a variety of organic dusts. It is characterized by an immune-mediated response that leads to inflammation of the alveoli, the small air sacs in the lungs.
Etiology[edit | edit source]
Hypersensitivity pneumonitis is caused by repeated inhalation of organic antigens. These antigens are typically found in occupational or environmental settings. Common sources include:
- Bird droppings and feathers (e.g., in bird fancier's lung)
- Moldy hay (e.g., in farmer's lung)
- Contaminated humidifiers or air conditioners
- Mold spores from compost
Pathophysiology[edit | edit source]
The pathophysiology of hypersensitivity pneumonitis involves a complex immune response. Upon inhalation of the antigen, the body mounts an immune response that involves both humoral and cell-mediated immunity. Key features include:
- Formation of immune complexes
- Activation of T cells
- Release of cytokines
- Recruitment of macrophages and neutrophils
This immune response leads to inflammation and damage to the alveoli, resulting in impaired gas exchange.
Clinical Presentation[edit | edit source]
The clinical presentation of hypersensitivity pneumonitis can vary depending on the duration and intensity of exposure. It is typically classified into three forms:
Acute[edit | edit source]
Subacute[edit | edit source]
- Gradual onset of symptoms
- Chronic cough and dyspnea
- Fatigue and weight loss
Chronic[edit | edit source]
- Progressive dyspnea
- Clubbing of fingers
- Pulmonary fibrosis
Diagnosis[edit | edit source]
Diagnosis of hypersensitivity pneumonitis is based on a combination of clinical history, imaging, and sometimes lung biopsy.
History[edit | edit source]
- Detailed occupational and environmental exposure history
- Identification of potential antigens
Imaging[edit | edit source]
- Chest X-ray: May show diffuse infiltrates
- High-resolution computed tomography (HRCT): Ground-glass opacities, nodules, and fibrosis
Lung Biopsy[edit | edit source]
- May be required in uncertain cases
- Shows interstitial inflammation, granulomas
Management[edit | edit source]
The primary treatment for hypersensitivity pneumonitis is avoidance of the offending antigen. Additional treatments include:
- Corticosteroids to reduce inflammation
- Immunosuppressive therapy in severe cases
Prognosis[edit | edit source]
The prognosis of hypersensitivity pneumonitis varies. Acute forms may resolve completely with antigen avoidance, while chronic forms can lead to irreversible lung damage and pulmonary fibrosis.
Prevention[edit | edit source]
Preventive measures include:
- Identification and control of environmental sources of antigens
- Use of protective equipment in occupational settings
See also[edit | edit source]
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Contributors: Kondreddy Naveen, Prab R. Tumpati, MD