Medical Care
Early diagnosis is imperative in management of hypersensitivity pneumonitis (HP), given that progression is largely preventable and adverse effects are largely reversible. Environmental and exposure control is the cornerstone of treatment. In cases in which elimination of antigen exposure does not result in full regression of disease, treatment with corticosteroids may be warranted.
Antigen avoidance
If the responsible inhaled antigen can be identified, the most effective therapy is complete avoidance. Acute disease remits without specific therapy. This may prove difficult or impractical when a new home or new job would be required. When complete elimination or avoidance of the allergen exposure is not possible, exposure minimization with protective equipment or environmental treatment is a potential alternative. Respirators may provide satisfactory personal air purification for workplace environments. Alternatively, use of fungicides, dehumidification, mold removal or other remediation services may also sufficiently reduce ambient antigen burden. Patients with disease progression in the setting of ongoing exposure should still be strongly counseled on antigen avoidance even if drastic measures such as relocation to a new job or home are required.
Corticosteroid therapy
Corticosteroid therapy may be indicated for acute symptomatic relief and may accelerate the initial recovery in persons with severe disease. [59] In long-term prospective follow-up studies, however, prognosis was not affected.
Treatment regimens for hypersensitivity pneumonitis vary according to the prescriber. A conceivable initial empiric treatment dose is prednisone 0.5-1 mg/kg/day for 1-2 weeks in acute hypersensitivity pneumonitis or 4-8 weeks for subacute/chronic hypersensitivity pneumonitis followed by a gradual taper to off or maintenance dose of approximately 10 mg/day. Continued therapy should be guided by clinical response, pulmonary function, and radiographic improvement. Maintenance doses are not always required, particularly if the patient is removed from exposure.
Other therapies
Outside of oral corticosteroids, several other alternative therapies have been explored in select cases. Inhaled corticosteroids, bronchodilators, cromolyn sodium, and antihistamines may be helpful in cases with obstructive physiology with reversibility. The use of low-dose macrolide antibiotics have been suggested for inflammation reduction, however, beneficial effects have not been verified in human studies. [60] The use of immunosuppressive agents such as azathioprine or cyclosporine has been documented in select pediatric cases, but not in the adult population. [3]
Prevention
Reduce the chances of contracting hypersensitivity pneumonitis (HP) by minimizing exposure to provocative antigens, reducing microorganism contamination in the environment, and/or using protective equipment.
Reduce the antigenic burden by altering the handling and storage of microbial antigens, wetting compost to decrease aerosolization, and using fungicides to decrease fungal growth.
Dehumidify the environment and remove stagnant water to discourage microbial overgrowth.
Perform preventive maintenance routinely on all heating, ventilation, and air-conditioning equipment. Remove water-damaged furnishings and carpeting.
When avoidance of causative antigens cannot be achieved easily, use protective devices such as personal respirators or air-purifier. Dust respirators do not provide adequate protection, and helmet-type air purifying respirators are efficacious but can be cumbersome to wear.
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A 60-year-old dairy farmer had an 8-year history of intermittent dyspnea. Chest radiograph shows bilateral reticulonodular interstitial infiltration secondary to subacute hypersensitivity pneumonitis.
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Chest radiograph of a patient with chronic hypersensitivity pneumonitis from pigeon breeder's disease. Bilateral reticulonodular densities are present.
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High-resolution CT scan of lungs shows ground-glass opacification in the acute phase of hypersensitivity pneumonitis.
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The chronic phase of hypersensitivity pneumonitis shows honeycombing in the right upper lung and traction bronchiectasis.
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High-resolution chest CT scan of a patient with subacute hypersensitivity pneumonitis demonstrates centrilobular nodules. These nodules are unlike those of sarcoidosis, in which the nodules are subpleural and along bronchovascular bundles.
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Light microscopy shows mononuclear infiltration and noncaseating granulomas usually observed in association with acute hypersensitivity pneumonitis, but it also can be observed in subacute and chronic disease.
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Giant cells are a characteristic feature of hypersensitivity pneumonitis.
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Chronic hypersensitivity pneumonitis shows interstitial inflammation associated with fibrosis.
Tables
Disease |
Source of Exposure |
Major Antigen |
Farmer's lung |
Moldy hay |
Saccharopolyspora rectivirgula (Micropolyspora faeni) |
Bagassosis |
Moldy sugar cane fiber |
Thermoactinomyces sacchari |
Grain handler's lung |
Moldy grain |
S rectivirgula,Thermoactinomyces vulgaris |
Humidifier/air-conditioner lung |
Contaminated forced-air systems, heated water reservoirs [13] |
S rectivirgula, T vulgaris, Candida guilliermondii |
Bird breeder's lung |
Pigeons, parakeets, fowl, rodents |
Avian or animal proteins [14] |
Cheese worker's lung |
Cheese mold |
Penicillium casei |
Malt worker's lung |
Moldy malt |
Aspergillus clavatus |
Paprika splitter's lung |
Paprika dust |
Mucor stolonifer |
Wheat weevil |
Infested wheat |
Sitophilus granarius |
Mollusk shell hypersensitivity |
Shell dust |
Sea snail shells |
Chemical worker's lung |
Manufacture of plastics, polyurethane foam, rubber |
Trimellitic anhydride, diisocyanate, methylene diisocyanate |
