Hypersensitivity Pneumonitis Treatment & Management

  • Author: Caleb Hsieh, MD, MS; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Sep 09, 2016
 

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.[51] 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.[52] The use of immunosuppressive agents such as azathioprine or cyclosporine has been documented in select pediatric cases, but not in the adult population.[2]

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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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Contributor Information and Disclosures
Author

Caleb Hsieh, MD, MS Department of Internal Medicine, Olive View-UCLA Medical Center

Caleb Hsieh, MD, MS is a member of the following medical societies: American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FCCM Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care Medicine, Vice-Chair, Department of Medicine, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: Academy of Persian Physicians, American Academy of Sleep Medicine, American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of Specialty Professors, California Sleep Society, California Thoracic Society, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, Trudeau Society of Los Angeles, World Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, Society of Critical Care Medicine, American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Michael Peterson, MD Chief of Medicine, Vice-Chair of Medicine, University of California, San Francisco, School of Medicine; Endowed Professor of Medicine, University of California, San Francisco-Fresno, School of Medicine

Michael Peterson, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Marine Demirjian, MD Resident Physician, Department of Internal Medicine, Ronald Reagan University of California in Los Angeles Medical Center

Marine Demirjian, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Medical Women's Association, and California Medical Association

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

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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.
Chest radiograph of a patient with chronic hypersensitivity pneumonitis from pigeon breeder's disease. Bilateral reticulonodular densities are present.
High-resolution CT scan of lungs shows ground-glass opacification in the acute phase of hypersensitivity pneumonitis.
The chronic phase of hypersensitivity pneumonitis shows honeycombing in the right upper lung and traction bronchiectasis.
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.
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.
Giant cells are a characteristic feature of hypersensitivity pneumonitis.
Chronic hypersensitivity pneumonitis shows interstitial inflammation associated with fibrosis.
Table. Selected Etiological Agents for Hypersensitivity Pneumonitis
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 S rectivirgula, T vulgaris
Bird breeder's lung Pigeons, parakeets, fowl, rodents Avian or animal proteins
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
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