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Pediatric Hypersensitivity Pneumonitis Treatment & Management

  • Author: Harold J Farber, MD, MSPH; Chief Editor: Girish D Sharma, MD, FCCP, FAAP  more...
Updated: May 20, 2016

Medical Care

The key to effective treatment of hypersensitivity pneumonitis (HP) is identifying the offending antigen and eliminating further exposure. These goals can be hard to achieve because the offending antigen may not be obvious and may endure long after the antigenic source is removed (ie, avian antigens).[89]

Removal from exposure usually results in complete resolution of symptoms, although substantially more time is required in subacute than in acute disease. In many patients, complete resolution requires weeks to months. Permanent lung damage, continued progression, or both may be seen in advanced cases of chronic hypersensitivity pneumonitis.

Corticosteroids can speed resolution of hypersensitivity pneumonitis; however, corticosteroid therapy does not eliminate or reduce the need to identify the causative antigen and elimination of exposure to it, nor does it change the long-term prognosis. If systemic corticosteroid therapy is used, the same dosage regimen should be continued until clinical improvement of pulmonary function is observed. The dosage should then be gradually tapered downward. In advanced chronic disease, progression of pulmonary fibrosis and death can occur despite aggressive corticosteroid therapy. If the patient has risk factors for tuberculosis, latent tuberculosis infection should be excluded prior to starting corticosteroid therapy.

Antibiotic therapy is not indicated for treatment of hypersensitivity pneumonitis. However, in many cases, antibiotic drugs are administered until a diagnosis of infectious pneumonia is ruled out.

A few case reports have described clinical improvement with rituximab when used as salvage therapy in adults with severe progressive chronic hypersensitivity pneumonitis.[90, 91] Rituximab is an anti-CD20 monoclonal antibody that depletes B cells from the peripheral circulation. One of the reports of clinical experience with rituximab in 6 adults with severe progressive hypersensitivity pneumonitis found that lung function stabilized or improved in 3 and continued to deteriorate in the other 3, all of whom died within 4 months of treatment.[91] There are no reports of pediatric experience with this medication in hypersensitivity pneumonitis.

In this author’s opinion, rituximab should not be considered standard therapy for chronic hypersensitivity pneumonitis. Rituximab may be considered as salvage therapy in a patient with severe, progressive, and life-threatening chronic hypersensitivity pneumonitis in whom standard therapies (including aggressive attempts to identify and eliminate exposure to the offending antigen) have clearly failed. This would be very unusual for a child.



Consulting a pediatric pulmonologist, an allergist, or both who have experience in treating hypersensitivity pneumonitis can be helpful for confirming the diagnosis, assessing complications, educating the patient and family, and providing long-term follow-up care for the patient.



No dietary restrictions are needed.



If the patient has pulmonary fibrosis, subpleural blebs, or airway obstruction, activities that may increase intrathoracic pressure (eg, scuba diving, playing horn instruments) are contraindicated because of the risk of pneumothorax. Otherwise, activity levels should be adjusted according to the patient's comfort; dyspnea causes most patients to spontaneously reduce their physical activity. If needed, tolerance of physical activity can be objectively assessed with 6-minute walk testing.

Contributor Information and Disclosures

Harold J Farber, MD, MSPH Associate Professor, Section of Pediatric Pulmonology, Baylor College of Medicine, Texas Children's Hospital

Harold J Farber, MD, MSPH is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.


R Paul Guillerman, MD Associate Professor of Radiology, Baylor College of Medicine

R Paul Guillerman, MD is a member of the following medical societies: American Roentgen Ray Society, Radiological Society of North America, Society for Pediatric Radiology, Children's Oncology Group

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO Professor, Chief, Department of Pediatrics and Pediatric Pulmonology, Tripler Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, Christian Medical and Dental Associations

Disclosure: Nothing to disclose.

Chief Editor

Girish D Sharma, MD, FCCP, FAAP Professor of Pediatrics, Rush Medical College; Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush Children's Hospital, Rush University Medical Center

Girish D Sharma, MD, FCCP, FAAP is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.


The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Bettina Hilman, MD, Nidhy Paulose Varghese, MD, Lori R Johnson, MD, and Laurianne Wild, MD. Leland Fan, MD, reviewed previous versions and provided helpful suggestions.

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Photomicrograph of a lung biopsy specimen reveals marked interstitial inflammation with lymphocytic predominance and a multinucleated giant cell (hematoxylin-eosin stain, original magnification 40X). Reprinted with permission from Farber and Budson, 2000.
Photomicrograph of a lung biopsy sample reveals interstitial fibrosis with active interstitial inflammation (hematoxylin-eosin stain, original magnification 10X). Reprinted with permission from Farber and Budson, 2000.
Photograph reveals precipitin lines produced by means of Ouchterlony immunodiffusion assay. Central wells contain the patient's serum. Peripheral wells contain serum or droppings from various birds. Reprinted with permission from Farber and Budson, 2000.
14-year-old girl with subacute hypersensitivity pneumonitis from avian antigen exposure. Chest radiograph demonstrates numerous tiny pulmonary nodules bilaterally.
Chest CT from same patient as previous image reveals widespread bilateral ill-defined centrilobular nodular opacities representing poorly formed granulomas.
10-year-old girl with chronic hypersensitivity pneumonitis from avian antigen exposure. Chest CT image shows irregular linear opacities and architectural distortion at the lung bases indicative of pulmonary fibrosis.
Table 1. Commonly Described Causes of Hypersensitivity Pneumonitis [46]
Exposure Disease Source of Antigen
Avian Bird fancier's lung, pigeon breeder's lung, poultry worker's lung, feather duvet lung Feathers, droppings, serum proteins, intestinal mucins, avian immunoglobulin A
Agriculture Farmer's lung, Bagasse (sugar cane) lung, mushroom worker's lung, potato riddler's lung, paprika slicer's lung, wine maker's lung Thermophilic actinomycetes, Aspergillus species, and other fungi in moldy hay or grains; moldy sugar cane; mushroom spores and thermophilic actinomycetes; moldy hay around potatoes, thermophilic actinomycetes, and others; Mucor stolonifer (on moldy paprika pods); B cinerea (noble rot on grapes)
Water-based systems Humidifier lung, hot-tub lung, sauna taker's lung, lifeguard's lung, sewage pneumonitis, wind instrument lung Aerosolized molds, endotoxins, mycobacteria, thermophilic actinomycetes, Penicillium species, others
Home environment Summer-type pneumonitis, mold-contaminated walls, humidifiers, wallpaper Trichosporon species, mold contamination in older and/or water-damaged homes


Chemicals Chemical worker's lung, epoxy-resin lung, pyrethrum pneumonitis Exposure to chemicals in manufacturing, laboratories, spray paints, heated epoxy resins, insecticides
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