eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Hypersensitivity Pneumonitis: Treatment & Medication

Author: Harold J Farber, MD, Associate Professor, Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine
Coauthor(s): Nidhy S Paulose Varghese, MD, Postdoctoral Fellow, Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine; Bettina C Hilman, MD, Consulting Staff, The Asthma and Allergy Center
Contributor Information and Disclosures

Updated: Apr 14, 2008

Treatment

The key to effective treatment is identifying the offending antigen and eliminating further exposure. These goals can be hard to achieve because the offending antigen may not be obvious. Some antigens, such as avian antigens, may persist in the home environment for a long time, even after the source of the antigen or its source (the bird) is removed.18 Patients or their families may find it difficult to remove treasured pets, abandon hobbies, move to a new home, or give up income-producing activity.

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 (HP). 

Corticosteroids can speed resolution of HP, especially in its subacute and chronic forms, however corticosteroid therapy does not eliminate or reduce the need to identify the causative antigen and elimination of exposure to it.  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, tuberculin skin testing should be considered before corticosteroid therapy is started.

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

Medical Care

See Treatment.

Consultations

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

Diet

No dietary restrictions are needed.

Activity

If the patient has pulmonary fibrosis, subpleural blebs, or airway obstruction, scuba diving is 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.

Medication

Systemic corticosteroid therapy speeds resolution of symptoms. Progression of pulmonary fibrosis and death can occur despite corticosteroid therapy. Corticosteroid therapy is not a substitute for identifying and eliminating the offending antigen.

Corticosteroids

These agents decrease inflammation, suppress leukocyte migration, reverse increased capillary permeability, and dampen the immune system.


Prednisone (Deltasone)

Decreases inflammation by reversing increased capillary permeability and suppressing PMN activity. Must be metabolized to the active metabolite prednisolone for effect.

Adult

0.5-1 mg/kg/d PO for 4-8 wk; slowly taper as symptoms resolve

Pediatric

1-2 mg/kg PO initially, followed by 1 mg/kg/d PO, usually for 4 wk until clinically significant improvement; taper slowly as symptoms resolve; long courses may be needed to treat chronic disease

Coadministration with estrogens may decrease clearance; concurrent use with digoxin, may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia when coadministered with diuretics

Documented hypersensitivity; peptic ulcer disease; hepatic dysfunction; untreated tuberculosis infection, or other serious infection; systemic fungal infection; varicella infection

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may result from glucocorticoid use

More on Hypersensitivity Pneumonitis

Overview: Hypersensitivity Pneumonitis
Differential Diagnoses & Workup: Hypersensitivity Pneumonitis
Treatment & Medication: Hypersensitivity Pneumonitis
Follow-up: Hypersensitivity Pneumonitis
Multimedia: Hypersensitivity Pneumonitis
References
Further Reading
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Further Reading

Fan LL. Hypersensitivity Pneumonitis in Children. Curr Opin Pediatr. 2002 Jun;14(3):323-6.

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Keywords

Hypersensitivity pneumonitis, HP, extrinsic allergic alveolitis, EAA, bird fancier's lung, pigeon fancier’s lung, bird breeder's lung, pigeon breeder's lung, farmer's lung, recurrent pneumonitis, pulmonary fibrosis, emphysema, hypersensitivity pneumonitides, farm worker's lung, thermophilic actinomycetes, winemaker's lung, Botrytis cinerea, coffee worker's lung, coffee bean dust, lifeguard's lung

aerosolized endotoxin, poultry worker's lung, avian antigens, laboratory worker's lung, rodent antigens, miller's lung, wheat weevil, woodworker's lung, Bacillus subtilis, epoxy-resin lung, Phthalic anhydride, spontaneous pneumothorax, end-stage lung disease, acute respiratory symptoms, pneumonia, digital clubbing, chronic cough, dyspnea, cyanosis, bird fancier's lung, pigeon breeder's lung, Aspergillus species, moldy hay, Mucor stolonifer, humidifier lung, hot-tub lung, sauna taker's lung, sewage pneumonitis, summer-type pneumonitis, Trichosporon species

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Contributor Information and Disclosures

Author

Harold J Farber, MD, Associate Professor, Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine
Harold J Farber, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Nidhy S Paulose Varghese, MD, Postdoctoral Fellow, Department of Pediatrics, Section of Pulmonology, Baylor College of Medicine
Nidhy S Paulose Varghese, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Bettina C Hilman, MD, Consulting Staff, The Asthma and Allergy Center
Bettina C Hilman, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Chest Physicians, American Heart Association, American Medical Association, American Pediatric Society, American Thoracic Society, and Louisiana State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Girish D Sharma, MD, Associate Professor, Department of Pediatrics, Rush University Medical Center, Rush Children's Hospital; Director of Pediatric Pulmonary Section and Rush Cystic Fibrosis Center
Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Charles Callahan, DO, Professor, Deputy Chief of Clinical Services, Walter Reed 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, and Christian Medical & Dental Society
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department of Clinical Pediatrics, State University of New York at Stony Brook
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics, American Heart Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD, Attending Physician, Pediatric Pulmonary Medicine, Columbia University Medical Center; Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons
Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society
Disclosure: Merck Honoraria Speaking and teaching

 
 
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