eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Hypersensitivity Pneumonitis: Differential Diagnoses & Workup

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

Differential Diagnoses

Coccidioidomycosis
Psittacosis
Drug-Induced Pulmonary Toxicity
Pulmonary Fibrosis, Idiopathic
Histoplasmosis
Sarcoidosis
Pneumonia, Bacterial
Tuberculosis

Other Problems to Be Considered

  • Acute hypersensitivity pneumonitis (HP) closely resembles viral or bacterial infections of the lower respiratory tract.
  • Bird exposure can place the patient at risk for psittacosis.
  • Granulomatous lung diseases (eg, tuberculosis, histoplasmosis, coccidiomycosis, sarcoidosis) can also produce findings similar to those of subacute HP.5
  • Lymphoid interstitial pneumonitis observed in patients with acquired immunodeficiency syndrome (AIDS) can manifest as dyspnea, crackles, interstitial infiltrates, and hypergammaglobulinemia. 
  • For patients residing or working in a farm setting, organic toxic dust syndrome can be provoked by bacterial endotoxins or fungal toxins.56
  • Zamboni disease (a toxic reaction to nitrogen oxides emitted from an ice-smoothing machine operated in an indoor ice rink) can mimic acute or subacute HP.57
  • Differentiating chronic HP from idiopathic pulmonary fibrosis is particularly important because the prognosis for the former improves when the offending antigen is identified and eliminated. 
  • Subacute and chronic HP has been misdiagnosed as asthma, a condition that can also cause cough, dyspnea, and exercise intolerance.2
  • Chronic HP may be misdiagnosed as anorexia nervosa. Anorexia, weight loss, and exercise intolerance are manifestations of both diseases.
  • Connective-tissue disease (eg, systemic lupus erythematosus) can cause noninfectious pneumonitis with fever and weight loss, but other clinical and laboratory features of the connective tissue disease are expected. 
  • Drug-induced pneumonitis is considered separately from pneumonitis triggered by inhaled antigens. Medications most often implicated in drug-induced pneumonitis include gold salts, methotrexate, and amiodarone. Rare causes of drug-induced pneumonitis are the nonsteroidal anti-inflammatory drugs aspirin and ibuprofen; the anticonvulsants carbamazepine and phenytoin; the antibiotics nitrofurantoin and dapsone; the sulfonamides sulfasalazine and sulfadoxine; the antimalarial chloroquine; the immunosuppressants penicillamine and cyclophosphamide; and the cytotoxic agents azathioprine, bleomycin, chlorambucil, cyclophosphamide, mitomycin, and vinblastine. For additional details, see the eMedicine article Lung, Drug-Induced Disease.

Workup

Laboratory Studies

  • Precipitating antibodies to the offending antigen are commonly present; however, this observation is considered marker of exposure and not the cause of the disease. It is also not specific to hypersensitivity pneumonitis (HP) because exposed persons without disease may have precipitating antibodies to the antigen.58,59 Reports have attributed missed diagnoses to false-negative results of precipitin studies, although repeat testing showed true-positive findings of precipitin in many cases.60
  • A preliminary study suggested that precipitating antibody titers (as opposed to simply the presence or absence) may be of help in diagnosis.61 Among adult pigeon fanciers, those who reported respiratory symptoms within 4-8 hours of pigeon exposure had much higher precipitin levels to pigeon serum, feathers, and droppings than those who had no symptoms from pigeon exposure. Further validation and standardization of this test is necessary to better determine the sensitivity and specificity before it can be considered ready for routine clinical use.
  • The erythrocyte sedimentation rate and C-reactive protein levels may be elevated, a rheumatoid factor may be present, and circulating immune complexes may be observed. However, these findings are not considered sufficiently specific to be useful for diagnosis.19
  • Hypergammaglobulinemia is a common finding but is neither sensitive nor specific.

Imaging Studies

HRCT is more sensitive than chest radiography for revealing pneumonitis; however, normal radiographic results have been observed in subjects who meet other diagnostic criteria for HP.62,63

  • Acute HP: Chest radiography may reveal a fleeting, micronodular, interstitial pattern in the lower and middle lung zones; however, chest radiography often reveals normal results. Airspace consolidation can be seen in patients with acute disease, especially after exposure to causative antigens. HRCT usually reveals a patchy, ground-glass attenuation with small, poorly defined centrilobular nodules.
  • Subacute HP: Radiographic findings are similar to those observed in acute disease, although abnormalities may be most prominent in the mid- to upper-lung zones, and focal emphysema may be seen in addition to mild fibrotic changes. As in acute HP, airspace consolidation can also be seen in subacute disease.
  • Chronic HP: The most severe radiographic abnormalities are observed in the upper zones of the lungs. The most common abnormalities observed include centrilobular nodules, areas of linear opacity, and increased lung density. In advanced disease, evidence of lung damage due to pulmonary fibrosis and emphysema with honeycombing can be seen with HRCT. The centrilobular nodules on HRCT of the chest correlate with the granulomatous areas seen in lung biopsy specimens.62

Other Tests

  • Pulmonary function studies
    • Acute HP: Pulmonary function may be normal between acute episodes of HP. Normal diffusing capacity observed between exacerbations of acute or subacute HP does not exclude the diagnosis. Testing during acute episodes of HP reveals predominately restrictive changes; however, obstruction and bronchial hyperreactivity can also be seen. Obstruction alone does not preclude a diagnosis of HP. Hypoxemia can be seen in patients with active pneumonitis whether the affected patient is at rest or exercising.28
    • Subacute HP: Pulmonary function testing may demonstrate mild hypoxemia, restriction and/or obstruction, and a reduced capacity for diffusing carbon monoxide.
    • Chronic HP: A reduced diffusing capacity of the lung for carbon monoxide may be the earliest abnormality observed. Pulmonary restriction, hypoxemia at rest, and/or desaturation during the 6-minute walk test indicates the presence of more advanced disease.
  • Provocation challenge: The role of inhalation challenge is controversial because it can provoke clinically significant disease and standardized antigen preparations are not yet available. Because of the risk for the late-phase severe reactions, patients should be closely observed for at least 24 hours after the inhalation challenge is administered.64
  • Natural challenge: Patients may be accidentally re-exposed during a “natural” challenge. The development of signs and symptoms after the patient is re-exposed to the antigenic environment supports a diagnosis of acute or subacute HP.
  • Skin testing:Skin testing is not helpful in assessing HP.65
  • Lung biopsy:If other measures are not adequate to establish the diagnosis, lung biopsy can be performed. In older children, transbronchial biopsy may be attempted before the more invasive transthoracic lung biopsy. Several biopsy specimens should be obtained from sites showing evidence of radiographic involvement. In patients with advanced disease, video-assisted thoracoscopic biopsy improves the diagnostic yield from that of transbronchial biopsy.64

Procedures

Analysis of BALF is the most sensitive tool for alveolitis detection in patients with suspected HP. Analysis of BALF in HP typically reveals the following:64

  • Lymphocytosis (>20% of WBCs recovered)
  • CD4+/CD8+ ratio reduced to less than 1
  • Elevated proportion of neutrophils (may be elevated to >5%), especially after recent antigenic exposure or in advanced disease
  • Elevated proportion of eosinophils (may be >5%), particularly in advanced disease

One study of BALF cytology reported that adults with HP have a greater percentage of NKT cells than adults with sarcoidosis (11% [range, 3-38%] vs 3% [range, 0-16%]).7  The NKT cells observed in patients with HP were predominantly of the CD8+CD56+ population. Although the clinical use of this observation remains to be determined, these data suggest that a high percentage of NKT cells in the BALF supports a diagnosis of HP, whereas a low percentage neither confirms nor excludes the diagnosis.

Histologic Findings

HP is a diffuse, predominantly mononuclear cell inflammation of the small airways and pulmonary parenchyma. The inflammation is often associated with poorly formed, nonnecrotizing granulomas.55 A bronchiolocentric distribution of the interstitial inflammation is believed to result from the airway being the portal of entry for the offending agent. Histologic findings may include the following:66

  • Bronchiolocentric, chronic interstitial inflammation in which lymphocytes predominate
  • Poorly formed, nonnecrotizing interstitial granulomas
  • Foamy macrophages within airspaces
  • Intra-alveolar foci of organizing pneumonia
  • Dense fibrosis, honeycombing, and fibroblastic foci in advanced, chronic disease

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
[ CLOSE WINDOW ]

References

  1. Krasnick J, Patterson R, Stillwell PC, et al. Potentially fatal hypersensitivity pneumonitis in a child. Clin Pediatr (Phila). Jul 1995;34(7):388-91. [Medline].

  2. Farber HJ, Budson D. A pediatric case of severe chronic interstitial lung disease presenting as spontaneous pneumothorax: blame it on the birds. Pediatr Asthma Allergy Immunol. 2000;14(1):75-85.

  3. Vergesslich KA, Götz M, Kraft D. [Bird breeder's lung with conversion to fatal fibrosing alveolitis]. Dtsch Med Wochenschr. Aug 19 1983;108(33):1238-42. [Medline].

  4. King TE. Epidemiology and causes of hypersensitivity pneumonitis (extrinsic allergic alveolitis) 2005. Up to Date. Available at http://www.uptodate.com/. Accessed January 30, 2006.

  5. Selman M. Hypersensitivity pneumonitis: a multifaceted deceiving disorder. Clin Chest Med. Sep 2004;25(3):531-47, vi. [Medline].

  6. Patel AM, Ryu JH, Reed CE. Hypersensitivity pneumonitis: current concepts and future questions. J Allergy Clin Immunol. Nov 2001;108(5):661-70. [Medline].

  7. Korosec P, Osolnik K, Kern I, Silar M, Mohorcic K, Kosnik M. Expansion of pulmonary CD8+CD56+ natural killer T-cells in hypersensitivity pneumonitis. Chest. Oct 2007;132(4):1291-7. [Medline].

  8. Gudmundsson G, Monick MM, Hunninghake GW. Viral infection modulates expression of hypersensitivity pneumonitis. J Immunol. Jun 15 1999;162(12):7397-401. [Medline].

  9. Denis M. Proinflammatory cytokines in hypersensitivity pneumonitis. Am J Respir Crit Care Med. Jan 1995;151(1):164-9. [Medline].

  10. Schaaf BM, Seitzer U, Pravica V, Aries SP, Zabel P. Tumor necrosis factor-alpha -308 promoter gene polymorphism and increased tumor necrosis factor serum bioactivity in farmer's lung patients. Am J Respir Crit Care Med. Feb 2001;163(2):379-82. [Medline].

  11. Gudmundsson G, Hunninghake GW. Interferon-gamma is necessary for the expression of hypersensitivity pneumonitis. J Clin Invest. May 15 1997;99(10):2386-90. [Medline].

  12. Diaz de la Vega V, Bialostosky D, Lupi E, et al. Familial pigeon breeder's disease. Possible association to HLA-Bw40 antigen. Rev Invest Clin. Oct-Dec 1980;32(4):401-7. [Medline].

  13. Muers MF, Faux JA, Ting A, Morris PJ. HLA-A, B, C and HLA-DR antigens in extrinsic allergic alveolitis (budgerigar fancier's lung disease). Clin Allergy. Jan 1982;12(1):47-53. [Medline].

  14. Rittner C, Sennekamp J, Mollenhauer E, et al. Pigeon breeder's lung: association with HLA-DR 3. Tissue Antigens. May 1983;21(5):374-9. [Medline].

  15. Gudmundsson G, Hunninghake GW. Respiratory epithelial cells release interleukin-8 in response to a thermophilic bacteria that causes hypersensitivity pneumonitis. Exp Lung Res. Apr-May 1999;25(3):217-28. [Medline].

  16. Dakhama A, Hegele RG, Laflamme G, et al. Common respiratory viruses in lower airways of patients with acute hypersensitivity pneumonitis. Am J Respir Crit Care Med. Apr 1999;159(4 Pt 1):1316-22. [Medline].

  17. Perez-Padilla R, Salas J, Chapela R, et al. Mortality in Mexican patients with chronic pigeon breeder's lung compared with those with usual interstitial pneumonia. Am Rev Respir Dis. Jul 1993;148(1):49-53. [Medline].

  18. Craig TJ, Hershey J, Engler RJ, et al. Bird antigen persistence in the home environment after removal of the bird. Ann Allergy. Dec 1992;69(6):510-2. [Medline].

  19. King TE. Classification and clinical manifestations of hypersensitivity pneumonitis 2005. Up to Date. Available at http://www.uptodate.com/. Accessed January 30, 2006.

  20. Arima K, Ando M, Ito K, et al. Effect of cigarette smoking on prevalence of summer-type hypersensitivity pneumonitis caused by Trichosporon cutaneum. Arch Environ Health. Jul-Aug 1992;47(4):274-8. [Medline].

  21. Cormier Y, Israel-Assayag E, Bedard G, Duchaine C. Hypersensitivity pneumonitis in peat moss processing plant workers. Am J Respir Crit Care Med. Aug 1998;158(2):412-7. [Medline].

  22. Blanchet MR, Israel-Assayag E, Cormier Y. Inhibitory effect of nicotine on experimental hypersensitivity pneumonitis in vivo and in vitro. Am J Respir Crit Care Med. Apr 15 2004;169(8):903-9. [Medline].

  23. Dangman KH, Storey E, Schenck P, Hodgson MJ. Effects of cigarette smoking on diagnostic tests for work-related hypersensitivity pneumonitis: data from an outbreak of lung disease in metalworkers. Am J Ind Med. May 2004;45(5):455-67. [Medline].

  24. Ohtsuka Y, Munakata M, Tanimura K, et al. Smoking promotes insidious and chronic farmer's lung disease, and deteriorates the clinical outcome. Intern Med. Oct 1995;34(10):966-71. [Medline].

  25. Earis JE, Marsh K, Pearson MG, Ogilvie CM. The inspiratory "squawk" in extrinsic allergic alveolitis and other pulmonary fibroses. Thorax. Dec 1982;37(12):923-6. [Medline].

  26. Reich JM. Chirping rales in bird-fancier's lung. Chest. Jul 1993;104(1):326-7. [Medline].

  27. Ando M, Suga M, Nishiura Y, Miyajima M. Summer-type hypersensitivity pneumonitis. Intern Med. Aug 1995;34(8):707-12. [Medline].

  28. Wild LG, Lopez M. Hypersensitivity pneumonitis: a comprehensive review. J Investig Allergol Clin Immunol. 2001;11(1):3-15. [Medline].

  29. Yee WF, Castile RG, Cooper A, Roberts M, Patterson R. Diagnosing bird fancier's disease in children. Pediatrics. May 1990;85(5):848-52. [Medline].

  30. Levenson T, Patterson R. Chronic cough in a child. Ann Allergy Asthma Immunol. Apr 1996;76(4):311-6. [Medline].

  31. Boyer RS, Klock LE, Schmidt CD, et al. Hypersensitivity lung disease in the turkey raising industry. Am Rev Respir Dis. Jun 1974;109(6):630-5. [Medline].

  32. Saltoun CA, Harris KE, Mathisen TL, Patterson R. Hypersensitivity pneumonitis resulting from community exposure to Canada goose droppings: when an external environmental antigen becomes an indoor environmental antigen. Ann Allergy Asthma Immunol. Jan 2000;84(1):84-6. [Medline].

  33. du Marchie Sarvaas GJ, Merkus PJ, de Jongste JC. A family with extrinsic allergic alveolitis caused by wild city pigeons: A case report. Pediatrics. May 2000;105(5):E62. [Medline].

  34. Bahna SL. A custodian cured the doctor!. Pediatrics. May 2000;105(5):E71. [Medline].

  35. Karakurum M, Doraswamy B, Bennuri SS. Index of suspicion. Case 1. Hypersensitivity pneumonitis. Pediatr Rev. Feb 1999;20(2):53-4. [Medline].

  36. Inase N, Ohtani Y, Endo J, Miyake S, Yoshizawa Y. Feather duvet lung. Med Sci Monit. May 2003;9(5):CS37-40. [Medline].

  37. Inase N, Ohtani Y, Sumi Y, Umino T, Usui Y, Miyake S. A clinical study of hypersensitivity pneumonitis presumably caused by feather duvets. Ann Allergy Asthma Immunol. Jan 2006;96(1):98-104. [Medline].

  38. Bureau MA, Fecteau C, Patriquin H, et al. Farmer's lung in early childhood. Am Rev Respir Dis. Apr 1979;119(4):671-5. [Medline].

  39. Thorshauge H, Fallesen I, Ostergaard PA. Farmer's lung in infants and small children. Allergy. Feb 1989;44(2):152-5. [Medline].

  40. Iyori H, Kawamura K, Seo K. Summer-type hypersensitivity pneumonitis in a child. Acta Paediatr Jpn. Aug 1991;33(4):488-91. [Medline].

  41. Swingler GH. Summer-type hypersensitivity pneumonitis in southern Africa. A report of 5 cases in one family. S Afr Med J. Jan 20 1990;77(2):104-7. [Medline].

  42. Apostolakos MJ, Rossmoore H, Beckett WS. Hypersensitivity pneumonitis from ordinary residential exposures. Environ Health Perspect. Sep 2001;109(9):979-81. [Medline].

  43. Aebischer CC, Frey U, Schoni MH. Hypersensitivity pneumonitis in a five-year-old boy: an unusual antigen source. Pediatr Pulmonol. Jan 2002;33(1):77-8. [Medline].

  44. Kristiansen JD, Lahoz AX. Riding-school lung? Allergic alveolitis in an 11-year-old girl. Acta Paediatr Scand. Mar 1991;80(3):386-8. [Medline].

  45. Saltos N, Saunders NA, Bhagwandeen SB, Jarvie B. Hypersensitivity pneumonitis in a mouldy house. Med J Aust. Sep 4 1982;2(5):244-6. [Medline].

  46. Hogan MB, Patterson R, Pore RS, et al. Basement shower hypersensitivity pneumonitis secondary to Epicoccum nigrum. Chest. Sep 1996;110(3):854-6. [Medline].

  47. Miller MM, Patterson R, Fink JN, Roberts M. Chronic hypersensitivity lung disease with recurrent episodes of hypersensitivity pneumonitis due to a contaminated central humidifer. Clin Allergy. Sep 1976;6(5):451-62. [Medline].

  48. Suda T, Sato A, Ida M, et al. Hypersensitivity pneumonitis associated with home ultrasonic humidifiers. Chest. Mar 1995;107(3):711-7. [Medline].

  49. Patterson R, Mazur N, Roberts M, et al. Hypersensitivity pneumonitis due to humidifier disease: seek and ye shall find. Chest. Sep 1998;114(3):931-3. [Medline].

  50. Banaszak EF, Thiede WH, Fink JN. Hypersensitivity pneumonitis due to contamination of an air conditioner. N Engl J Med. Aug 6 1970;283(6):271-6. [Medline].

  51. Rose CS, Martyny JW, Newman LS, et al. "Lifeguard lung": endemic granulomatous pneumonitis in an indoor swimming pool. Am J Public Health. Dec 1998;88(12):1795-800. [Medline].

  52. Embil J, Warren P, Yakrus M, et al. Pulmonary illness associated with exposure to Mycobacterium-avium complex in hot tub water. Hypersensitivity pneumonitis or infection?. Chest. Mar 1997;111(3):813-6. [Medline].

  53. Hanak V, Kalra S, Aksamit TR, et al. Hot tub lung: presenting features and clinical course of 21 patients. Respir Med. Apr 2006;100(4):610-5. [Medline].

  54. Glazer CS, Rose CS, Lynch DA. Clinical and radiologic manifestations of hypersensitivity pneumonitis. J Thorac Imaging. Oct 2002;17(4):261-72. [Medline].

  55. Fan LL. Hypersensitivity pneumonitis in children. Curr Opin Pediatr. Jun 2002;14(3):323-6. [Medline].

  56. Seifert SA, Von Essen S, Jacobitz K, et al. Organic dust toxic syndrome: a review. J Toxicol Clin Toxicol. 2003;41(2):185-93. [Medline].

  57. Morgan WK. 'Zamboni disease'. Pulmonary edema in an ice hockey player. Arch Intern Med. Dec 11-25 1995;155(22):2479-80. [Medline].

  58. doPico GA, Reddan WG, Chmelik F, et al. The value of precipitating antibodies in screening for hypersensitivity pneumonitis. Am Rev Respir Dis. Apr 1976;113(4):451-5. [Medline].

  59. Dodge RR, Reed CE, Barbee RA. The absence of a relationship between serum precipitins and pulmonary disease in a community. Chest. May 1978;73(5):608-12. [Medline].

  60. Patterson R, Greenberger PA, Castile RG, et al. Diagnostic problems in hypersensitivity lung disease. Allergy Proc. Mar-Apr 1989;10(2):141-7. [Medline].

  61. McSharry C, Dye GM, Ismail T, Anderson K, Spiers EM, Boyd G. Quantifying serum antibody in bird fanciers' hypersensitivity pneumonitis. BMC Pulm Med. 2006;6:16. [Medline].

  62. Lynch DA, Rose CS, Way D. Hypersensitivity pneumonitis: sensitivity of high-resolution CT in a population-based study. AJR Am J Roentgenol. Sep 1992;159(3):469-72. [Medline].

  63. Nasser-Sharif FJ, Balter MS. Hypersensitivity pneumonitis with normal high resolution computed tomography scans. Can Respir J. Mar-Apr 2001;8(2):98-101. [Medline].

  64. King TE. Diagnosis of hypersensitivity pneumonitis. Up to Date. Available at http://www.uptodate.com/. Accessed January 30, 2006.

  65. Salvaggio JE. Robert A. Cooke memorial lecture. Hypersensitivity pneumonitis. J Allergy Clin Immunol. Apr 1987;79(4):558-71. [Medline].

  66. Fink JN, Ortega HG, Reynolds HY, Cormier YF, Fan LL, Franks TJ. Needs and opportunities for research in hypersensitivity pneumonitis. Am J Respir Crit Care Med. Apr 1 2005;171(7):792-8. [Medline].

[ CLOSE WINDOW ]

Further Reading

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

[ CLOSE WINDOW ]

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

[ CLOSE WINDOW ]

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

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.