eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Children's Interstitial Lung Disease (ChILD): Treatment & Medication

Author: James S Hagood, MD, Director, Pediatric Pulmonary Center, Professor of Pediatrics, Cell Biology, Pathology and Biochemistry and Molecular Genetics, Department of Pediatrics, University of Alabama School of Medicine
Coauthor(s): Gulnur Com, MD, Pediatric Pulmonologist, University of Arkansas for Medical Sciences Children's Hospital; David J Vaughan, MBBCh, Consultant Pediatrician, Department of Pediatrics, Our Lady of Lourdes Hospital, Ireland; Daniel William Young, MD, FACR, Clinical Professor of Radiology, Clinical Professor of Pediatrics, University of Alabama School of Medicine; Active Staff, Department of Pediatric Imaging, Children's Hospital of Alabama; Vice-President, Pediatric Radiology Associates, PC; Elizabeth C Mroczek-Musulman, MD, Clinical Associate Professor of Pathology, Associate Pathologist, Department of Pathology, University of Alabama Schools of Medicine and Dentistry, The Children's Hospital of Alabama; Lisa R Young, MD, Assistant Professor, Pediatric Pulmonary Medicine and Pulmonary Critical Care and Sleep Medicine, University of Cincinnati; Director of Pediatric Rare Lung Diseases Program and Consulting Physician, Cincinnati Children's Hospital Medical Center; Consulting Physician, University Hospital, Cincinnati
Contributor Information and Disclosures

Updated: Sep 11, 2009

Treatment

Medical Care

 
The multiple possible diagnostic entities and lack of randomized clinical trials make offering specific recommendations regarding treatment of children’s interstitial lung disease (ChILD) impossible. If the process is secondary to an underlying condition, patients should be treated for the underlying disease.
 
The same principles that apply to all children with chronic pulmonary diseases apply to those with interstitial lung disease (ILD). These include meticulous attention to growth and nutrition, immunizations (including influenza and pneumococcal prophylaxis), and treatment of secondary infections.
 

  • Treatment with bronchodilators, inhaled steroids, or both may be appropriate if any component of airway reactivity is demonstrated on PFT. However, this therapy has not been proven to modify the clinical course of most types of ILD.
  • Oxygen therapy, either continuously or during sleep, may be necessary to provide symptomatic relief and to decrease the risk or halt the progression of pulmonary hypertension and cor pulmonale related to alveolar hypoxia.
  • Active and passive smoking should be avoided. Smoking cessation should be actively pursued for caregivers who smoke.
  • Many medications have been used to treat different forms of ILD. No therapeutic regimen has been subjected to the rigors of a randomized control trial in the pediatric population. Numerous broad treatment strategies have been attempted, including anti-inflammatory medications (eg, steroids, cytotoxic agents, immunosuppressive therapies), collagen synthesis inhibitors, antifibrotic agents, hydroxychloroquine, intravenous immunoglobulin (IVIG), antioxidants, and cytokine inhibitors.
  • Hypersensitivity pneumonitis is the most treatable condition among chILDs. Fan et al (2004) reported 86 cases of pediatric hypersensitivity pneumonitis that had an excellent response to steroids.34 Other steroid-responsive conditions include NSIP, LIP, COP, eosinophilic pneumonia syndromes, sarcoidosis, pulmonary hemosiderosis, and ILD associated with connective tissue disease.6
  • Treatment of specific conditions resulting in ILD includes antiviral agents against CMV and EBV, antiretroviral therapy in addition to prednisolone for AIDS-associated LIP, surgical approach for lymphangiomatosis, therapeutic BAL for PAP, and PPI and Nissen fundoplication for GER-associated chronic aspiration. Reports indicate that infliximab (an inhibitor of tumor necrosis factor [TNF]-alpha) may be beneficial for ILD associated with rheumatoid arthritis.44 Several studies have demonstrated successful use of subcutaneous treatments with GM-CSF in adults with PAP.6
  • In patients with associated PAH, sildenafil and/or anticoagulant therapy should be considered.
  • In patients with congenital PAP due to GM-CSF receptor mutation or acquired receptor dysfunction secondary to autoantibody formation, subcutaneous or inhaled GM-CSF treatment has been reported to be beneficial.45 ,46

Surgical Care

 

  • Surgical consultation is usually sought for diagnostic biopsy (see Procedures).
  • Patients with end-stage idiopathic forms of ILD, severe lung disease associated with SFTPB or ABCA3 mutations, as well as some pulmonary veno-occlusive diseases, may be candidates for lung or heart/lung transplantation. These patients are considered on an individual basis at the few centers specializing in pediatric lung transplantation.
  • In children, the establishment of lung transplantation has been slower than in adults. Only 5% of all patients receiving transplants for this reason have been younger than 18 years. For some diseases, such as SP-B and ABCA3 deficiencies and alveolar capillary dysplasia, lung transplantation remains the only effective treatment.
  • Huddleston et al (2002) reported a 77% overall survival rate for the first year after transplantation in children.45 The 3- and 5-year survival declined to 63% and 54%, respectively. The authors observed no statistical relationship between pretransplantation diagnoses and long-term survival. The same authors reported 19 infants younger than 6 months who underwent lung transplantation: Seven had SP-B deficiency, 4 had PAP of other etiology, 3 had congenital interstitial pneumonitis, 2 had alveolar-capillary dysplasia, and 10 had pulmonary vascular disease.

Consultations

  • Pediatric pulmonologist: All children with ILD should be treated in consultation with a pediatric pulmonologist.
  • Pediatric ILD specialist: In addition, referral to or telephone consultation with a center with clinicians specializing in childhood ILD is advised.
  • Pediatric cardiologist: As a result of the existence of cardiovascular diseases masquerading as ILD, all patients should see a pediatric cardiologist.
  • Pediatric rheumatologist: A pediatric rheumatologist should be involved in the management of ILD associated with connective tissue disease.
  • Pediatric radiologist: Consult a pediatric radiologist regarding interpretation of imaging studies.
  • In addition, consider consultation with the following specialists:
    • Infectious disease specialist
    • Immunologist
    • Rheumatologist
    • Transplantation specialist
  • Pathologist: Consultation with a pathologist is recommended before tissue is obtained to ensure that adequate specimens are collected and that they are correctly processed. Consider consultation with a pathologist knowledgeable about ChILD.

Diet

No specific diet is necessary. However, as with patients with any chronic disease, patients with ChILD should receive sufficient kilojoules to maintain adequate growth. Decreased lung compliance increases the work of breathing and energy expenditure. Energy supplementation should be undertaken with consideration to the added difficulty in handling high carbohydrate loads with chronic lung disease. Consult a nutritionist experienced in the management of chronic pulmonary conditions in children. Young infants with feeding difficulties resulting from dyspnea may require a transpyloric or gastrostomic feeding tube.
 

Activity

Activity may be limited by the patient's degree of dyspnea. Oxygen saturation during exercise should be measured. A prescribed, monitored, exercise program may be beneficial to prevent deconditioning in older children. Conditions that may exacerbate pulmonary symptoms (high levels of ozone or other environmental pollutants) should be avoided. Patients with hypersensitivity pneumonitis should be removed from exposure to the precipitating substances (eg, birds, organic dusts). Air travel or travel to high altitudes must be carefully planned in patients with arterial desaturation.

Medication

Corticosteroids have been the mainstay of therapy in most children and adults with interstitial lung disease (ILD), despite little conclusive evidence of their efficacy. The theoretical basis for the use of corticosteroids is the assumption that the lung remodeling is in large part the result of persistent inflammation. This paradigm has recently been challenged in IPF (see Pathophysiology). Steroids may be administered daily or by pulse. Steroid responsiveness is often considered an important prognostic indicator. Data in adults indicate that the specific histopathologic pattern seen on biopsy specimens correlates with the degree of response to steroids. This has not been verified in children. Time to response is variable, but steroids should be continued for at least 8-12 weeks at full dose before therapy is deemed to have failed. Improvement may be seen in symptoms, physical signs, or chest radiographic appearance alone.

Glucocorticoids

These agents elicit anti-inflammatory properties and cause profound and varied metabolic effects. They modify the immune response of the body to diverse stimuli. Suppression of immune-mediated alveolitis and repair mechanisms may reduce the progression of fibrosis. Data from small studies suggest that pulse administration with intravenous (IV) corticosteroids may improve survival and lessen toxicity compared with prolonged courses of oral steroids.


Prednisone (Deltasone, Meticorten, Orasone, Sterapred)

Most widely used agent, particularly for UIP, DIP, and hypersensitivity pneumonitis. May decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) activity.

Adult

Pediatric

2 mg/kg/d PO for 6-8 wk; not to exceed 60-80 mg/d; continue 8-12 wk at full dose, gradually taper or adjust dose to clinical response and PFT results; symptom relapse warrants return to maximum dosing

Barbiturates, phenytoin, and rifampin increase clearance of corticosteroids; ketoconazole and troleandomycin decrease clearance of corticosteroids; increases clearance of salicylates; may impair vaccine or toxoid effectiveness; effects on anticoagulants varies; administration of live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses; coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; serious infection (ie, bacterial, viral, especially varicella, fungal)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Extensive adverse reactions associated with corticosteroids, mostly with long-term administration; fluid and electrolyte disturbances, hypertension, musculoskeletal problems (including osteoporosis), GI bleeding, neurologic disturbances, hypercoagulable states, endocrine disturbances (most notably adrenocortical suppression and growth impairment in children), and ophthalmic disturbances
Increased risk of disseminating infections (eg, chickenpox, measles); prophylaxis may be indicated if exposure to these infections cannot be avoided; may mask symptoms of serious infections; abrupt discontinuation of glucocorticoids may cause adrenal crisis


Methylprednisolone (Solu-Medrol)

Decreases inflammation by suppressing migration of PMN leukocytes and reversing increased capillary permeability. Can decrease frequency in patients with stable clinical course.

Adult

Pediatric

10-30 mg/kg/d IV for 3 d each month; in patients with stable clinical course, interval may be gradually increased

Barbiturates, phenytoin, and rifampin increase clearance of corticosteroids; ketoconazole and troleandomycin decrease clearance of corticosteroids; increases clearance of salicylates; may impair vaccine or toxoid effectiveness; have variable effects on anticoagulants; administration of live or live-attenuated vaccines is contraindicated in patients receiving immunosuppressive doses; coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; monitor patients for hypokalemia with concurrent administration with diuretics

Documented hypersensitivity; serious infections (ie, bacterial, viral, especially varicella and fungal)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Extensive adverse reactions associated with corticosteroids, mostly with long-term administration; fluid and electrolyte disturbances, hypertension, musculoskeletal problems (including osteoporosis), GI bleeding, neurologic disturbances, hypercoagulable states, endocrine disturbances (most notably adrenocortical suppression and growth impairment in children), and ophthalmic disturbances
Increased risk of disseminating infections, eg, chickenpox, measles; prophylaxis may be indicated if exposure to these infections cannot be avoided; may mask symptoms of serious infections; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, hypokalemia, euphoria, psychosis, myopathy, and GI irritation or ulceration may be more likely in pulse administration

Immunomodulating and immunosuppressive agents

The use of hydroxychloroquine and chloroquine has been reported, with variable results. Hydroxychloroquine has been used most frequently as a corticosteroid sparing agent with anecdotal success in ILD and alveolar hemorrhage syndromes. The mechanism of action is unknown. Recent data suggest that the efficacy of these agents may be related in part to alkalization of macrophages, which may reduce the secretion of TNF-alpha and impair antigen presentation.

Rosen et al (2005) reported an infant with SP deficiency that was treated successfully with hydroxychloroquine.47 They suggested that, in addition to its anti-inflammatory properties, hydroxychloroquine inhibits intracellular processing of the precursor of SP-C, which may be the mechanism of action in that disorder.

Azathioprine, MTX, cyclophosphamide, or penicillamine may be used as second-line therapy if response to corticosteroids has not occurred, if a steroid-sparing effect is desired, or as an adjunctive agent to steroids in severe or rapidly progressive disease. The mechanism of action is presumed to be immunosuppression by means of relative myelosuppression. The potential for pulmonary toxicity from MTX and cyclophosphamide has limited their use.


Hydroxychloroquine (Plaquenil)

Inhibits chemotaxis of eosinophils and locomotion of neutrophils and impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200 mg equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate. Dose and duration not tested in controlled trials, but, case reports describe children receiving 5-10 mg/kg/d for years. In adults, usually discontinued if no clinical response after 6 months.

Adult

Pediatric

10 mg/kg/d PO hydroxychloroquine base; not to exceed 400 mg/d hydroxychloroquine sulfate

Increases digoxin levels; cimetidine increases serum levels; magnesium trisilicate may decrease absorption; coadministration with gold increases risk of blood dyscrasias; may increase levels and toxicities of substrates (eg, metoprolol, opioid analgesics, tricyclic antidepressants [TCAs], antipsychotics) because is cytochrome P450 2D6 (CYP2D6) inhibitor

Documented hypersensitivity; psoriasis; porphyria; retinal and visual field changes attributable to 4-aminoquinolones

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use in pregnancy should be avoided because of potential fetal ocular toxicity; numerous adverse effects reported and more likely in children than adults: neurotoxicity, ocular toxicity, muscle weakness, dermatologic changes, blood dyscrasias, and GI irritation; caution in hepatic disease, glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, psoriasis, and porphyria; long-term use not recommended in children; perform ophthalmologic examinations and blood counts at baseline and q3-6mo; periodically test for muscle weakness; abrupt or premature cessation associated with exacerbation of symptoms


Chloroquine phosphate (Aralen)

Generally not used in young children who are unable to comply with thorough color-vision testing. Anti-inflammatory activity from lymphocyte transformation suppression. Dose and duration not tested in controlled trials, but case reports describe children receiving 5-10 mg/kg/d for years. In mostly uncontrolled case reports and small series of infants <6 mo with ILD, mortality rates 66% with corticosteroids alone vs 16% with chloroquine. Most infants responded clinically within first 2 mo of treatment.

Adult

Pediatric

5 mg/kg/d (as base) PO; not to exceed 300 mg/d (as base) PO; doses up to 10 mg/kg/d PO reported

Cimetidine increases serum levels; magnesium trisilicate or kaolin may decrease absorption; coadministration with gold increases risk of blood dyscrasias; decreases gastric emptying and may decrease bioavailability of various drugs (eg, ampicillin, bacampicillin); increases thyroid-stimulating hormone (TSH) levels, decreasing effectiveness of levothyroxine; increases cyclosporine and penicillamine levels

Documented hypersensitivity; psoriasis; retinal and visual field changes attributable to 4-aminoquinolones

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use in first trimester of pregnancy should be avoided because of potential fetal ocular toxicity; numerous adverse effects reported and more likely in children than adults: neurotoxicity, ocular toxicity, muscle weakness, dermatologic changes, blood dyscrasias, and GI irritation; caution in hepatic disease, G-6-PD deficiency, psoriasis, and porphyria; long-term use not recommended in children; perform ophthalmologic examinations and blood counts at baseline and q3-6mo; periodically test for muscle weakness; may cause auditory reactions (eg, tinnitus); abrupt or premature cessation associated with exacerbation of symptoms


Azathioprine (Imuran)

Antagonizes purine metabolism and inhibits DNA, RNA, and protein synthesis. May decrease proliferation of immune cells, which lowers autoimmune activity.

Adult

Pediatric

1 mg/kg/d PO for 6-8 wk initially; increase by 0.5 mg/kg/d q4wk up to 2.5 mg/kg/d or until response

Inhibits azathioprine metabolism by 30% (decrease azathioprine dose by 67-75%); concomitant cotrimoxazole or ACE inhibitors may exaggerate leukopenia; may decrease effects of anticoagulants, neuromuscular blockers, and cyclosporine

Documented hypersensitivity; low levels of serum thiopurine S-methyltransferase (TPMT)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Principal toxicities are hematologic (eg, leukopenia) and GI (eg, nausea, vomiting, hepatotoxicity); monitor blood counts frequently (eg, q1wk first month, q2wk second and third months, monthly thereafter); caution in liver or renal disease


Methotrexate (Rheumatrex)

Unknown mechanism of action in treatment of inflammatory reactions; may affect immune function.

Adult

Pediatric

Specific dosing for ILD not standardized
In inflammatory conditions, such as JRA, 10 mg/m2/wk PO has been administered as single dose qwk; not to exceed 15 mg/wk

Salicylates and NSAIDs may reduce tubular secretion and enhance toxicity; protein displacement by phenytoin, phenylbutazone, sulfonamides, and probenecid may increase toxicity; penicillins reduce renal clearance; concomitant retinoids can enhance hepatotoxicity; tetracycline and chloramphenicol decrease absorption; folic acid can decrease effectiveness, whereas folic acid deficiency can increase toxicity; decreases clearance of theophylline

Documented hypersensitivity; alcoholism; hepatic insufficiency; documented immunodeficiency syndromes; preexisting blood dyscrasias (eg, bone marrow hypoplasia, leukopenia, thrombocytopenia, significant anemia); renal insufficiency

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Folic acid usually prescribed concurrently as 1 mg/d; common adverse reactions are ulcerative stomatitis, leukopenia, nausea, malaise, and fatigue; risk of opportunistic infection increased; may elevate hepatic enzyme levels and persistent elevation may indicate hepatotoxicity or cirrhosis; monitor blood CBC counts at baseline and monthly; may cause pulmonary fibrosis but usually not at doses used for inflammatory conditions; reduce dose in patients with renal failure, ascites, or pleural effusions


Cyclophosphamide (Cytoxan)

Chemically related to nitrogen mustards. As an alkylating agent, mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Adult

Pediatric

5-10 mg/kg IV q2-3wk; not to exceed adult range of 500-1800 mg/dose

Chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity; severely depressed bone marrow function; active infection

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in impaired hepatic or renal function; nausea, vomiting, alopecia, and myelosuppression frequent; hemorrhagic cystitis and bladder fibrosis may occur; can impair fertility, sometimes irreversibly; pulmonary fibrosis reported; use antineoplastic handling and disposal; monitor CBC counts, urinalysis, electrolyte, and serum creatinine results


Penicillamine (Cuprimine)

Metal-chelating agent. Use in patients with ILD reported. Mechanism of action unknown.

Adult

Pediatric

3 mg/kg/d PO for 3 mo, not to exceed 250 mg/d; then 6 mg/kg/d PO divided bid for 3 mo, not to exceed 500 mg/d; not to exceed final maximum dose of 10 mg/kg/d PO divided tid/qid

Increases effects of immunosuppressants, phenylbutazone, and antimalarials; decreases digoxin effects; coadministration of zinc salts, antacids, gold, or iron may decrease effects

Documented hypersensitivity; renal insufficiency; previous penicillamine-related aplastic anemia; chronic lead poisoning

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Potential cross-sensitivity with penicillin allergy; many adverse effects reported; potential for severe hematologic and renal reactions; Goodpasture syndrome, obliterative bronchiolitis, myasthenia syndrome, and lupus-like syndrome reported; wound healing impaired; all patients should receive pyridoxine 25 mg/d; iron deficiency may develop; measure CBC counts q2wk for first 6 mo then monthly; advise patients to promptly report signs suggesting bone marrow failure (eg, bleeding, sore throat, fevers)

More on Children's Interstitial Lung Disease (ChILD)

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Differential Diagnoses & Workup: Children's Interstitial Lung Disease (ChILD)
Treatment & Medication: Children's Interstitial Lung Disease (ChILD)
Follow-up: Children's Interstitial Lung Disease (ChILD)
Multimedia: Children's Interstitial Lung Disease (ChILD)
References
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Further Reading

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Keywords

children’s interstitial lung disease, ChILD, ILD, diffuse infiltrative lung disease, pulmonary disease, lung disease, interstitial disease, idiopathic pulmonary fibrosis, IPF, nonidiopathic interstitial pulmonary fibrosis, usual interstitial pneumonia, UIP, desquamative interstitial pneumonia, DIP, bronchiolitis obliterans with interstitial pneumonia, BIP, lymphoid interstitial pneumonia, lymphocytic interstitial pneumonia, LIP, giant cell interstitial pneumonia, giant-cell interstitial pneumonia, GIP, respiratory bronchiolitis interstitial lung disease, RBILD

nonspecific interstitial pneumonia, NSIP, bronchiolitis obliterans organizing pneumonia, BOOP, cryptogenic organizing pneumonia, COP, cryptogenic fibrosing alveolitis, CFA, pulmonary histiocytosis X, eosinophilic granuloma, Langerhans cell histiocytosis, LCH, acute interstitial pneumonia, AIP, idiopathic BOOP, nonclassifiable ILD, neuroendocrine cell hyperplasia of infancy, NEHI, pulmonary interstitial glycogenosis, PIG, idiopathic interstitial pneumonia, cryptogenic fibrosing alveolitis, chronic pneumonitis of infancy, cellular interstitial pneumonitis

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Contributor Information and Disclosures

Author

James S Hagood, MD, Director, Pediatric Pulmonary Center, Professor of Pediatrics, Cell Biology, Pathology and Biochemistry and Molecular Genetics, Department of Pediatrics, University of Alabama School of Medicine
James S Hagood, MD is a member of the following medical societies: American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Gulnur Com, MD, Pediatric Pulmonologist, University of Arkansas for Medical Sciences Children's Hospital
Gulnur Com, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Cystic Fibrosis Foundation
Disclosure: Nothing to disclose.

David J Vaughan, MBBCh, Consultant Pediatrician, Department of Pediatrics, Our Lady of Lourdes Hospital, Ireland
David J Vaughan, MBBCh is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Daniel William Young, MD, FACR, Clinical Professor of Radiology, Clinical Professor of Pediatrics, University of Alabama School of Medicine; Active Staff, Department of Pediatric Imaging, Children's Hospital of Alabama; Vice-President, Pediatric Radiology Associates, PC
Daniel William Young, MD, FACR is a member of the following medical societies: Alpha Omega Alpha, American College of Radiology, Radiological Society of North America, and Society for Pediatric Radiology
Disclosure: Nothing to disclose.

Elizabeth C Mroczek-Musulman, MD, Clinical Associate Professor of Pathology, Associate Pathologist, Department of Pathology, University of Alabama Schools of Medicine and Dentistry, The Children's Hospital of Alabama
Elizabeth C Mroczek-Musulman, MD is a member of the following medical societies: American Society for Clinical Pathology and College of American Pathologists
Disclosure: Nothing to disclose.

Lisa R Young, MD, Assistant Professor, Pediatric Pulmonary Medicine and Pulmonary Critical Care and Sleep Medicine, University of Cincinnati; Director of Pediatric Rare Lung Diseases Program and Consulting Physician, Cincinnati Children's Hospital Medical Center; Consulting Physician, University Hospital, Cincinnati
Lisa R Young, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Central Society for Clinical Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Susanna A McColley, MD, Director of Cystic Fibrosis Center; Head, Division of Pulmonary Medicine; Associate Professor, Department of Pediatrics, Children's Memorial Medical Center of Chicago, Northwestern University
Susanna A McColley, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Sleep Disorders Association, and American Thoracic Society
Disclosure: Genentech Honoraria Speaking and teaching; Genentech Honoraria Consulting; Novartis Honoraria Consulting; Altus  Consulting fee Consulting; Axcan Scandi Consulting fee Consulting; Boston Scientific Consulting fee Consulting; Gilead  Speaking and teaching

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Professor of Clinical Pediatrics, State University of New York at Stony Brook; Director of Children's Sleep Services, Winthrop University Hospital
Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians
Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD, Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center
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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