title: Overlap of atopic, eosinophilic, and TH2-high asthma phenotypes in a general population with current asthma.
abstract: BACKGROUND
  Atopic, eosinophilic, and TH2-high asthma phenotypes may overlap, but the extent is unknown. Understanding the overlap across these phenotypes may be useful in guiding asthma patient care.
  
  
  OBJECTIVE
  To examine the frequency and overlap of atopic, eosinophilic, and TH2-high asthma phenotypes.
  
  
  METHODS
  We analyzed 2005 to 2006 data from the National Health and Nutrition Examination Survey. Patients with asthma were identified based on the participant self-report. Eosinophilic asthma was defined as a blood eosinophil cutoff point of ≥150, 300, or 400/μL. Atopic asthma was defined as having an allergen-specific IgE level of ≥0.35 IU/mL for any of the 9 perennial allergens tested. TH2-high asthma was defined as a total serum IgE of ≥100 IU/mL and a blood eosinophil count of ≥140/μL.
  
  
  RESULTS
  The study included 269 children and 310 adults. Depending on the eosinophil cutoff used, 31% to 78% of children and 21% to 69% of adults with asthma were classified as having eosinophilic asthma. In addition, 63% of children and 61% of adults were classified as having atopic disease and 48% of children and 37% of adults as having TH2-high asthma. At a higher eosinophil cutoff point, a greater proportion of eosinophilic asthma can be classified as atopic or TH2 high, but a lower proportion of atopic or TH2-high asthma can be classified as eosinophilic. Approximately 70% or more of children and adults with asthma were 1 of these 3 phenotypes.
  
  
  CONCLUSIONS
  A considerable overlap among eosinophilic, atopic, and TH2-high asthma phenotypes exists in a general asthma population.
authors.affiliation: Global Medicine Development, AstraZeneca, Gaithersburg, Maryland. Electronic address: trantr@medimmune.com.
authors.forename: Trung N
authors.initials: TN
authors.lastname: Tran
authors.affiliation: Kaiser Permanente Southern California, San Diego, California.
authors.forename: Robert S
authors.initials: RS
authors.lastname: Zeiger
authors.affiliation: Wake Forest School of Medicine, Winston-Salem, North Carolina.
authors.forename: Stephen P
authors.initials: SP
authors.lastname: Peters
authors.affiliation: Global Medicine Development, AstraZeneca, Gaithersburg, Maryland.
authors.forename: Gene
authors.initials: G
authors.lastname: Colice
authors.affiliation: Translational Medicine, MedImmune, Gaithersburg, Maryland.
authors.forename: Paul
authors.initials: P
authors.lastname: Newbold
authors.affiliation: Global Medicine Development, AstraZeneca, Gaithersburg, Maryland.
authors.forename: Mitchell
authors.initials: M
authors.lastname: Goldman
authors.affiliation: Capital Allergy & Respiratory Disease Center, Sacramento, California.
authors.forename: Bradley E
authors.initials: BE
authors.lastname: Chipps
mesh_terms: D000293:Adolescent; D000328:Adult; D000485:Allergens / Q000276:immunology; D001249:Asthma / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D002648:Child; D004802:Eosinophilia / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000097:blood / Q000453:epidemiology* / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009749:Nutrition Surveys; D010641:Phenotype; D018418:Th2 Cells / Q000276:immunology; D014481:United States / Q000453:epidemiology; D055815:Young Adult
chemical_list: D000485:Allergens; D007073:Immunoglobulin E