title: Asthma: a syndrome composed of heterogeneous diseases.
abstract: OBJECTIVE
  To review the concept that asthma comprises distinct heterogeneous inflammatory disorders characterized by patients showing different phenotypes with distinct genetic components, environmental causes, and immunopathologic signa-
  
  
  METHODS
  Ovid MEDLINE and PubMed databases from 1950 to the present time were searched for relevant articles and references regarding the heterogeneity of asthma.
  
  
  METHODS
  Articles that described the various phenotypes of asthma were used for this review.
  
  
  RESULTS
  Asthma is unlikely to be a single disease but rather a series of complex, overlapping individual diseases or phenotypes, each defined by its unique interaction between genetic and environmental factors. These conditions include syndromes characterized by allergen-exacerbated, nonallergic, and aspirin-exacerbated factors along with syndromes best distinguished by their pathologic findings (eosinophilic, neutrophilic, pauci-granulocytic), response to therapy (corticosteroid resistant), and natural history (remodeling prone). Additional phenotypes will almost certainly be identified as advances in genetics and other profiling methods are made and will be accompanied by the availability of clear biomarkers for distinguishing among them.
  
  
  CONCLUSIONS
  Responses to asthma medications vary considerably among patients, likely reflecting, at least in part, the differing sensitivities of the various asthma phenotypes. Selecting the best possible treatment course in individual patients will be aided by clearly identifying the different phenotypes. Physicians need to recognize this when making decisions to adjust treatment to improve asthma control.
authors.affiliation: Asthma and Allergic Disease Center, Carter Center for Immunology Research, University of Virginia Health System, Charlottesville, Virginia, USA. lb4m@virginia.edu
authors.forename: Larry
authors.initials: L
authors.lastname: Borish
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Culp
mesh_terms: D000485:Allergens / Q000276:immunology*; D001241:Aspirin / Q000276:immunology / Q000378:metabolism; D001249:Asthma / Q000276:immunology* / Q000473:pathology*; D016207:Cytokines / Q000276:immunology / Q000378:metabolism; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D008407:Mast Cells / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism; D012307:Risk Factors
chemical_list: D000485:Allergens; D016207:Cytokines; D007073:Immunoglobulin E; D001241:Aspirin