title: Expansion of activated eosinophils in infants with severe atopic dermatitis.
abstract: BACKGROUND
  There is increasing concern in Japan over infants with atopic dermatitis (AD) who present with severe systemic complications, such as hypoproteinemia, electrolyte disturbances, and delayed growth and development. They are often associated with extremely increased numbers of circulating eosinophils. However, the clinical significance of eosinophil expansion has not been thoroughly investigated.
  
  
  METHODS
  This study attempted to determine the significance of eosinophilia and eosinophil activation in infant cases of AD by comparing multiple clinical parameters, indexes of eosinophil activation, and levels of serum cytokines. CD69 expression was determined by flow cytometry. The clinical severity of AD was graded by the severity SCORing of atopic dermatitis (SCORAD) method. Patients were classified into two groups, with and without CD69 on eosinophils. Nuclear lobes were evaluated under a microscopy. Serum levels of eosinophil-derived neurotoxin (EDN), interleukin (IL)-12, IL-18, IL-4, IL-5 and interferon (IFN)-gamma were determined by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Patients with CD69-positive eosinophils had significantly higher numbers of eosinophils and platelets, total IgE, and eosinophil nuclear lobes. They also showed growth failure, developmental delay, low serum albumin, and electrolyte disturbances. EDN and IL-18 levels were significantly increased in this group, but the levels of IL-4, IL-5 and IL-12 were not significantly different between the two groups. IFN-gamma was not detectable in all patients with AD. Surface expression of CD69 indicates intense systemic allergic inflammation induced in severe cases of AD.
  
  
  CONCLUSIONS
  Evaluation of eosinophil activation and early therapeutic intervention is mandatory for the treatment of severe AD during infancy.
authors.affiliation: Department of Pediatrics, Graduate School of Medical Science, Faculty of Medicine, Kanazawa University, Kanazawa 920-0942, Japan.
authors.forename: Tomoko
authors.initials: T
authors.lastname: Toma
authors.forename: Kazunori
authors.initials: K
authors.lastname: Mizuno
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Okamoto
authors.forename: Chiharu
authors.initials: C
authors.lastname: Kanegane
authors.forename: Kazuhide
authors.initials: K
authors.lastname: Ohta
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Ikawa
authors.forename: Masayoshi
authors.initials: M
authors.lastname: Miura
authors.forename: Mondo
authors.initials: M
authors.lastname: Kuroda
authors.forename: Yo
authors.initials: Y
authors.lastname: Niida
authors.forename: Shoichi
authors.initials: S
authors.lastname: Koizumi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Yachie
mesh_terms: D015703:Antigens, CD / Q000097:blood; D000945:Antigens, Differentiation, T-Lymphocyte / Q000097:blood; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D003876:Dermatitis, Atopic / Q000097:blood / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000276:immunology*; D004804:Eosinophils / Q000166:cytology / Q000276:immunology*; D005260:Female; D006801:Humans; D007223:Infant; D037181:Lectins, C-Type; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D008297:Male; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016207:Cytokines; D037181:Lectins, C-Type; D000099192:CD69 Antigens