title: Increase in serum levels of autoantibodies after attack of seasonal allergic rhinitis in patients with Graves' disease.
abstract: BACKGROUND
  The prevalence of allergic disease is increasing worldwide, but its influence on the clinical course of autoimmune diseases is unknown.
  
  
  OBJECTIVE
  The purpose of this study was to assess the effect of seasonal allergic rhinitis on the clinical course of Graves' disease, which has been considered a Th2-dominant autoimmune disease.
  
  
  METHODS
  Ten patients with Graves' disease, who were considered to be in a state of remission or near remission, were serially examined for 18 months starting from August. Five of them had seasonal allergic rhinitis due to Japanese cedar pollen, and the remaining patients had no such allergic disorders. Peripheral eosinophil counts, serum concentrations of cedar-pollen-specific IgE, anti-TSH-receptor antibody, anti-thyroid-peroxidase antibody and antithyroglobulin antibody were assessed at 2- to 4-month intervals. Serum thyroid hormones and TSH levels were also measured to evaluate disease activity.
  
  
  RESULTS
  All patients with pollinosis had attacks of allergic rhinitis caused by cedar pollen in early March. Subsequently, peripheral eosinophil counts, pollen-specific IgE activity and serum levels of anti-thyroid-peroxidase and antithyroglobulin autoantibodies markedly increased. Serum levels of anti-TSH-receptor antibody increased in 3 patients in association with an increase in serum thyroid hormones but were always negative in 2 patients. The control patients without pollinosis showed no consistent change of these parameters.
  
  
  CONCLUSIONS
  Seasonal allergic rhinitis aggravated the clinical course of Graves' disease and induced an increase in serum antithyroid autoantibody concentrations as well as an increase in pollen-specific IgE concentration. These data suggest that environmental antigens induce not only local allergic reactions, but also stimulate thyroid immune reactions toward Th2 proliferation, and finally aggravate Th2-dependent autoimmune thyroid disease.
authors.affiliation: Department of Laboratory Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
authors.forename: Keiko
authors.initials: K
authors.lastname: Takeoka
authors.forename: Yoh
authors.initials: Y
authors.lastname: Hidaka
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hanada
authors.forename: Tomoko
authors.initials: T
authors.lastname: Nomura
authors.forename: Susumu
authors.initials: S
authors.lastname: Tanaka
authors.forename: Toru
authors.initials: T
authors.lastname: Takano
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Amino
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D004804:Eosinophils / Q000502:physiology; D005260:Female; D006111:Graves Disease / Q000276:immunology*; D006801:Humans; D008875:Middle Aged; D011989:Receptors, Thyrotropin / Q000276:immunology; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D001323:Autoantibodies; D011989:Receptors, Thyrotropin