title: Heightened IgE response to mite antigens in inflammatory neuropathies.
abstract: In order to clarify the IgE response to common environmental antigens, we measured the serum total IgE and allergen-specific IgE in 50 patients with Guillain-Barré syndrome (GBS), nine patients with Fisher syndrome (FS), 14 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 18 patients with mononeuritis multiplex (MNM), 43 patients with neurodegenerative disorders and 82 healthy controls by ELISA. The total IgE level was significantly higher in patients with GBS (median = 135 U/ml, P<0.05), CIDP (median = 175 U/ml, P<0.05) and MNM (median= 199 U/ml, P<0.05), than in the healthy controls (median = 79 U/ml), but not in those patients with neurodegenerative disorders. The specific IgE to Dermatophagoides pteronyssinus was significantly higher in the patients with GBS (56%, P<0.01) and MNM (72%, P<0.005) than in the healthy controls (32%). The level of specific IgE to Dermatophagoides farinae tended to be higher in the patients with GBS than in the healthy controls (0.05<P<0.1). The patients with CIDP and MNM also showed a similar increase in the frequency of mite antigen-specific IgE. As a result, the heightened IgE responses to mite antigens may therefore in part be related to the mechanism of inflammatory neuropathies. On the other hand, such heightened IgE responses in these inflammatory neuropathies may be a reflection of Th2 cell overactivity, which may induce an intense synthesis of autoantibodies against the peripheral nerves.
authors.affiliation: Department of Neurology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Horiuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Kawano
authors.forename: K
authors.initials: K
authors.lastname: Yamasaki
authors.forename: H
authors.initials: H
authors.lastname: Matsuo
authors.forename: M
authors.initials: M
authors.lastname: Minohara
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Hashiguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Ohyagi
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: J
authors.initials: J
authors.lastname: Kira
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000818:Animals; D000941:Antigens / Q000276:immunology*; D003711:Demyelinating Diseases / Q000097:blood / Q000276:immunology*; D005260:Female; D020275:Guillain-Barre Syndrome / Q000097:blood / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019846:Miller Fisher Syndrome / Q000097:blood / Q000276:immunology; D008925:Mites / Q000276:immunology*; D009443:Neuritis / Q000097:blood / Q000276:immunology; D019636:Neurodegenerative Diseases / Q000097:blood / Q000276:immunology*
chemical_list: D000941:Antigens; D007073:Immunoglobulin E