title: High prevalence of GAD65 (and IA-2) antibodies in Japanese IDDM patients by a new immunoprecipitation assay based on recombinant human GAD65.
abstract: Marked differences have been reported in the prevalence of glutamic acid decarboxylase (GAD) antibodies between Caucasian (63-84%) and Japanese (30-50%) or Asian (5-50%) IDDM patients. Using a new immunoprecipitation assay based on 125I-labelled recombinant human GAD65 we have reassessed prevalence of GAD65 antibodies in Japanese patients. We also assessed prevalence of IA-2 antibodies. GAD65 antibodies were detected in 83.3% of sera taken within 1 year of onset, comparable to the prevalence reported in Caucasian patients. Positivity decreased to 66.7% after 2 to 3 years and to 54.3% after 3 years from onset, still higher than previously reported Asian prevalence. Except in one patient, high antibody levels persisted chronically, up to 12 years. There was no difference in the prevalence of GAD65 antibodies between Japanese IDDM patients with and without autoimmune thyroid disease (AITD). IA-2 antibodies were detected in 64.7% of sera taken within 1 year of onset. Prevalence of IA-2 antibodies was lower than that of GAD65 antibodies. The difference in positivity in Asian IDDM patients between present and previous reports arose from the sensitivity of our assay for GAD65 antibodies. Additionally, the patients we studied had classic IDDM with a well-defined onset. We conclude that prevalence of GAD65 antibodies in Japanese IDDM patients is comparable to that in Western studies. There was no relationship of GAD65 antibody positivity to coexistence of AITD. Our results suggest that autoimmunity is the most significant cause of Japanese IDDM.
authors.affiliation: Second Department of Internal Medicine, University of the Ryukyus School of Medicine, Okinawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Akamine
authors.forename: I
authors.initials: I
authors.lastname: Komiya
authors.forename: T
authors.initials: T
authors.lastname: Shimabukuro
authors.forename: T
authors.initials: T
authors.lastname: Asawa
authors.forename: H
authors.initials: H
authors.lastname: Tanaka
authors.forename: N
authors.initials: N
authors.lastname: Yagi
authors.forename: T
authors.initials: T
authors.lastname: Taira
authors.forename: K
authors.initials: K
authors.lastname: Nagata
authors.forename: K
authors.initials: K
authors.lastname: Arakaki
authors.forename: T
authors.initials: T
authors.lastname: Wakugami
authors.forename: N
authors.initials: N
authors.lastname: Takasu
authors.forename: M J
authors.initials: MJ
authors.lastname: Powell
authors.forename: J
authors.initials: J
authors.lastname: Furmaniak
authors.forename: B R
authors.initials: BR
authors.lastname: Smith
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology / Q000378:metabolism; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000276:immunology* / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000276:immunology; D005260:Female; D005500:Follow-Up Studies; D005968:Glutamate Decarboxylase / Q000032:analysis / Q000276:immunology*; D006801:Humans; D007457:Iodine Radioisotopes; D007564:Japan; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011233:Precipitin Tests; D011994:Recombinant Proteins / Q000032:analysis; D012016:Reference Values; D013961:Thyroid Gland / Q000276:immunology*; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000276:immunology; D013997:Time Factors
chemical_list: D001323:Autoantibodies; C096322:ICA512 autoantibody; D007457:Iodine Radioisotopes; D011994:Recombinant Proteins; D005968:Glutamate Decarboxylase