title: Antibodies to glutamic acid decarboxylase in Japanese diabetic patients with secondary failure of oral hypoglycaemic therapy.
abstract: Some patients with non-insulin-dependent (Type 2) diabetes mellitus (NIDDM) are positive for antibodies to glutamic acid decarboxylase (anti-GAD), which have been shown to be a useful marker for the diagnosis and prediction of insulin-dependent (Type 1) diabetes mellitus (IDDM). Anti-GAD positive NIDDM patients tend to develop insulin deficiency. We investigated the prevalence of anti-GAD in 200 NIDDM with secondary failure of oral hypoglycaemic therapy (SF) and 200 NIDDM well controlled by diet and/or sulphonylurea agents (NSF). Twenty-two of 200 (11%, p < 0.05) SF patients and 6 of 200 (3%) NSF patients were anti-GAD positive. The positive. The positive rate for anti-GAD was as high as 23.8% in the non-obese and insulin deficient SF patients. The SF patients with anti-GAD tended to be non-obese and to have an impaired release of endogenous insulin. The internal before development of secondary failure was not associated with the presence of anti-GAD in this study. In conclusion we found that anti-GAD was positive in as many as 11% of the SF patients, suggesting that autoimmune mechanisms may play an important role in the pathogenesis of secondary failure or sulphonylurea therapy.
authors.affiliation: First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fukui
authors.forename: K
authors.initials: K
authors.lastname: Nakano
authors.forename: H
authors.initials: H
authors.lastname: Shigeta
authors.forename: K
authors.initials: K
authors.lastname: Yoshimori
authors.forename: M
authors.initials: M
authors.lastname: Fujii
authors.forename: Y
authors.initials: Y
authors.lastname: Kitagawa
authors.forename: H
authors.initials: H
authors.lastname: Mori
authors.forename: S
authors.initials: S
authors.lastname: Kajiyama
authors.forename: N
authors.initials: N
authors.lastname: Nakamura
authors.forename: N
authors.initials: N
authors.lastname: Abe
authors.forename: H
authors.initials: H
authors.lastname: Obayashi
authors.forename: I
authors.initials: I
authors.lastname: Fukui
authors.forename: K
authors.initials: K
authors.lastname: Ohta
authors.forename: M
authors.initials: M
authors.lastname: Ohta
authors.forename: M
authors.initials: M
authors.lastname: Kondo
mesh_terms: D000704:Analysis of Variance; D000906:Antibodies / Q000032:analysis / Q000737:chemistry; D001323:Autoantibodies / Q000032:analysis; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy / Q000276:immunology*; D005215:Fasting / Q000097:blood; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007003:Hypoglycemia / Q000628:therapy*; D007328:Insulin / Q000008:administration & dosage; D007564:Japan; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000276:immunology; D013997:Time Factors; D017211:Treatment Failure; D014556:Urine / Q000737:chemistry
chemical_list: D000906:Antibodies; D001323:Autoantibodies; D002096:C-Peptide; D007328:Insulin; D005968:Glutamate Decarboxylase