title: Anti-glutamic acid decarboxylase antibody in Graves' disease is a possible indicator for the unlikelihood of going into remission with antithyroid agents.
abstract: The prevalence and titer of glutamic acid decarboxylase antibody (GADAb) in type 1 diabetes mellitus (T1DM) has been reported to be higher in patients with autoimmune thyroid diseases (AITD) than those without them. However, we have no data about the influence of GADAb on AITD. We therefore studied the clinical characteristics of Graves' disease (GD) with GADAb in order to clarify the influence of GADAb on GD. Twelve GD patients with GADAb were enrolled and were compared to 40 GD patients without DM. The male to female ratio and age of onset of GD showed no statistical difference. The titer of TSH receptor antibody (TRAb) at the onset of GD was similar in both groups. Initial treatment with methimazole (MMI) was started in all patients with GADAb but radioactive iodine (RI) therapy was carried out in five patients because of adverse effects of MMI or poor control of hyperthyroidism. The initial titer of TRAb was significantly lower in patients treated with MMI alone compared to that in RI treated patients but none of the patients treated with MMI alone went into remission after more than 3-years of follow up. We also compared these GADAb-positive patients with 14 patients with diabetes mellitus who had matched clinical features. The number of diabetic patients who remained in possible remission was significantly higher than that of GADAb-positive patients (5 in 14 vs 0 in 12). Moreover, the rate of remission in the diabetic patients was no different from that of 21 control patients without diabetes followed for more than 7 years (5 in 14 vs 7 in 21). These data suggested that GADAb-positive patients are unlikely to go into remission with antithyroid agents. Therefore, definitive therapies might be preferable for the initial treatment of GADAb-positive patients.
authors.affiliation: Department of Medicine, Institute of Clinical Endocrinology, Tokyo Women's Medical University, Tokyo, Japan.
authors.forename: Ai
authors.initials: A
authors.lastname: Yoshihara
authors.forename: Osamu
authors.initials: O
authors.lastname: Isozaki
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Okubo
authors.forename: Kazue
authors.initials: K
authors.lastname: Takano
mesh_terms: D000328:Adult; D000368:Aged; D013956:Antithyroid Agents / Q000276:immunology / Q000627:therapeutic use*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000276:immunology; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006111:Graves Disease / Q000150:complications / Q000188:drug therapy / Q000276:immunology* / Q000532:radiotherapy; D006801:Humans; D018828:Immunoglobulins, Thyroid-Stimulating / Q000276:immunology; D007457:Iodine Radioisotopes / Q000627:therapeutic use; D008297:Male; D008713:Methimazole / Q000627:therapeutic use; D008875:Middle Aged
chemical_list: D013956:Antithyroid Agents; D018828:Immunoglobulins, Thyroid-Stimulating; D007457:Iodine Radioisotopes; C094372:thyrotropin-binding inhibitory immunoglobulin; D008713:Methimazole; D005968:Glutamate Decarboxylase