Autoantibodies to glutamic acid decarboxylase in patients with IDDM and autoimmune thyroid disease

Kawasaki, Eiji; Takino, Hirofumi; Yano, M.; Uotani, S.; Matsumoto, K.; Takao, Y.; Yamaguchi, Yoshihiko; Akazawa, S.; Nagataki, Shigenobu

doi:10.2337/diabetes.43.1.80

Cited by 65 publications

(61 citation statements)

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“…In addition, in subjects with high titres of ICA, GAD itself is also recognized by ICA, as shown by the predominant b cell pattern of the ICA-positive sera and the partial or total inhibition of ICA reactivity after preabsorption with recombinant GAD. These data are in accordance with previous works showing a strong reactivity to GAD in patients whose diabetes was associated with a thyroid autoimmune disease (8).…”

Section: Journal Of Endocrinology (1997) 137supporting

confidence: 83%

“…The proportion of polyendocrine ICApositive patients who developed type 1 diabetes was dramatically smaller than ICA-positive first degree relatives, another high risk population (6). Antibodies to glutamic acid decarboxylase (GAD)/64 kDa protein have also been detected in diabetic and non-diabetic endocrine patients (7)(8)(9)(10). More recently, the predictive value of 37/40 kDa antibodies, identified as IA2 and phogrin proteins (11)(12)(13)(14)(15), has been reported in nondiabetic patients with organ-specific autoimmune disease (16).…”

Section: Introductionmentioning

confidence: 96%

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Anti-pancreatic autoimmunity and Graves' disease: study of a cohort of 600 Caucasian patients

Maugendre¹,

Verite²,

Guilhem³

et al. 1997

European Journal of Endocrinology

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The aim of this study was to investigate the frequencies of clinical diabetes and humoral markers of anti-pancreatic autoimmunity in a homogeneous population of 600 Caucasian patients with recently diagnosed Graves' disease (GD), in order to characterize the specific features of this group of endocrine patients among subjects at risk of diabetes.Ten were already diabetic at GD diagnosis. Among the 590 non-diabetic patients, 29 had islet cell antibodies (ICA), including 15 with low titre ICA and only 1 ICA-positive subject with a familial history of diabetes. Twenty-four patients had insulin autoantibodies, including three in association with ICA. Glutamic acid decarboxylase (GAD)/64 kDa antibodies were found in 16 of the 150 tested sera, including 13 of the 29 ICA-positive sera. Four ICA-positive patients displayed 37/40 kDa antibodies, including three in association with GAD/64 kDa antibodies. During follow-up, one of the ICA-positive patients developed insulin-dependent diabetes, 14 years after the GD diagnosis.To summarize, this anti-pancreatic autoimmunity study was focused on a large but specific and homogeneous group of subjects at risk for diabetes: recently diagnosed GD patients. This population was characterized by a high prevalence of GAD/64 kDa antibodies but also by a low frequency of evolution towards diabetes and the slowness of the process which could be due to the fact that only a minority of subjects possessed a sufficient combination of anti-pancreatic markers at the same time.

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Section: Journal Of Endocrinology (1997) 137supporting

confidence: 83%

Section: Introductionmentioning

confidence: 96%

Anti-pancreatic autoimmunity and Graves' disease: study of a cohort of 600 Caucasian patients

Maugendre¹,

Verite²,

Guilhem³

et al. 1997

European Journal of Endocrinology

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show abstract

“…GAD65Abs are less frequent among boys developing diabetes before the age of 10 years, but in older children, teenagers, and young adults, the diagnostic sensitivity is ϳ80% in both males and females. GAD65Ab titers are higher and more prevalent in patients with other associated autoimmune diseases, such as thyroiditis (48). IA2Abs have been reported in 32-75% of subjects with newly diagnosed type 1 diabetes (4).…”

Section: Diabetes Classification and Daasmentioning

confidence: 99%

Autoantibodies in Diabetes

et al. 2005

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Islet cell autoantibodies are strongly associated with the development of type 1 diabetes. The appearance of autoantibodies to one or several of the autoantigens-GAD65, IA-2, or insulin-signals an autoimmune pathogenesis of ␤-cell killing. A ␤-cell attack may be best reflected by the emergence of autoantibodies dependent on the genotype risk factors, isotype, and subtype of the autoantibodies as well as their epitope specificity. It is speculated that progression to ␤-cell loss and clinical onset of type 1 diabetes is reflected in a developing pattern of epitopespecific autoantibodies. Although the appearance of autoantibodies does not follow a distinct pattern, the presence of multiple autoantibodies has the highest positive predictive value for type 1 diabetes. In the absence of reliable T-cell tests, dissection of autoantibody responses in subjects of genetic risk should prove useful in identifying triggers of islet autoimmunity by examining seroconversion and maturation of the autoantibody response that may mark time to onset of type 1 diabetes. The complexity of the disease process is exemplified by multiple clinical phenotypes, including autoimmune diabetes masquerading as type 2 diabetes in youth and adults. Autoantibodies may also provide prognostic information in clinically heterogeneous patient populations when examined longitudinally. Diabetes 54 (Suppl. 2):S52-S61, 2005

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“…With regard to the clinical characteristics of APS3v (including both patients with T1D plus GD and those with T1D plus Hashimoto's thyroiditis), marked female predominance, a slowly progressive clinical course with older T1D onset age, a higher prevalence of GAD antibodies and a higher level of GAD antibodies were observed in APS3v patients compared to T1D patients without AITD (4,8). The prevalence of IA-2 antibodies was significantly higher in acute-onset T1D than in slowly progressive T1D among APS3v patients (4).…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

et al. 2013

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Two unrelated Japanese women, 41 and 27 years of age, were admitted with histories of thirst, weight loss and palpitations of a few weeks' duration. Both were diagnosed to have diabetic ketosis or ketoacidosis with acute-onset type 1 diabetes (T1D) and Graves' disease (GD) (autoimmune polyglandular syndrome type 3 variant; APS3v), and were treated with intensive insulin therapy and anti-thyroid drugs. Human leukocyte antigen examinations showed that both cases had the HLA-A2, A24, B54, and DRB1*04:05-DQA1*03:03-DQB1*04:01 haplotype, which made them susceptible not only to APS3v, but also to both acute-onset T1D and GD. The genetic background of patients strongly contributes to the simultaneous occurrence of T1D and GD.

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Autoantibodies to glutamic acid decarboxylase in patients with IDDM and autoimmune thyroid disease

Cited by 65 publications

References 0 publications

Anti-pancreatic autoimmunity and Graves' disease: study of a cohort of 600 Caucasian patients

Anti-pancreatic autoimmunity and Graves' disease: study of a cohort of 600 Caucasian patients

Autoantibodies in Diabetes

Simultaneous Occurrence of Type 1 Diabetes Mellitus and Graves' Disease: A Report of Two Cases and a Review of the Literature

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