title: What are the characteristics of phenotypic type 2 diabetic patients with low-titer GAD65 antibodies?
abstract: Type 2 diabetes results from combined insulin resistance and β-cell deficiency. Type 1 diabetes results from β-cell destruction associated with islet autoantibodies, including those directed against glutamate decarboxylase (GAD65 antibodies [GADA]). Clinical impact of low GADA positivity (<60 U/ml) in type 2 diabetes is debated, being rarely performed in routine care. The aim of our study was to determine the prevalence and cardiometabolic/autoimmune phenotype of GADA[+] patients. 524 type 2 diabetes consecutive outpatients were assessed for glucose homeostasis using homeostasis model assessment (HOMA): insulin sensitivity (HOMA S); β-cell function (HOMA B) and annualized loss in [BXS]. GADA prevalence was 6% (n = 30). There were no differences between groups for age, diabetes duration and family history of diabetes. There were proportionately more women (33 vs. 53%) in GADA[+]. There were no differences in body mass index, waist circumference or visceral fat. HOMA S was lower than normal, with no difference between groups, as was HOMA B. Annualized rate of [BXS] loss was 1.26%/year (GADA[+]) versus 1.34%/year (GADA[-]; NS). HbA1c was 7.8% (GADA[+]) versus 7.6% (GADA[-]; NS). Among all patients, prevalence of autoimmune thyroid disease was 10%. In GADA[+], this prevalence was significantly increased and equally affected both sexes: 29% (men) versus 25% (women), while for GADA[-] the prevalence was 5% (men) versus 18% (women; p < 0.0001). Low-titer GADA autoimmunity among type 2 diabetes patients was not associated with accelerated β-cell function, nor with any distinctive cardiometabolic phenotype, but for a markedly increased prevalence of autoimmune thyroid disease, especially among men.
authors.affiliation: Service d'Endocrinologie et Nutrition, Cliniques Universitaires St-Luc, Université Catholique de Louvain, Avenue Hippocrate UCL 54.74, 1200, Brussels, Belgium, myovan@hotmail.com.
authors.forename: Yovan P
authors.initials: YP
authors.lastname: Mahadeb
authors.forename: Damien
authors.initials: D
authors.lastname: Gruson
authors.forename: Martin
authors.initials: M
authors.lastname: Buysschaert
authors.forename: Michel P
authors.initials: MP
authors.lastname: Hermans
mesh_terms: D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D002318:Cardiovascular Diseases / Q000097:blood / Q000453:epidemiology / Q000209:etiology; D003430:Cross-Sectional Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications / Q000453:epidemiology / Q000628:therapy; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D015995:Prevalence; D013967:Thyroiditis, Autoimmune / Q000097:blood / Q000453:epidemiology / Q000209:etiology
chemical_list: D001323:Autoantibodies; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2