Becerril Ángeles Martín, García Lara Sergio Enrique, González Bárcena David, Ibarra Olmos María Alicia, Torres Ambriz Pedro, Angeles Garay Ulises
Servicio de Alergia e Inmunología Clínica, Unidad Médica de Alta Especialidad, Hospital de Especialidades Dr. Antonio Fraga Mouret, Centro Médico Nacional La Raza, Instituto Mexicano del Seguro Social, México, DF, Mexico.
Rev Alerg Mex. 2010 Nov-Dec;57(6):190-5.
Pancreatic cell destruction causing type 1 diabetes is associated to diverse autoantibodies. Antibodies against glutamic acid decarboxylase have been found in type 1 (DM1) and type 2 diabetic patients (DM2). Their presence in siblings is unknown.
To determine the presence of anti-GAD65 autoantibodies in diabetic patients and their siblings.
Sixty-eight individuals were included and distributed in four groups: group 1 DM1, group 2 DM2, group 3 and 4 healthy siblings of patients from groups 1 and 2. Anti-GAD65, peptide C, serum glucose, total cholesterol and triglycerides were obtained. Body mass index and hip-waist ratio were measured.
Anti-GAD65 antibodies were positive in 23% of DM1, in 14% of DM2, and in 7.7% and 9.5% in siblings of both groups, respectively. Using Mann-Whitney's U the mean of anti-GAD65 in diabetic type 1 and 2 patients was p = 0.022; between DM1 and their siblings and between DM2 and their siblings there was no statistical significance. C peptide was low in cases of positive anti-GAD65 of DM1 and DM2; and it was normal in patients with negative anti-GAD65.
Anti-GAD65 autoantibodies are more frequent in type 1 diabetic patients. There were no meaningful differences regarding the presence of anti-GAD65 in patients and their siblings.
