Islet autoantibodies in cord blood from patients who developed type 1 diabetes mellitus at 15-30 years of age.

Islet cell autoantibodies are early markers for type 1 diabetes. The aim of this study was to determine whether islet autoantibodies were present at birth in young adults who developed type 1 diabetes at 15-30 years of age. Cord blood sera from 30 patients who developed type 1 diabetes between 15 and 25 years of age and sera from 320 randomly selected control children were tested for islet cell antibodies (ICA) by indirect immunofluorescence and autoantibodies against the 65 kD isoform of glutamic acid decarboxylase (GADA), islet cell antigen-2 (IA-2A) and insulin (IAA) by radiobinding assays. The young adults who developed type 1 diabetes did not differ from controls in the cord blood prevalence of any of the four islet autoantibodies. This is in contrast to our previous findings that children who developed type 1 diabetes below 15 years of age had an increased prevalence of cord blood islet autoantibodies. Our present data suggest that, in contrast to children, pre- and perinatal risk factors are less likely to be involved in the development of type 1 diabetes in young adults.

Islet cell autoantibodies in cord blood from children with blood group incompatibility or hyperbilirubinemia.

Blood group incompatibility is a risk factor for type 1 diabetes. Our aim was to test the hypothesis that islet cell autoantibodies, as markers for beta cell autoimmunity, are increased in cord blood from newborns with a diagnosis of blood group incompatibility. Using the diagnosis register of the Malmö University Hospital we obtained cord blood from 151 children with ABO immunization, 311 children with hyperbilirubinemia and a control group of 320 other children born during the same time period. The cord blood samples were analyzed for islet cell antibodies (ICA) by indirect immunofluorescence and autoantibodies against the Islet Cell Antigen-2 (IA-2Ab) and the 65 kDa isoform of glutamic acid decarboxylase (GAD65Ab) by standard radioligand binding assays. The prevalence of ICA was increased compared to controls (0.6%) not only in children with ABO immunization (4.0%, p = 0.02), but also in newborn children with hyperbilirubinemia (4.2%, p = 0.003). The prevalence of IA2Ab, but not of GAD65Ab, was increased in children with ABO immunization (3.3%) compared to the hyperbilirubinemia group without incompatibility (0.6%, p = 0.04), or the controls (0.3%, p = 0.02). Our findings that hyperbilirubinemia is associated with an increased prevalence of ICA, and blood group incompatibility with both ICA and IA-2, suggests that intra-uterine factors may be associated with islet cell autoimmunity.