Measuring levels of autoantibodies in the blood can predict the development of type 1 diabetes in young children, according to new research.
The study, known as ”The Environmental Determinants of Diabetes in the Young” (or TEDDY) and published in Diabetologia, indicates that autoantibodies reveal whether or not the immune system is attacking insulin-producing beta cells in the pancreas, thereby causing type 1 diabetes in children.
Antibodies are proteins found in the blood. Their presence indicates that the immune system has attacked a foreign body. Autoantibodies indicate autoimmune disease. That is, they suggest that the immune system is attacking healthy, beneficial cells, such as insulin-producing beta cells. This kind of abnormal immune system behaviour is the cause of type 1 diabetes.
If the first autoantibody found in young children attacks insulin, this could indicate the presence of type 1 diabetes. Similarly, if the autoantibody targets GAD65 (a protein found inside insulin-producing beta cells), the child may be likely to develop type 1 diabetes. In some cases, autoantibodies targeting both insulin and GAD65 will be found simultaneously.
The research followed 8,600 children from Sweden, the United States, Germany, and Finland, all of whom were highly likely to develop hereditary type 1 diabetes. 6.5 per cent of them had their first autoantibody before the age of six.
Of these children, 44 per cent had an autoantibody targeting insulin, 38 per cent had GAD65 autoantibodies before two, and 14 per cent had both autoantibodies by the age of three.
The study suggests that autoantibodies can appear earlier than previously thought.
Although the kind of autoantibody was determined by the child’s genetic risk factors, researchers still do not know why the immune attacks insulin-producing beta cells in the pancreas.
Ake Lernmark, lead researcher of the study, suggested that a virus may be responsible: ”It is possible that there are two different diseases involved. Perhaps one virus triggers the autoantibodies against insulin and another one the autoantibodies against GAD65.”
The 6 year incidence of diabetes-associated autoantibodies in genetically at-risk children: the TEDDY study
AbstractAims/hypothesis
Islet autoantibodies, in addition to elevated blood glucose, define type 1 diabetes. These autoantibodies are detectable for a variable period of time before diabetes onset. Thus, the occurrence of islet autoantibodies is associated with the beginning of the disease process. The age at, and order in, which autoantibodies appear may be associated with different genetic backgrounds or environmental exposures, or both.
Methods
Infants with HLA-DR high-risk genotypes (DR3/4, DR4/4, DR4/8 and DR3/3) were enrolled and prospectively followed with standardised autoantibody assessments quarterly throughout the first 4 years of life and then semi-annually thereafter.
Results
Autoantibodies appeared in 549/8,503 (6.5%) children during 34,091 person-years of follow-up. Autoantibodies at 3 (0.1%) and 6 (0.2%) months of age were rare. Of the 549, 43.7% had islet autoantibodies to insulin (IAA) only, 37.7% had glutamic acid decarboxylase autoantibodies (GADA) only, 13.8% had both GADA and IAA only, 1.6% had insulinoma antigen-2 only and 3.1% had other combinations. The incidence of IAA only peaked within the first year of life and declined over the following 5 years, but GADA only increased until the second year and remained relatively constant. GADA only were more common than IAA only in HLA-DR3/3 children but less common in HLA-DR4/8 children.
Conclusions/interpretation
Islet autoantibodies can occur very early in life and the order of appearance was related to HLA-DR-DQ genotype.
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