The role of GaD65, ZNTS, IA-2, and IAA as predictive biomarkers for type 1 diabetes mellitus in children

Abstract

Background Type 1 diabetes mellitus (T1DM) is a chronic disorder characterized by immune-mediated harm to the pancreatic β-cells that produce insulin. The four major autoantibodies implicated in the pathophysiology are insulin autoantibodies, glutamic acid decarboxylase antibodies, tyrosine phosphatase antibodies, and zinc transporter 8 antibodies. Objective We examined whether children with T1DM have particular antibodies related to T1DM and their association with clinical features. Materials and methods The study involved 60 Iraqi children who had been diagnosed with T1DM within the last 3 years, as well as a control group of 60 healthy individuals without diabetes or autoimmune diseases. Blood samples were collected from all participants to analyze the levels of serum autoantibodies, specifically insulin (IAA), glutamic acid decarboxylase (GADA), tyrosine phosphatase (IA-2A), and zinc transporter 8 (ZnT8A), using an enzyme-linked immunosorbent assay (Sandwich-ELISA). Results and conclusion The findings revealed that a significant number of patients with diabetes had elevated levels of antibodies against zinc transporter 8 (P<0.001), tyrosine phosphatase (P<0.001), insulin autoantibodies (P<0.001), and glutamic acid decarboxylase (P<0.001). Glutamic acid decarboxylase 65 antibodies were found to be the most prevalent. All four biomarkers showed remarkable effectiveness in distinguishing positive and negative cases. Logistic regression analysis revealed that glutamic acid decarboxylase 65 and insulin antibodies were significantly associated with the outcome, while tyrosine phosphatase and zinc transporter 8 did not show such a relationship. These findings indicate that measurements of anti-zinc transporter 8, tyrosine phosphatase, insulin autoantibodies, and glutamic acid decarboxylase could be important diagnostic markers for identifying patients with T1DM, aiding in early detection and understanding the disease process.