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Several autoantibodies can be used in clinical practice to document the presence of islet autoimmunity. These are antibodies directed against Glutamic Acid Decarboxylase (GAD‐65), insulin, tyrosine phosphatases, insulinoma‐associated protein 2 (IA‐2 and IA‐2β), and the zinc transporter (ZnT8). The greater the number of autoantibodies that are positive and the higher the titer of these antibodies, the more likely that islet autoimmunity is present [40]. However, people with a clinical presentation compatible with type 1 diabetes are often antibody negative. The opposite sometimes applies. Indeed, in a cohort of Belgian patients with type 1 diabetes presenting before age 40, 24% did not have autoantibodies [41]. In the Botnia study, 4.4% of healthy individuals had GAD antibodies [42].

Latent autoimmune diabetes of adults (LADA) likely represents a “forme fruste” of type 1 diabetes where a lower genetic burden of predisposition results in a later age at presentation, decreased amount and degree of autoantibody positivity, and a longer persistence of endogenous insulin secretion. Patients with LADA tend to have a lower BMI than patients with type 2 diabetes. Of note, antibodies against insulin and IA‐2 are rarely present in late‐onset diabetes. Islet autoantibodies are most useful in screening family members of patients with type 1 diabetes for risk of developing the disease [43].