Читать книгу Clinical Dilemmas in Diabetes - Группа авторов - Страница 42

Although the process by which pancreatic β‐cells are destroyed is not well understood, several risk factors and immune‐ related markers are known to accurately identify first‐degree relatives of patients with T1D who may develop the disease. Since we now can predict the development of T1D, investigators have begun to explore the use of intervention therapy to halt or even prevent β‐cell destruction in such individuals. The autoimmune pathogenesis of T1D determines the efforts to prevent it. Susceptible individuals are identified by searching for evidence of autoimmune activity directed against β‐cells. While direct evaluation of T‐cell activity might be preferable, antibody determinations are generally used for screening because these assays are more robust. Antibody titers are often used in combination with an assessment of the genetic susceptibility, primarily evaluated by HLA typing. In the near future, testing for oxPTM‐INS‐Ab may help to identify children progressing to overt diabetes.

Interventions are generally designed to delay or prevent T1D by impacting some phases of the immune pathogenesis of the disease. As discussed below, current trials are attempting to modify the course of disease progress at many points along the presumed pathogenic pathway. Most prevention trials include only relatives of T1D patients, a group in which risk prediction strategies are most established. Trials in genetically at‐risk infants evaluate whether avoiding one of the putative environmental triggers for T1D can delay or prevent its onset.