[Prevention strategies of type 1 diabetes: the focus in 2003]

Type 1 diabetes is caused by a progressive autoimmune destruction of insulin-producing B cells of the pancreatic islets of Langerhans. The autoimmune process begins years before the B-cell destruction becomes complete, thereby providing an opportunity for early intervention. Genetic susceptibility markers have been identified and autoantibody assays make possible the identification of individuals at high risk of the disease. Prevention strategies could be implemented in first-degree relatives of type 1 diabetic patients at high risk of developing the disease because of the presence of several autoantibodies. Alternatively, they may also be considered at time of clinical diagnosis of type 1 diabetes mellitus in order to maintain residual endogenous insulin secretion that markedly contributes to long-term better glycaemic stability. Thus, the goals of prevention are to preserve B cells during the preclinical period and/or after early diagnosis by modifying immunological pathogenic processes. Several molecules have been administered or are currently investigated to achieve this protection. This article summarizes the hopes and deceptions of previous clinical trials and describes the rationale and protocols of ongoing trials dealing with the prevention of type 1 diabetes.