Last update:
10-Sep-2004

Type 1 diabetes mellitus (Τ1DM, insulin dependent diabetes mellitus) is caused by the destruction of the insulin-secreting β-cells of the islets of Langerhans. It is believed that the disease is caused by nongenetic (environmental) factors operating in a genetically susceptible host to initiate a destructive immune process. The autoimmune reactions are pronounced at the onset of disease when an infiltration of the islets with T and B-lymphocytes, plasma cells and macrophages can be observed. There is a long prodromal phase prior to the onset of clinical diabetes, during which clinical, immune and metabolic changes can be detected. Using genetic, immunological and metabolic markers, testing individuals at risk or conducting population screening programs can help in the recognition of subclinical insulitis. The progress made in the prediction of Τ1DM has led to the emergence of strategies for intervention in the development of the disease prior to the total destruction of the β-cell mass. Each of the stages leading to the clinical onset of Τ1DM can be seen as an opportunity for intervention directed at prevention of the disease. Some of the approaches currently being explored include dietary interventions, generalized immunosuppression (e.g. cyclosporin, azathioprine), use of drugs that protect the β-cell from damage (e.g. nicotinamide), peptide-mediated immunotherapy (e.g. insulin), use of monoclonal antibodies and cytokines and gene therapy. Ideally the recognition of specific diabetogenic antigens will allow the planning of immunization of the general population against diabetes. Programs aiming at prediction and prevention of Τ1DM have been launched or are in the planning phase in several countries, including Greece.

Key words: Prevention, Type 1 diabetes mellitus.