Immunomodulation for the prevention of SPIDDM and LADA

Abstract

Type 1 diabetes may occur at any age, in young individuals before or after adolescence, during middle age life, or even in the elderly. When diagnosed in adults it is characterized by the presence of islet cell-related autoantibodies (ICA), in particular GAD and IA2 (less common) and very rarely insulin autoantibodies (IAA). Baseline C-peptide at diagnosis of type 1 diabetes can identify different patient populations according to when the disease is diagnosed depending on age. A key question is whether the process of beta cell destruction follows the same pattern in patients diagnosed in young age, soon after adolescence, or in adult age. The terms SPIDDM--slowly progressive insulin-dependent diabetes mellitus, and LADA--latent autoimmune diabetes in adults, have been considered synonymous on most grounds based on the fact that with this form of diabetes we intend a form of diabetes that has an autoimmune basis that eventually will require insulin for its treatment sometime after diagnosis. Therapeutic approaches are similar for prevention and treatment of SPIDDM or LADA, including both specific and nonspecific immunomodulation. For specific immunomodulation the attention is focused on DiaPep277, GAD, and insulin, and for nonspecific immunomodulation on 1,25 dihydroxy-vitamin D3 (calcitriol) and thiazolidinediones. Current trials in SPIDDM/LADA with both specific and nonspecific immunomodulation seem promising. Response to therapy varies according to age and residual beta cell function at diagnosis of SPIDMM/LADA. Results in beta cell protection with different agents can also help to identify differences, if any, between SPIDMM and LADA.