Type 1 diabetes is caused by the immune-mediated destruction of islet insulin-secreting B-cells. This chronic destructive
process is associated with both cellular and humoral immune changes in the peripheral blood that can be detected months or even years before the onset of clinical diabetes.
A fraction of individuals with humoral immunological changes have clinical diabetes that initially is not insulin-requiring. The onset of diabetes in these patients is usually in adult life, and because their diabetes is at least initially not insulin-requiring, they appear clinically to be affected by type 2 diabetes. . A genetic susceptibility as well as autoantibodies to islet antigens, low insulin secretion, and a higher rate of progression to insulin
dependency.
Such patients probably have the same disease process as patients with type 1 diabetes in that they have similar HL. These patients are defined as being affected by an autoimmune diabetes of the adult (LADA). Special attention should be paid to diagnose such patients because therapy may influence the speed of progression toward insulin dependency, and in this respect, efforts should be made to protect residual peptide secretion. LADA can serve as a model for designing new strategies for prevention of type 1diabetes but also a target group for prevention in its own right.
The recent new
classification of diabetes is the third attempt in the last 30 years to recomprise the many different disease entities comprised in the term diabetes under a single classification criterion. Age was the main classification criterion in the early 1970s, and it was son abandoned because the different forms of diabetes can be present at any age, although a few are typical of young age and others of adult age. Insulin dependency, a clinical criterion, was then used because of its ease of use in a clinical setting, and it was considered for subgrouping cases with different pathogenetic mechanisms. (362) For many years (maybe too many), insulin dependency was thought to specifically characterize those forms of diabetes with an autoimmune pathogenesis. More recently, attention has been paid to the fact the clinical criterion (i.e. insulin dependency, and the pathogenetic criterion, ie., the presence of autoimmune mechanisms leading to B-cell damage) do not match in a number of cases. An etiologic classification criterion was therefore chosen to subgroup the different types of diabetes. Type 1 diabetes is characterized by the destruction of the insulin-secreting B-cells of the islets of Langerhans, by the production of little or no insulin, and, in most cases, by immune-mediated pathogenetic mechanism highlighted by the presence of islet cell auto-antibodies and by an altered frequency of immune-regulating genes in the HLA region. This form of diabetes often develops in children, although it may occur at any age and often, but not always requires insulin treatment. For a clinician, the distinction between type 1 and type 2 diabetes is not always straightforward. The presence or absence of islet auto antibodies is one of the more direct ways to distinguish between type 1 and type 2 diabetic patients. If a search is done for these auto antibodies in all new cases of diabetes, it is now believed that among that the non-insulin- requiring diabetic subject at diagnosis, a significant minority are islet cell antibody – positive. These patients who clinically are difficult to distinguish from type 2 diabetic subjects test positive for those markets that characterize patients with type 1 diabetes.
The term latent autoimune diabetes in adults (LADA) was introduced to define adult diabetic patients initially non-insulin-requiring but with immune markers of type 1 diabetes that, in a number of cases, progress to insulin dependency (3). This term has been largely used in the last few years when referring to autoimmune forms of diabetes not requiring insulininitially. Now it is clea