LADA: pathophysiological and clinical aspects

Abstract

LADA is a specific form of type 1 diabetes that develops in adulthood and that is characterized by slow development of clinical symptoms. The presence of chronic immune-mediated mechanism leads to the destruction of the insulin-secreting beta-cells of the islets of Langerhans. Typical features of LADA are age at diagnosis usually over 30 years, circulating type 1 diabetes related antibodies, low C-peptide level, lack of obesity, initially good response to diet and oral medications and fast progression to clinical insulin dependency. LADA patients are often diagnosed initially with type 2 diabetes. It is very important to make a right diagnosis because early intervention with insulin may protect beta-cells, maintain their residual function over longer period of time and result in better metabolic control. The diagnosis of autoimmune diabetes is based on the presence of type 1 diabetes related antibodies, particularly glutamic acid decarboxylase antibodies (GADA). There were several studies performed on genetic background of LADA. In general the role of HLA in LADA, similarly to typical type 1 diabetes, has been confirmed. The role of other genes such as for example insulin, cytotoxic T-Lymphocyte Antigen-4 (CTLA-4) and protein tyrosine phosphatase type 22 (PTPN22) has not been defined.