Latent autoimmune diabetes in adults

Abstract

Recently, diabetes has become a medical and social problem due to its widespread ever-increasing incidence. The latent autoimmune diabetes in adults (LADA) accounts for up to 10% of all cases and stands high among the new identified forms of the disease. With the manifestation of LADA, which occurs, as a rule, before the age of 35 years, patients show clinical symptoms of type 2 diabetes in combination with autoantibody destruction of beta-cells of the pancreas, which is characteristic for type 1 diabetes. Genetic predisposition associated with histocompatibility antigens HLA DR4-DQ8, DR3-DQ2 and others, in combination with resolving factors contributes to autoimmune β-cell damage. Unlike type 1 diabetes, LADA is featured by constant blood circulation of antibodies against cytoplasmic structures of β-cells (most often to glutamatdecarboxylase - GAD), insulin and thyroperoxidase. The developing insulitis is combined with intact and compensatory hypertrophied islets. Subsequently, atrophy and sclerosis of the Langerhans islets as well as stromal proliferation are identified in pancreatic tissue. The debute of LADA is diagnosed in the young age of the patient with normal body weight (body mass index up to 25 kg/m2) by low blood level of insulin C-peptide and presence of anti- β-cell autoantibodies. The treatment of LADA (with early administration of insulin drugs even in clinically compensated patients) aims to maintain their own secretion of insulin. As a result, the functional load on β-cells is decreased and their autoimmune damage is diminished.