[Latent autoimmune diabetes of adult or slim type 2 diabetes mellitus?].
The prevalence of latent autoimmune diabetes of the adult (LADA) varies according to the population studied, criteria used and antibodies analyzed. In a series of 256 patients > 25 years, we found that 26 (10.2%) were anti-GAD antibody (GADA) positive and 16 of them (6.3%) progressed without initial insulin requirement. Although controversy exists, the following diagnostic criteria for LADA are suggested: age between 25 and 65 years; absence of ketoacidosis or symptomatic hyperglycemia at diagnosis or immediately thereafter, without insulin requirement for 6-12 months; and presence of autoantibodies (especially GADA). Autoimmunity and insulin resistance coexist in LADA and the contribution of these factors seems to be reflected in GADA titers. A subgroup, which is phenotypically and in terms of insulin requirement similar to type 2 diabetic patients, seems to be better identified based on the presence of low GADA titers, especially when these antibodies are present alone. On the other hand, subjects with high GADA titers and multiple antibodies show a phenotype close to that of classical DM 1 and are at a higher risk of premature beta-cell failure. Compared to GADA-negative diabetics, patients with LADA present a higher prevalence of other autoantibodies (anti-TPO, anti-21-hydroxylase and antibodies associated with celiac disease) and a higher frequency of genotypes and haplotypes indicating a risk for DM 1. Patients with high GADA titers may benefit from early insulinization and avoiding the use of sulfonylureas, delaying beta-cell failure. In contrast, patients with low GADA titers do not seem to have any disadvantage when managed as type 2 diabetic patients (GADA negative).
Calsolari
Maria Regina
MR
Serviço de Endocrinologia, Santa Casa de Belo HorizonteMG, Brasil.
Rosário
Pedro W Souza do
PW
Reis
Janice Sepúlveda
JS
Silva
Saulo Cavalcanti da
SC
Purisch
Saulo
S
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000032:analysis; D015551:Autoimmunity / Q000502:physiology; D015415:Biomarkers / Q000032:analysis; D001938:Brazil / Q000453:epidemiology; D002096:C-Peptide / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology; D003924:Diabetes Mellitus, Type 2 / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology / Q000276:immunology; D003937:Diagnosis, Differential; D020022:Genetic Predisposition to Disease; D005968:Glutamate Decarboxylase / Q000032:analysis / Q000276:immunology; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007328:Insulin / Q000627:therapeutic use; D007333:Insulin Resistance / Q000502:physiology; D008875:Middle Aged; D015995:Prevalence; D055815:Young Adult
D001323:Autoantibodies; D015415:Biomarkers; D002096:C-Peptide; D007004:Hypoglycemic Agents; D007328:Insulin; D005968:Glutamate Decarboxylase