Comment on: Gale EAM (2005) Latent autoimmune diabetes in adults: a guide for the perplexed. Diabetologia 48:2195–2199

Abstract

A definition of LADA has recently been issued by the Immunology of Diabetes Society [6]. However, it is unclear how a disease entity with poorly defined aetiology and heterogeneous clinical features can be so rigorously defined; we seem to have returned to definition of diabetes by age (>30 years) and therapy (no insulin requirement within 6 months of diagnosis) and a test for autoantibodies with low positive predictive value for insulin therapy requirement post-diagnosis [1]. In conclusion, there appears to be a continuum with age of both genetic and clinical factors in juvenile- and adult-onset autoimmune diabetes; there is a decreased frequency of predisposing HLA variants and diminished severity in clinical course of disease with increasing age of onset in cohorts of children (diagnosed under 25 years) and of adults (>30 years). We agree with the Editor that there is no scientific or clinical evidence to suggest that the overall aetiology of LADA is different from that of childhood-onset autoimmune diabetes. The qualitative differences in clinical features at onset are likely to result from a combination of varying genetic susceptibility and its interaction with the environment. Opinions differ regarding treatment of adult-onset patients, but the UKPDS LADA study shows that the actual therapy received by patients with autoimmune diabetes did not significantly affect the clinical course of the disease. Defining differences on the basis of age of onset is likely to hinder rather than help understanding of autoimmune diabetes so that interventions can be appropriately devised for children and adults alike.