Background & Aim
Latent autoimmune diabetes in adults (LADA) is characterised by circulating pancreatic islet autoantibodies yet great heterogeneity exists. LADA remains a relatively poorly understood form of diabetes with many clinicians believing it is ‘type 2 diabetes with coincidental islet autoantibodies’. This study aimed to profile the frequency of organ-specific autoimmunity in patients classified with LADA.
Clinical, family history and autoantibody data were obtained from hospital records, diabetes databases and patient questionnaires. Autoantibodies assessed included glutamic acid decarboxylase (GADA), tyrosine phosphatase-like insulinoma antigen-2 (IA2A), insulin (IAA), tissue transglutaminase (TTGA), thyroid peroxidase (TPOA), parietal cell (PCA) and intrinsic factor (IFA). This ‘real world’ clinical audit involved 237 LADA patients who had islet autoantibody data and smaller subgroups with other organ specific antibody data (TTG N=150, TPOA N=105, PCA N=49, IFA N=45).
A majority of patients with LADA had a symptomatic diabetes presentation (64%) and a family history of diabetes (72%). GADA positivity was present in 97% and IA2A positivity in 24% (IA2A positive alone 3%). Patients with at least two positive islet autoantibody specificities were more often symptomatic at presentation, diagnosed with LADA earlier after diabetes diagnosis, had a higher family history of autoimmune disease and started insulin earlier compared to those positive for a single autoantibody specificity. A family history of an organ-specific autoimmune disease in a first and/or second degree relative was present in 38% of patients. In LADA patients, TPOA positivity was present in 42%, TTGA positivity in 5%, PCA positivity in 24%, IFA positivity in 2%. Higher prevalence of other organ-specific autoimmunity was significantly associated with higher islet autoantibody concentration but not multiple islet autoantibody positivity.
LADA is a heterogeneous form of diabetes with variable (auto)immunopathology evident. Approximately 40% of individuals had evidence of thyroid autoimmunity and a family history of organ-specific autoimmunity.