Antibody profile in families with mono- and polyglandular autoimmunity

Abstract

Elevated autoantibody (Ab) titres may indicate underlying autoimmune disorders. This study examined the antibody profile in families with different severity of endocrine autoimmunity. 60 patients with polyglandular autoimmunity (PGA), 54 with monoglandular autoimmunity and associated non-glandular autoimmune disease (MGA2) and their relatives (14 monoglandular autoimmunity, MGA; 15 non-glandular autoimmunity, NGA; 82 healthy subjects) were screened for Ab against alpha-fodrin-IgA/IgG, SSA/SSB, TPO, intrinsic factor (IF), parietal cells (PCA), gliadin-IgA/IgG, transglutaminase-(tTG)-IgA/IgG, ASCA-IgA/IgG, 21-OH, 17-OH, side-chain-cleavage, antinuclear antibodies (ANA) and anti-neutrophile cytoplasmic Ab (ANCA) using ELISA and/or RIA. Group comparisons were performed with chi-square tests. Methods comparison (ELISA vs. RIA for tTG-Ig-Ab; ELISA vs. ELISA for IF, PCA, gliadin, TPO, ANA, and ANCA) was done with Kappa statistic, 95% confidence interval (CI), and McNemar test. Overall Ab prevalence in patients with PGA, MGA2, relatives with MGA, NGA, and healthy relatives was 92%, 87%, 79%, 67%, and 56%, respectively. For prevalence of PCA in subjects with PGA (32%), MGA2 (43%), MGA (3/14, 21%), NGA (1/15, 7%), and healthy relatives (6%), group differences were significant (chi-square=30.1, p<0.0001). Prevalences for TPO were also different between PGA, MGA2, MGA, NGA, and healthy relatives amounting 50%, 54%, 50%, 13% (2/15), and 12%, respectively, (chi-square=37.6, p<0.0001). There were no statistically significant group differences with respect to the other autoantibodies. With respect to PCA, comparison of two ELISAs yielded different results (45 vs. 35 Ab-positive subjects, McNemar test: p=0.019; kappa=0.702, 95%CI=0.58 to 0.83). In conclusion, we show a high prevalence of silent antibodies in families with endocrine autoimmunity. The prevalence of these Ab is associated with the number of involved glands. Thus, these Ab may be predictive for the development of future autoimmune endocrine diseases.