Background: The elevation of serum immunoglobulin E (IgE) has been recently reported to be associated with Graves disease (GD). Interleukin 13 (IL-13) is a major cytokine involved in IgE synthesis and therefore may be a potential candidate gene influencing the clinical course of the GD. The aim of this study are to evaluate whether the atopic parameter such as total IgE is related to TSH receptor antibody (TRAb, thyrotropin-binding inhibitory immunoglobulin: TBII) and whether IL-13 gene polymorphisms are associated with the course of GD.
Methods: In 405 patients with GD, we investigated the history of common allergic diseases by questionnaire and measured total IgE and TRAb. We also examined IL-13 gene single-nucleotide polymorphisms in the 5 promoter region at position −1112 (C to T change, C-1112T) and in exon 4 at position −2044 (G to A change, G2044A).
Results: Log-transformed TRAb was higher in patients who had clinical symptoms of asthma (2.30±1.44 vs 1.79±1.36, P=0.011) and treatment history of it within a year (3.37±2.15 vs 1.84±1.36, P=0.014). Log-transformed TRAb was related positively with log-tranformed total IgE (r=0.136, P<0.01). Subdividing GD patients according to the clinical symptoms of asthma, −1112T/T+C/T genotypes had significantly increased in patients with asthma symptoms (42 vs 26%; χ2=5.788; P=0.016). Subdividing them according to the treatment history of asthma within a year, −2044A/A+G/A genotypes had significantly increased in patients with treatment history (100 vs 51%; χ2=4.687; P=0.030).
Discussion: TRAb was significantly related with total IgE, known as an atopic marker. TRAb and IL-13 gene polymorphisms were both significantly increased in patients with clinical symptoms or treatment history of asthma. Our results suggest that there might be a possible common link between autoimmune thyroid disease and allergic immune response.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology