An elevation of serum immunoglobulin E provides a new aspect of hyperthyroid Graves' disease

Abstract

Graves' disease is an autoimmune disorder characterized by circulating TSH receptor antibodies (TRAb), the majority of which lies in the immunoglobulin G (IgG) class. However, there may be a role of other immunoglobulins in the induction and maintenance of hyperthyroid Graves' disease. We focus on the role of IgE on these issues. One third of hyperthyroid Graves' disease shows IgE elevation (greater than 170 U/mL). This prevalence is significantly higher than other thyroid diseases and controls, suggesting IgE elevation appears associated with autoimmune Graves' disease. Half of Graves' patients with IgE elevation have hereditary and/or allergic conditions such as bronchial asthma and pollen allergy. There is a significantly smaller decrease in TRAb in patients with IgE elevation than in those with normal IgE during methimazole treatment. The remission rate is significantly less in patients with IgE elevation than in those with normal IgE. These findings suggest that TRAb synthesis is increased when IgE synthesis is stimulated. There is an elevation of interleukin (IL)-13, but not of IL-4, in two thirds of patients with IgE elevation in the absence of detectable helper T-cell-1 marker, IFN gamma. It seems that TH2 cells are stimulated in hyperthyroid Graves' disease to secrete excess IL-13, following stimulation of B cells to secrete TRAb and IgE. IgE elevation as a result of aggravating complex (IL-13-IgE synthesis), thus, may play a role in the participation of thyroid autoimmunity rather than its pathogenesis.