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

In hyperthyroid Graves' disease, short-term methimazole is sufficient to in duce lasting remission in some patients, but even longterm treatment fails to do so in others. We have evaluated the role of autoimmune abnormalities in the helper T cell type 2 (TH2)-interleukin-13 (IL-13)-TSH receptor syste m in maintaining hyperthyroidism by comparing IgE levels in patients with v arious thyroid diseases. One hundred and ninety-three patients with hyperthyroid Graves' disease wer e treated with methimazole, and blood samples were obtained to measure seru m levels of T-4, T-3, TSH, thyroglobulin, antimicrosomal antibody, TSH bind ing inhibitory Ig (TBII), thyroid-stimulating antibody, thyroid stimulation -blocking antibody, IgE, interferon-gamma, IL-4, and IL-13. Elevation of se rum IgE (greater than or equal to 170 U/mL) was found in 35.5% of patients with hyperthyroid Graves' disease, and serum levels of T-4, T-3, antimicros omal antibody, and TBII were significantly greater in patients with IgE ele vation than in those with normal serum IgE. During methimazole treatment, t here was a parallel decrease in the serum T, concentration in the presence or absence of an IgE elevation. However, there was a significantly smaller decrease in TBII in patients with elevated IgE than in those with normal Ig E. As a result, the remission rate was significantly greater in patients wi th normal IgE than in those with IgE elevation. Serum levels of IL-13 were elevated in 64.7% of patients with IgE elevation in the absence of detectab le TH1 marker, interferon-gamma. These findings suggest that in one third of patients with hyper thyroid Gra ves' disease, TH2 cells are stimulated and secrete excess amounts of IL-13, which subsequently stimulates B cells to synthesize more TSH receptor anti body and IgE, so that during methimazole treatment TBII decreases less in p atients with IgE elevation, producing a lower remission rate.