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Triiodothyronine autoantibodies in Graves' disease: Their changes after antithyroid therapy and relationship with the thyroglobulin antibodies

  • P. W. Wang*
  • , M. J. Huang
  • , R. T. Liu
  • , C. D. Chen
  • *Corresponding author for this work
  • Chang Gung Memorial Hospital

Research output: Contribution to journalJournal Article peer-review

10 Scopus citations

Abstract

Sera of 63 patients with Graves' disease, and 49 control subjects were assayed for T3 autoantibodies by a sensitive radioimmunoassay after being stripped of the endogeneous thyroid hormone. T3 autoantibodies were demonstrated in 27% of patients with Graves' disease. After antithyroid treatment, T3 autoantibodies in 75% of the patients with positive antibody before therapy changed to negative titre during a follow-up period of 1 to 12 months. Also, a significant decrease of T3 autoantibodies was observed at 1 month after therapy in all patients who received antithyroid treatment. A further study of T3 autoantibodies and anti-thyroglobulin antibodies showed that the latter were demonstrated in 100% of patients with positive T3 autoantibodies and that T3 autoantibodies existed in about one third of patients with positive anti-thyroglobulin antibodies. The results suggested that T3 autoantibodies could be a subpopulation of the heterogeneous anti-thyroglobulin antibodies. Although the fall of T3 autoantibodies in some patients was correlated to that of anti-thyroglobulin antibodies, the overall correlation between T3 autoantibodies and anti-thyroglobulin antibodies was poor. In conclusion: 1. T3 autoantibodies may be suppressed by antithyroid drugs. 2. Being a subpopulation of anti-thyroglobulin antibodies, T3 autoantibodies may be caused by an antigenic site within the big thyroglobulin molecule, whereas their titre was correlated with that of the overall heterogeneous anti-thyroglobulin antibodies.

Original languageEnglish
Pages (from-to)22-28
Number of pages7
JournalActa Endocrinologica
Volume122
Issue number1
DOIs
StatePublished - 1990
Externally publishedYes

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