1990European Journal of EndocrinologyRequires access

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

Pei‐Wen Wang, Miau‐Ju Huang, Rue‐Tsuan Liu, Chung Dar Chen

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Abstract

UNLABELLED: 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 endogenous 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 heterogenous 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 not correlated with that of the overall heterogenous anti-thyroglobulin antibodies.

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UNLABELLED: 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 endogenous 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 heterogenous 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 not correlated with that of the overall heterogenous anti-thyroglobulin antibodies.

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Available abstract

UNLABELLED: 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 endogenous 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 heterogenous 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 not correlated with that of the overall heterogenous anti-thyroglobulin antibodies.

Key concepts: Thyroglobulin, Autoantibody, Internal medicine, Endocrinology, Graves' disease, Medicine, Triiodothyronine, Antibody

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