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. 1988 Jun;72(3):481–485.

Graves' disease: changes in TSH receptor and anti-microsomal antibodies after thyroidectomy.

T W De Bruin 1, N A Patwardhan 1, R S Brown 1, L E Braverman 1
PMCID: PMC1541569  PMID: 3168323

Abstract

It has been suggested that intrathyroidal plasma cells are the major site of TSH receptor antibody synthesis in Graves' disease (GD). To investigate this hypothesis, serial serum levels of TSH receptor antibodies, as determined by a recently developed immunoprecipitation assay (IPA), were measured in 13 patients with GD before and after subtotal thyroidectomy (Tx). Pretreatment TSH receptor antibody levels (86.4 +/- 26.8 pM/ml; mean +/- s.d.) decreased significantly due to antithyroid drug therapy to 60.3 +/- 21.5 pM/ml (P less than 0.05) just before Tx. However, 4 h after Tx, there was a significant increase (84.9 +/- 35.5 pM/ml; P less than 0.05) due to leakage of antibodies from the manipulated thyroid gland. After Tx, no major decrease in autoantibody levels occurred; TSH receptor antibodies were still detectable 1 to 7 months after Tx (88.7 +/- 44.6 pM/ml). Neither an acute change nor an overall reduction in anti-microsomal (M) antibody titres was observed after Tx. Our conclusions are that serum TSH antibody levels exhibited a drug-induced decrease before Tx and an immediate, but transient, post-operative increase. The post-operative increase was caused by leakage of preformed TSH receptor antibodies from the manipulated thyroid gland. Several months after Tx, TSH receptor and anti-M antibodies were present in the same serum concentrations as before treatment. The present data does not support the hypothesis that plasma cells in the thyroid gland are the major site of autoantibody synthesis in GD at the time of Tx.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Adams D. D. Thyroid-stimulating autoantibodies. Vitam Horm. 1980;38:119–203. doi: 10.1016/s0083-6729(08)60485-9. [DOI] [PubMed] [Google Scholar]
  2. Arqueros M. C., Niepomniszcze H., Moreno J. Thyroid glands in patients with Graves' disease are sources of thyrotropin-binding inhibitory (TBI) activity. Acta Endocrinol (Copenh) 1986 Jul;112(3):351–354. doi: 10.1530/acta.0.1120351. [DOI] [PubMed] [Google Scholar]
  3. Burman K. D., Baker J. R., Jr Immune mechanisms in Graves' disease. Endocr Rev. 1985 Spring;6(2):183–232. doi: 10.1210/edrv-6-2-183. [DOI] [PubMed] [Google Scholar]
  4. De Bruin T. W., Braverman L. E., Brown R. S. Further evaluation of an immunoprecipitation assay for TSH-receptor autoantibodies in Graves' disease. Metabolism. 1986 Dec;35(12):1101–1105. doi: 10.1016/0026-0495(86)90022-3. [DOI] [PubMed] [Google Scholar]
  5. Hardisty C. A., Talbot C. H., Munro D. S. The effect of partial thyroidectomy for Graves' disease on serum long-acting thyroid stimulator protector (LATS-P). Clin Endocrinol (Oxf) 1981 Feb;14(2):181–188. doi: 10.1111/j.1365-2265.1981.tb00614.x. [DOI] [PubMed] [Google Scholar]
  6. Kendall-Taylor P., Knox A. J., Steel N. R., Atkinson S. Evidence that thyroid-stimulating antibody is produced in the thyroid gland. Lancet. 1984 Mar 24;1(8378):654–656. doi: 10.1016/s0140-6736(84)92171-8. [DOI] [PubMed] [Google Scholar]
  7. McLachlan S. M., Pegg C. A., Atherton M. C., Middleton S. L., Clark F., Rees Smith B. TSH receptor antibody synthesis by thyroid lymphocytes. Clin Endocrinol (Oxf) 1986 Feb;24(2):223–230. doi: 10.1111/j.1365-2265.1986.tb00766.x. [DOI] [PubMed] [Google Scholar]
  8. Teng C. S., Yeung R. T., Khoo R. K., Alagaratnam T. T. A prospective study of the changes in thyrotropin binding inhibitory immunoglobulins in Graves' disease treated by subtotal thyroidectomy or radioactive iodine. J Clin Endocrinol Metab. 1980 Jun;50(6):1005–1010. doi: 10.1210/jcem-50-6-1005. [DOI] [PubMed] [Google Scholar]
  9. Torrigiani G., Doniach D., Roitt I. M. Serum thyroglobulin levels in healthy subjects and in patients with thyroid disease. J Clin Endocrinol Metab. 1969 Mar;29(3):305–314. doi: 10.1210/jcem-29-3-305. [DOI] [PubMed] [Google Scholar]
  10. Tötterman T. H., Andersson L. C., Häyry P. Evidence for thyroid antigen-reactive T lymphocytes infiltrating the thyroid gland in Graves' disease. Clin Endocrinol (Oxf) 1979 Jul;11(1):59–68. doi: 10.1111/j.1365-2265.1979.tb03046.x. [DOI] [PubMed] [Google Scholar]
  11. Tötterman T. H., Karlsson F. A., Bengtsson M., Mendel-Hartvig I. Induction of circulating activated suppressor-like T cells by methimazole therapy for Graves' disease. N Engl J Med. 1987 Jan 1;316(1):15–22. doi: 10.1056/NEJM198701013160104. [DOI] [PubMed] [Google Scholar]
  12. Uller R. P., Van Herle A. J. Effect of therapy on serum thyroglobulin levels in patients with Graves' disease. J Clin Endocrinol Metab. 1978 May;46(5):747–755. doi: 10.1210/jcem-46-5-747. [DOI] [PubMed] [Google Scholar]
  13. Weetman A. P., McGregor A. M. Autoimmune thyroid disease: developments in our understanding. Endocr Rev. 1984 Spring;5(2):309–355. doi: 10.1210/edrv-5-2-309. [DOI] [PubMed] [Google Scholar]
  14. de Bruin T. W., van der Heide D. Anti-thyrotrophin receptor antibodies in Graves' disease as demonstrated directly by immunoprecipitation assay. Acta Endocrinol (Copenh) 1983 Jan;102(1):49–56. doi: 10.1530/acta.0.1020049. [DOI] [PubMed] [Google Scholar]
  15. de Bruin T. W., van der Heide D. Solubilized human thyrotrophin receptors behave as one class of high-affinity binding sites. Mol Cell Endocrinol. 1984 Oct;37(3):337–348. doi: 10.1016/0303-7207(84)90104-7. [DOI] [PubMed] [Google Scholar]

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