Exp Clin Endocrinol Diabetes 2004; 112(4): 171-174
DOI: 10.1055/s-2004-817930
Review

J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

TSH-Receptor Autoantibodies - Differentiation of Hyperthyroidism between Graves' Disease and Toxic Multinodular Goitre

H. Wallaschofski1 , T. Kuwert2 , T. Lohmann1
  • 1Department of Internal Medicine I, Friedrich-Alexander University of Erlangen-Nürnberg, Germany
  • 2Department of Nuclear Medicine, Friedrich-Alexander University of Erlangen-Nürnberg, Germany
Further Information

Publication History

Received: October 1, 2002 First decision: March 17, 2003

Accepted: July 14, 2003

Publication Date:
04 May 2004 (online)

Abstract

Previous studies indicate pre-existing subclinical Graves' disease in many patients with the scintigraphic diagnosis of toxic multinodular goitre type A, equivalent to the in Germany so-called disseminated thyroid autonomy. Furthermore, after radioiodine treatment an increase or the induction of TSH-receptor antibodies (TRAb) in patients with Graves' disease or toxic multinodular goitre has been repeatedly reported.

The distinction between both hyperthyroid conditions, Graves' disease and toxic multinodular goitre type A, depends on the diagnostic power of the TSH-receptor antibody determination. Bioassays using CHO cell lines expressing the hTSH-receptor or a new TBII assay based on competitive binding to recombinant human TSH-receptor showed a higher sensitivity for the detection of TSH-receptor antibodies in patients with Graves' disease than previous assays using solubilized porcine epithelial cell membranes. In up to 50 % of patients with toxic multinodular goitre A without antithyroid drug pretreatment TSH-receptor antibodies were detectable with a high correlation between thyroid-stimulating antibodies in the bioassay and the h-TBII assay. Moreover, in a recent study the development of TSH-receptor antibodies after radioiodine treatment was detectable in 36 % of patients with toxic multinodular goitre type A, whereas TSH-receptor antibodies were not detectable in patients with toxic multinodular goitre type B or in patients with toxic adenoma.

In conclusion, thyroid-stimulating antibodies in a bioassay or TSH-receptor antibodies detected with the h-TBII assay have the highest diagnostic power to differentiate Graves' disease from toxic multinodular goitre. Because of its less cumbersome assay technique the h-TBII should be performed in all patients with hyperthyroidism to differentiate Graves' disease from non-autoimmune hyperthyroidism such as toxic multinodular goitre to select the appropriate therapy for these patients.

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Henri Wallaschofski

Medizinische Klinik I mit Poliklinik
Universitätsklinikum

Ulmenweg 18

91054 Erlangen

Germany

Phone: + 4991318535230

Fax: + 49 9 13 18 53 52 31

Email: Henri.Wallaschofski@med1.imed.uni-erlangen.de

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