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The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 12 4630-4634
Copyright © 2000 by The Endocrine Society


Original Studies

Low Frequency of Autoantibodies to the Human Na+/I- Symporter in Patients with Autoimmune Thyroid Disease1

Jochen Seissler, Sandra Wagner, Matthias Schott, Melanie Lettmann, Joachim Feldkamp, Werner A. Scherbaum and Nils G. Morgenthaler

German Diabetes Research Institute and Department of Endocrinology, University of Dusseldorf (J.S., S.W., M.S., M.L., J.F., W.A.S.), D-40225 Dusseldorf, Germany; and Research Department, B.R.A.H.M.S Diagnostica, Biotechnology Center (N.G.M.), D-16761 Hennigsdorf/Berlin, Germany

Address all correspondence and requests for reprints to: J. Seissler, M.D., German Diabetes Research Institute, University of Dusseldorf, Auf’m Hennekamp 65, D-40225 Dusseldorf, Germany. E-mail: sei{at}dfi

Several studies suggest that the sodium-iodide symporter (NIS) may represent a major autoantigen in autoimmune diseases of the thyroid. The aim of the present paper was to investigate the importance of autoantibodies to human NIS (hNIS-Ab) in patients suffering from Hashimoto’s thyroiditis (HT) and Graves’ disease (GD). Full-length human NIS (hNIS) was cloned from thyroid tissue, expressed by in vitro transcription and translation in the presence of [35S]methionine, and used to analyze autoantibodies in a direct binding assay. The structurally similar glucose transporter, GLUT-2, was produced in the same system as control protein. Autoradiography revealed that full-length hNIS was expressed, recognized by a NIS monoclonal antibody, and strongly bound by some sera from patients with autoimmune thyroid disease, which did not react with the GLUT-2 control protein. Using the 95.2th percentile of healthy controls as threshold for positivity, 19 of 177 (10.7%) patients with GD and 15 of 72 (20.8%) patients with HT had hNIS-Ab, respectively. Applying more stringent cut-off criteria (99.4th percentile of normal controls), hNIS-Ab were found in only 5.6% of patients with GD and 6.9% of patients with HT. In HT significantly higher hNIS-Ab levels were observed compared with GD and normal controls (P < 0.001). There was no correlation between hNIS-Ab and TSH receptor antibodies and only a weak correlation to thyroid peroxidase antibodies (P < 0.05). Comparison of hNIS-Ab, thyroid peroxidase, and TSH receptor antibodies in individual sera revealed that the additional detection of hNIS-Ab did not increase the diagnostic power for GD or HT. Our data indicate that hNIS is not a major antigen in autoimmune thyroid disease, as it is the target of humoral autoimmunity in only a few patients with GD and HT. The frequency of hNIS-Ab may be lower than that reported in previous studies.




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