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Department of Nuclear Medicine, Kyoto University School of Medicine Kyoto, Japan
The Department of Psychosomatic Medicine, Kyushu University School of Medicine (H. T.) Fukuoka, Japan
Kuma Hospital (T.M., K.K.) Kobe, Japan
The Departments of Internal Medicine (T.I.) and Nuclear Medicine (K.I.), Kobe Central Municipal Hospital Kobe, Japan
Address all correspondence and requests for reprints to: Kanji Kasagi, M.D., Department of Nuclear Medicine, Kyoto University Hospital, 54 Kawahara-cho, Sakyo-ku, Kyoto 606, Japan.
TSH binding inhibitor immunoglobulin (TBII) and thyroid-stimulating antibody (TSAb) activities were measured serially for 4–32 months in nine patients before and during development of hyperthyroidism due to Graves disease. Initially, all were euthyroid, seven had thyroid enlargement, one had proptosis, and seven had high serum titers of antithyroid microsomal antibodies. The occurrence of hyperthyroidism was preceded by detection of both TBII and TSAb in four patients and detection of TSAb alone in four patients. One patient had neither TBII nor TSAb when euthyroid. The mean initial TBII and TSAb activities were 10.2 ± 15.2% (±SD) and 2677 ± 4620%, respectively, when these patients were euthyroid. When they became hyperthyroid, both TBII and TSAb activities increased in all patients. At that time, TBII was detected in all but one (eight of nine subjects; 88.9%), with a mean activity of 58.8 ± 23.4% (±SD), and TSAb was detected in all nine patients, with a mean value of 4508 ± 4429%. These findings not only indicate the crucial role of TSH receptor antibodies in the development of hyperthyroidism due to Graves disease, but also suggest that a certain period of subclinical Graves disease exists before the onset of overt hyperthyroidism in most patients, in the sense that they have TSH receptor antibodies, especially TSAb, in their serum even though they are euthyroid.
Received August 15, 1988.
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