Article

Journal of Endocrinological Investigation

, Volume 20, Issue 8, pp 452-461

First online:

Thyroid-stimulating antibody and TSH-binding inhibitor immunoglobulin in 277 Graves’ patients and in 686 normal subjects

  • Nobuyuki TakasuAffiliated withSecond Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus
  • , C. OshiroAffiliated withSecond Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus
  • , H. AkamineAffiliated withSecond Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus
  • , I. KomiyaAffiliated withSecond Department of Internal Medicine, Faculty of Medicine, University of the Ryukyus
  • , A. NagataAffiliated withYamasa Corporation
  • , Y. SatoAffiliated withYamasa Corporation
  • , H. YoshimuraAffiliated withIto Hospital
  • , K. ItoAffiliated withIto Hospital

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Abstract

TSH receptor antibodies (TRAb) are believed to cause hyperthyroidism of Graves’ disease. Thyroid-stimulating antibody (TSAb) and TSH-binding inhibitor immunoglobulin (TBII) have been measured as TRAb to diagnose Graves’ disease and to follow Graves’ patients. We intended to evaluate the clinical value of TRAb (TSAb and TBII) assay in establishing the diagnosis of Graves’ disease and in predicting its clinical course. TSAb and TBII were studied in 686 normal subjects and in 277 Graves’ patients before antithyroid drug therapy. We followed serial changes of TSAb and TBII in 30 Graves’ patients before, during and after antithyroid drug therapy over 3.5–9 yr. We measured TSAb as a stimulator assay and TBII as a receptor assay. Both TSAb and TBII were distributed normally in 686 normal subjects. ROC curves demonstrated that both TSAb and TBII had high sensitivity and specificity for the diagnosis of Graves’ disease, and were equally sensitive and specific; 150% was chosen as cut-off value for TSAb and 10% for TBII. Of the 277 untreated Graves’ patients, 254 (92%) had positive TSAb and positive TBII. All of the 277 untreated Graves’ patients had positive TRAb (TSAb and/or TBII). We followed the serial changes of TSAb and TBII in 30 Graves’ patients over 3.5–9 yr. During antithyroid drug therapy, TSAb and TBII activities decreased and disappeared in 27 patients (Group A), but continued to be high in the other 3 (Group B). The former 27 Group A patients achieved remission, but the latter 3 Group B patients continued to have hyperthyroidism. Of the 27 Group A patients, 16 (59%) had parallel decreases of TSAb and TBII activities; in 6, the changes were predominantly observed in either TSAb or TBII, and in 4, complex changes in TSAb and TBII activities were observed. Disappearance of TSAb and appearance of TSBAb was seen in one. The other 3 Group B patients continued to have high TSAb and TBII activities and to have hyperthyroidism. In conclusion, TSAb and TBII are of clinical value in establishing the diagnosis of Graves’ disease and in predicting its clinical course. We clearly demonstrated its diagnostic usefulness. Both TSAb and TBII have high sensitivity and specificity. All of the 277 untreated Graves’ patients had TRAb (TSAb and/or TBII). Serial changes of TSAb and TBII during therapy differ from one patient to another, and can be classified into several groups. Changes in TSAb and TBII activities reflect the clinical courses of Graves’ patients. The simultaneous measurement of both TSAb and TBII is clinically useful, since TSAb and TBII reflect two different aspects of TRAb. TSAb and TBII are different.

Key-words

Graves’ disease TRAb (TSH receptor antibody) thyroid stimulating antibody (TSAb) TSH-binding inhibitor immunoglobulin (TBII)