THYROTROPHIN BINDING INHIBITING IMMUNOGLOBULINS IN GRAVES'DISEASE BEFORE, DURING AND AFTER ANTITHYROID THERAPY, AND ITS RELATION …

R Docter, G Bos, TJ Visser… - Clinical …, 1980 - Wiley Online Library
R Docter, G Bos, TJ Visser, G Hennemann
Clinical Endocrinology, 1980Wiley Online Library
Thyrotrophin binding inhibiting immunoglublins (TBII) were measured in twenty‐five patients
with unequivocal hyperthyroid Graves' disease with a radioreceptor assay for TSH before,
during and at the end of treatment with antithyroid drugs and triiodothyronine. To assess the
outcome of this therapy patients were followed for 10–90 months (mean 63 months). Before
treatment there was a significant correlation between TBII activity and serum thyroxine (r=−
0· 48, P< 0· 05) and between TBII activity and 24 hour 131I thyroid uptake (r=− 0· 57, P< 0 …
Summary
Thyrotrophin binding inhibiting immunoglublins (TBII) were measured in twenty‐five patients with unequivocal hyperthyroid Graves' disease with a radioreceptor assay for TSH before, during and at the end of treatment with antithyroid drugs and triiodothyronine. To assess the outcome of this therapy patients were followed for 10–90 months (mean 63 months). Before treatment there was a significant correlation between TBII activity and serum thyroxine (r =−0·48, P < 0·05) and between TBII activity and 24 hour 131I thyroid uptake (r =−0·57, P < 0·01). No relationship was found between TBII activity and 20 min, 4 hour and 48 hour 131I thyroid uptakes before institution of therapy. During treatment a significant correlation between TBII index and 20 min 131I thyroid uptake was found (r =−0·55, P < 0·001). Both before and during treatment there was a significant correlation between TBII and LATS activity (r =−0·65, P < 0·001). From the magnitude of this correlation coefficient it can be concluded that related, although not the same immunoglobulins, are measured with the two assay techniques. It is not possible to predict the occurrence of a relapse from the presence or absence of TBII activity at the end of treatment in this group of patients. The relapse rate was four out of eight for patients without TBII activity in their serum at the end of treatment and five out of nine for patients with TBII activity. From the data presented it can be concluded that although there is a significant relation between TBII activity and some indices of thyroid function before and during treatment, the correlation coefficients are too small to conclude that TBII alone is responsible for the hyperfunction of the thyroid. The same conclusion can be drawn from the fact that TBII activity has no prognostic value in relation to a possible relapse.
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