We previously reported that two sisters with juvenile hypothyroidism due to Hashimoto's thyroiditis (Case 1 : 13 years old, Case 2 : 10 years old) had antibodies against thyroid hormones. Treatment was started with 12.5μg of L-T
4 per day in Jan. 1980. The doses were gradually increased, and after 1 year of treatment, both patients were clinically euthyroid on 100μg of L-T
4 per day, and the heights of Case 1 and of Case 2 had increased by 9cm and by 10cm, respectively. Serum TSH levels were decreased from 1088μU/ml to 1.7μU/ml in Case 1, and from 1300μU/ml to 2.1μU/ml in Case 2. The titers of antithyroglobulin antibodies as measured by solid phase RIA decreased in both patients after the treatment.
The bindings of
125I-T
3 and of
125I-T
4 to sera in the presence of 8-anilino-1- naphthalene sulfonic acid to block binding to TBG (non-treated sera) were markedly higher in the two patients before therapy than those in ten normal controls (11.8% and 52.3% in Case 1, 46.8% and 21.5% in Case 2, and 5.9 ± 0.6% and 4.1 ± 0.5% (mean ± SD) in the controls, respectively). After the 1 year treatment, the bindings of
125I-T
3 and
125I-T
4 decreased to normal levels in Case 1 (5.8% and 3.8%, respectively). In Case 2, the
125I-T
4 binding decreased to the normal level (4.7%), whereas the
125T
3 binding decreased but still remained above the normal level (10.6%). In order to exclude the interference of endogenous and/or therapeutic thyroid hormones with the binding of labelled hormones to sera, the sera were treated with dextran-coated charcoal at pH3.0 (acid-treated sera). The bindings of
125-T
3 and
125 I-T
4 to acid-treated sera were clearly higher in both patients before therapy than those in ten normal controls (16.9% and 60.7% in Case 1, 75.0% and 46.4% in Case 2, and 6.9 ± 0.7% and 6.8 ± 0.7% (mean ± SD) in the controls, respectively), and these values were compatible with those from non-treated sera. After the 1 year treatment, however, the results of acid-treated sera were different from those of non-treated sera. That is, the bindings of
125I-T
3 and of
125I-T
4 to acid-treated sera from both patients decreased but remained above normal levels (9.3% and 26.5% in Case 1, and 29.4% and 22.5% in Case 2, respectively). These results indicate the presence of antibodies against thyroid hormones even in the euthyroid state during L-T
4 treatment, and also the data obtained from the non-treated sera were affected by endogenous and/or therapeutic thyroid hormones. The importance of acid-charcoal treatment for the detection of anti-thyroid hormone antibodies during thyroid hormone administration was suggested.
In the serum from another sister of the reported patients, we also found unusual T
4binding proteins which were only detected by the acid-charcoal treatment. The implications of decrement of anti-thyroglobulin antibodies and of anti-thyroid hormone antibodies were discussed.
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