OBJECTIVE: In patients with hypothyroid goitrous Hashimoto's thyroiditis, the recovery from hypothyroidism seems to be due to a spontaneous decrease of antibodies (Ab) to the TSH-receptor (R). In contrast, in patients with Graves' disease made euthyroid by antithyroid drug therapy, the suppression of TSH secretion by thyroid hormone during antithyroid drug treatment decreases the production of Ab to TSH-R. We investigated in patients with initially euthyroid or hypothyroid goitrous Hashimoto's thyroiditis the relationships between thyroid status and the serum TSH-R, peroxidase (TPO) and thyroglobulin (Tg) Ab concentrations in untreated or L-thyroxine (T4) treated patients. PATIENTS: A prospective study of 174 consecutive patients, referred with goitrous Hashimoto's disease in an initially euthyroid (group I, n = 78) or hypothyroid (group II, n = 96) state. The patients with positive (> or = 7%) TSH-RAb (group I, n = 18; group II, n = 22) were reinvestigated 12 months after the initiation of L-T4 therapy. After which, (1) L-T4 was continued and an evaluation performed 2 months later (i.e. 14 months after L-T4 initiation) in 9 patients of group I and in 11 patients of group II or (2) L-T4 was withdrawn and an evaluation performed 2 months later in 9 patients of group I and in 11 patients of group II. MEASUREMENTS: Measurements of basal plasma TSH, free T4 (FT4) and total T3 and serum TSH-R, TPO and TgAb. RESULTS: The prevalence of positive TSH-RAb levels did not differ between group I (23.1%) and group II (22.9%). However, the mean TSH-RAb level in group I (9.4 +/- 0.4%) was lower (P < 0.01) than in group II (11.6 +/- 0.5%). In the patients with positive TSH-R Ab, (1) the prevalences of positive TSH-RAb decreased (P < 0.001) under L-T4 therapy (group I = 22.2%, group II = 21.2%) and increased again (P < 0.01) 2 months after L-T4 cessation (group I = 77.7%, group II = 63.6%) to reach lower levels (group I, P < 0.05; group II, P < 0.01) than those obtained prior to L-T4 treatment. Statistical analysis of TSH levels through the course of the study confirmed these results. (2) In contrast to the variations of the mean TgAb values, the variations of the mean TPOAb levels in each group were in good agreement with those of TSH-RAb through the course of the study. (3) There were significant correlations between some parameters of thyroid status and both TSH-RAb (TSH, r = 0.43, P < 0.001; FT4, r = -0.35, P < 0.01) and TPOAb (TSH, r = 0.42, P < 0.001; FT4, r = -0.31; P < 0.01) levels. In contrast, no correlations were found between thyroid status and TgAb values. CONCLUSIONS: This study demonstrates that thyroid status can modulate thyroid autoimmunity expression, such as TSH-RAb and TPOAb, in patients with euthyroid or hypothyroid goitrous Hashimoto's thyroiditis. Similar results have been reported in patients with Graves' disease made euthyroid by the administration of thyroid hormone during antithyroid drug treatment.
OBJECTIVE: In patients with hypothyroid goitrous Hashimoto's thyroiditis, the recovery from hypothyroidism seems to be due to a spontaneous decrease of antibodies (Ab) to the TSH-receptor (R). In contrast, in patients with Graves' disease made euthyroid by antithyroid drug therapy, the suppression of TSH secretion by thyroid hormone during antithyroid drug treatment decreases the production of Ab to TSH-R. We investigated in patients with initially euthyroid or hypothyroid goitrous Hashimoto's thyroiditis the relationships between thyroid status and the serum TSH-R, peroxidase (TPO) and thyroglobulin (Tg) Ab concentrations in untreated or L-thyroxine (T4) treated patients. PATIENTS: A prospective study of 174 consecutive patients, referred with goitrous Hashimoto's disease in an initially euthyroid (group I, n = 78) or hypothyroid (group II, n = 96) state. The patients with positive (> or = 7%) TSH-RAb (group I, n = 18; group II, n = 22) were reinvestigated 12 months after the initiation of L-T4 therapy. After which, (1) L-T4 was continued and an evaluation performed 2 months later (i.e. 14 months after L-T4 initiation) in 9 patients of group I and in 11 patients of group II or (2) L-T4 was withdrawn and an evaluation performed 2 months later in 9 patients of group I and in 11 patients of group II. MEASUREMENTS: Measurements of basal plasma TSH, free T4 (FT4) and total T3 and serum TSH-R, TPO and TgAb. RESULTS: The prevalence of positive TSH-RAb levels did not differ between group I (23.1%) and group II (22.9%). However, the mean TSH-RAb level in group I (9.4 +/- 0.4%) was lower (P < 0.01) than in group II (11.6 +/- 0.5%). In the patients with positive TSH-R Ab, (1) the prevalences of positive TSH-RAb decreased (P < 0.001) under L-T4 therapy (group I = 22.2%, group II = 21.2%) and increased again (P < 0.01) 2 months after L-T4 cessation (group I = 77.7%, group II = 63.6%) to reach lower levels (group I, P < 0.05; group II, P < 0.01) than those obtained prior to L-T4 treatment. Statistical analysis of TSH levels through the course of the study confirmed these results. (2) In contrast to the variations of the mean TgAb values, the variations of the mean TPOAb levels in each group were in good agreement with those of TSH-RAb through the course of the study. (3) There were significant correlations between some parameters of thyroid status and both TSH-RAb (TSH, r = 0.43, P < 0.001; FT4, r = -0.35, P < 0.01) and TPOAb (TSH, r = 0.42, P < 0.001; FT4, r = -0.31; P < 0.01) levels. In contrast, no correlations were found between thyroid status and TgAb values. CONCLUSIONS: This study demonstrates that thyroid status can modulate thyroid autoimmunity expression, such as TSH-RAb and TPOAb, in patients with euthyroid or hypothyroid goitrous Hashimoto's thyroiditis. Similar results have been reported in patients with Graves' disease made euthyroid by the administration of thyroid hormone during antithyroid drug treatment.