Stimulation of thyroid-stimulating hormone (TSH) receptor antibody production following painless thyroiditis.
OBJECTIVE
Development or recurrence of Graves' disease (GD) following painless thyroiditis (PT) has been documented. Therefore, we measured titres of TSH receptor antibodies (TSHR Ab) using a novel sensitive TSHR Ab assay in patients with PT to determine whether PT enhances TSHR Ab production, possibly triggering the development or recurrence of GD.


METHODS
Ninety-two patients who developed PT were studied. Group G consisted of 40 patients with a history of GD (19 patients in remission, 21 who had stopped taking antithyroid drugs during pregnancy). Group P consisted of 52 patients with no history of GD. Serum thyroid hormone levels, thyroid autoantibodies including TSHR Ab, and 123I uptake at 24 h (RAIU) were measured in these patients at the time of PT onset. TSHR Abs were measured by radioreceptor assay using porcine TSH receptors (pTBII) or human TSH receptors (hTBII).


RESULTS
There were no significant differences in serum thyroid hormone levels or pTBII values between groups G and P. Nor was there any significant difference between p- and h-TBII values in group P. There was also no significant difference in pTBII levels before, compared to at the time of PT onset in group G patients. However, hTBII values at the PT onset were significantly higher in the group G than in the group P (7.7 +/- 9.8%vs. 1.4 +/- 5.4%, P = 0.0014). The rate of hTBII positivity was also significantly higher in group G than in group P (12/40 vs. 3/52, P = 0.002). Furthermore, the RAIU in group G patients was significantly higher than that in group P patients (2.8 +/- 2.4%vs. 1.3 +/- 0.9%, P = 0.0002). GD recurrence was observed in seven patients in group G, whose hTBII levels were significantly higher than those of other patients in this group (17.0 +/- 11.8%vs. 5.7 +/- 8.2%, P = 0.02). Of these seven with relapses, five had hTBII values exceeding 15%.


CONCLUSIONS
TBII elevation at the onset of PT in patients with a history of GD was detected by a sensitive hTBII assay. Destruction of the thyroid by PT may trigger GD recurrence in patients with a history of GD.
Iitaka
Makoto
M
Department of Internal Medicine 4, Saitama Medical School, 38 Morohongo, Moroyama, Iruma-gun, Saitama, Japan.
Morgenthaler
Nils G
NG
Momotani
Naoko
N
Nagata
Atsuo
A
Ishikawa
Naofumi
N
Ito
Koichi
K
Katayama
Shigehiro
S
Ito
Kunihiko
K
D000328:Adult; D001323:Autoantibodies / Q000097:blood*; D005260:Female; D006111:Graves Disease / Q000276:immunology*; D006801:Humans; D007457:Iodine Radioisotopes; D008297:Male; D008875:Middle Aged; D011989:Receptors, Thyrotropin / Q000097:blood / Q000276:immunology*; D012008:Recurrence; D018709:Statistics, Nonparametric; D013961:Thyroid Gland / Q000378:metabolism; D013963:Thyroid Hormones / Q000097:blood; D013966:Thyroiditis / Q000276:immunology*
D001323:Autoantibodies; D007457:Iodine Radioisotopes; D011989:Receptors, Thyrotropin; D013963:Thyroid Hormones