scholarly journals Decrease in TSH Receptor Autoantibodies during Antithyroid Treatment: Relationship with a Long Noncoding Heg RNA and Cdk1 mRNA in Mononuclear Cells

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Niels Juel Christensen ◽  
Gurli Habekost ◽  
Palle Bratholm

We have previously shown that a long noncoding RNA transcript Heg is negatively correlated with TSH receptor autoantibodies (TRAb) in patients with untreated Graves' disease and with CD14 mRNA in treated patients and controls. Thus patients with high concentrations of Heg RNA have low levels of TRAb or CD14 mRNA, respectively. Here we show that an additional factor, gene expression of Cdk1 in mononuclear cells, is positively related to concentrations of TRAb in patients with untreated Graves' disease. Cdk1 mRNA is very important for regulation of cell cycle activity. It is well known that TRAb decrease significantly during treatment with antithyroid drugs. This decrease during treatment cannot be explained by Heg RNA, which remains unchanged. Cdk1 mRNA decreased significantly during treatment to values below values obtained in normal subjects. Thus both Heg RNA and Cdk1 mRNA may influence the level of TSH receptor autoantibodies but by different mechanisms.

Medicina ◽  
2021 ◽  
Vol 57 (10) ◽  
pp. 1016
Author(s):  
Yoon-Kyung Ji ◽  
Shin-Hee Kim

Here, we report a case of an increase in serum creatine kinase (CK) concentration in an 11-year-old girl being treated for Graves’ disease with antithyroid drugs (ATDs). The patient complained of myalgia two weeks after methimazole treatment. Triiodothyronine (T3) and free thyroxine (FT4) levels were normal, but the serum CK level was significantly elevated. After switching to propylthiouracil, the serum CK level decreased to normal, and the myalgia was resolved. The development of myopathy during the treatment of hyperthyroidism may be considered as an adverse reaction of MMI. In this report, we present a rare pediatric case, along with a discussion on the possible causes of myopathy that occurred during the treatment of Graves’ disease. A careful follow-up (serum CK levels and thyroid function) and treatment reassessment should always be considered after antithyroid treatment.


2005 ◽  
Vol 90 (11) ◽  
pp. 6093-6098 ◽  
Author(s):  
Dominique Luton ◽  
Isabelle Le Gac ◽  
Edith Vuillard ◽  
Mireille Castanet ◽  
Jean Guibourdenche ◽  
...  

Abstract Background: Fetuses from mothers with Graves’ disease may experience hypothyroidism or hyperthyroidism due to transplacental transfer of antithyroid drugs (ATD) or anti-TSH receptor antibodies, respectively. Little is known about the fetal consequences. Early diagnosis is essential to successful management. We investigated a new approach to the fetal diagnosis of thyroid dysfunction and validated the usefulness of fetal thyroid ultrasonograms. Methods: Seventy-two mothers with past or present Graves’ disease and their fetuses were monitored monthly from 22 wk gestation. Fetal thyroid size and Doppler signals, and fetal bone maturation were determined on ultrasonograms, and thyroid function was evaluated at birth. Thyroid function and ATD dosage were monitored in the mothers. Results: The 31 fetuses whose mothers were anti-TSH receptor antibody negative and took no ATDs during late pregnancy had normal test results. Of the 41 other fetuses, 30 had normal test results at 32 wk, 29 were euthyroid at birth, and one had moderate hypothyroidism on cord blood tests. In the remaining 11 fetuses, goiter was visualized by ultrasonography at 32 wk, and fetal thyroid dysfunction was diagnosed and treated; there was one death, in a late referral, and 10 good outcomes with normal or slightly altered thyroid function at birth. The sensitivity and specificity of fetal thyroid ultrasound at 32 wk for the diagnosis of clinically relevant fetal thyroid dysfunction were 92 and 100%, respectively. Conclusion: In pregnant women with past or current Graves’ disease, ultrasonography of the fetal thyroid gland by an experienced ultrasonographer is an excellent diagnostic tool. This tool in conjunction with close teamwork among internists, endocrinologists, obstetricians, echographists, and pediatricians can ensure normal fetal thyroid function.


1995 ◽  
Vol 132 (1) ◽  
pp. 62-68 ◽  
Author(s):  
Yoshimichi Ueda ◽  
Hideo Sugawa ◽  
Takashi Akamizu ◽  
Jyoji Okuda ◽  
Michiko Ueda ◽  
...  

Ueda Y, Sugawa H, Akamizu T, Okuda J, Ueda M, Kosugi S, Ohta C, Kihou Y, Mori T. Thyroidstimulating antibodies in sera from patients with Graves' disease are heterogeneous in epitope recognition. Eur J Endocrinol 1995;132:62–8. ISSN 0804–4643 Two synthetic peptides, P354-14 (amino acid nos. 354 to 367) and P338-16 (nos. 338 to 353), corresponding to the partial amino acid sequences of the hTSH receptor structure were studied for their ability to bind specifically serum IgGs from patients with Graves' disease and to inhibit thyroid stimulating TSH receptor antibody (TSH-R SAb) activity. IgG binding was measured by an ELISA using sera from 102 Graves', 20 Hashimoto patients, and 9 normal subjects. Both peptides showed significantly increased IgG binding of Graves' sera compared with those of Hashimoto and normal sera. There was a significant correlation (r = 0.529) between the amount of IgG bound by the two peptides, but neither of these values correlated well with their TSH-R SAb activity nor thyrotropin-binding inhibitor TSH receptor antibody (TSH-R IAb) activity. TSH-R SAb inhibiting effects of these peptides were then analysed by measuring TSH-R SAb activity after incubation with the peptides. Among eight Graves' IgGs tested the TSH-R SAb activity of three was inhibited by both peptides, two were inhibited only by P354-14 and three were not affected by either. These TSH-R SAb inhibiting effects were dose-dependent and reproducible. To confirm these findings, a peptide-sepharose gel affinity absorption study was performed. Eleven Graves' IgGs were applied to both peptide gels and the TSH-R SAb activity of the unabsorbed fraction was measured. The TSH-R SAb activity of five IgGs was strongly absorbed only by P354-14 and five others were absorbed by both peptides to an almost similar extent. One IgG was not affected by either of the peptides. None of the IgG activities tested was absorbed only or predominantly by P338-16. Most of Graves' IgGs could bind to region no. 338 to no. 367 of the hTSH receptor. There was apparent heterogeneity among Graves' TSH-R SAb IgGs as shown by their absorption by the peptides, and the existence of at least three heterogeneous species in epitopic recognition among Graves' TSH-R SAb was demonstrated. Toru Mori, Department of Laboratory Medicine, Kyoto University School of Medicine, 54-Shogoin Kawaharacho, Sakyo-ku, Kyoto 606-01, Japan


1986 ◽  
Vol 113 (2) ◽  
pp. 233-241 ◽  
Author(s):  
Hans-Wilhelm Müller-Gärtner ◽  
Claus Schneider ◽  
Sören Schröder

Abstract. Out of 256 patients with Graves' disease and a characteristically low echogenic ultrasound appearance of the thyroid gland, 12 patients (4.7%) showed additionally one single or several intrathyroidal focal alterations with high echogenicity. Their volume was 0.2 to 7.0 cm (x̄ ± sd: 1.75 ± 2.24 cm). A common characteristic of the 12 patients was a longstanding history of Graves' disease and antithyroid treatment with thiamazol or carbimazol and a mean age of 55 ± 9 (sd) years (range 42–75 years). The foci with high echogenicity had a normal or macrofollicular histological structure (mean follicle lumen diameter 119.7 μm, as proven by histology in 4 cases) which was significantly higher than follicle lumina of the surrounding Graves' disease tissue (mean follicular lumen diameter 38.3 μm; P < 0.001). The height of follicle epithelium and the nuclei cross-section area of such foci was similar to corresponding normal tissue parameter in 5 out of 7 foci. The 99mTc-uptake of the foci amounted to 40 to 80% in comparison with Graves' disease tissue. 131-iodine autoradiography, thyroglobulin immunochemistry and 125-iodine-TSH binding analysis performed in selected cases confirmed the heterogenicity of these foci. The data provided evidence that the foci were unresponsive to TSH-receptor mediated stimulation through Graves' immunoglobulins. It is concluded that longstanding Graves' disease can be associated with tissue foci which are in a functional sense resistant to immunogenic stimulation by TSH-receptor autoantibodies.


1990 ◽  
Vol 122 (1) ◽  
pp. 22-28 ◽  
Author(s):  
Pei-Wen Wang ◽  
Miau-Ju Huang ◽  
Rue-Tsuan Liu ◽  
Chung Dar Chen

Abstract. Sera of 63 patients with Graves' disease, and 49 control subjects were assayed for T3 autoantibodies by a sensitive radioimmunoassay after being stripped of the endogenous thyroid hormone. T3 autoantibodies were demonstrated in 27% of patients with Graves' disease. After antithyroid treatment, T3 autoantibodies in 75% of the patients with positive antibody before therapy changed to negative titre during a follow-up period of 1 to 12 months. Also, a significant decrease of T3 autoantibodies was observed at 1 month after therapy in all patients who received antithyroid treatment. A further study of T3 autoantibodies and anti-thyroglobulin antibodies showed that the latter were demonstrated in 100% of patients with positive T3 autoantibodies and that T3 autoantibodies existed in about one third of patients with positive anti-thyroglobulin antibodies. The results suggested that T3 autoantibodies could be a subpopulation of the heterogenous anti-thyroglobulin antibodies. Although the fall of T3 autoantibodies in some patients was correlated to that of anti-thyroglobulin antibodies, the overall correlation between T3 autoantibodies and anti-thyroglobulin antibodies was poor. In conclusion: 1. T3 autoantibodies may be suppressed by antithyroid drugs. 2. Being a subpopulation of anti-thyroglobulin antibodies, T3 autoantibodies may be caused by an antigenic site within the big thyroglobulin molecule, whereas their titre was not correlated with that of the overall heterogenous anti-thyroglobulin antibodies.


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