Relevance of TSH-Receptor stimulating and blocking autoantibody measurement for the prediction of relapse in Graves' disease

2005 ◽  
Vol 113 (S 1) ◽  
Author(s):  
M Schott ◽  
WB Minich ◽  
C Papewalis ◽  
J Seissler ◽  
WA Scherbaum ◽  
...  
2005 ◽  
Vol 37 (12) ◽  
pp. 741-744 ◽  
Author(s):  
M. Schott ◽  
W. B. Minich ◽  
H. S. Willenberg ◽  
C. Papewalis ◽  
J. Seissler ◽  
...  

Endocrine ◽  
2014 ◽  
Vol 48 (1) ◽  
pp. 89-95 ◽  
Author(s):  
Sena Hwang ◽  
Dong Yeob Shin ◽  
Mi Kyung Song ◽  
Eun Jig Lee

1983 ◽  
Vol 102 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Tjerk W. A de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol

Abstract. An immunoprecipitation assay was developed to determine the presence of antibodies against human TSH1 receptors. With this assay we were able to demonstrate that in comparison with sera from normal controls, 24 out of 30 (80%) sera from patients with untreated Graves' disease could immunoprecipitate more [125I]TSH-TSH receptor complexes. In 9 assays, an average of 14.1 ± 3.7% (sd) of the [125I]TSH-TSH receptor complexes was immunoprecipitated by the 30 Graves' sera vs 9.8 ± 3.0% by the normal pool serum (n = 23) (P < 0.001) and 7.7 ± 2.8% by the 22 normal sera (P < 0.001). One serum of the 24 positive Graves' sera was studied in detail. The results suggest that this serum contained an anti-TSH receptor auto-antibody directed towards a different determinant on the TSH receptor than the TSH binding site.


2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Samer El-Kaissi ◽  
Jack R. Wall

Background. To examine factors contributing to extraocular muscle (EOM) volume enlargement in patients with Graves’ hyperthyroidism.Methods. EOM volumes were measured with orbital magnetic resonance imaging (MRI) in 39 patients with recently diagnosed Graves’ disease, and compared to EOM volumes of 13 normal volunteers. Thyroid function tests, uptake on thyroid scintigraphy, anti-TSH-receptor antibody positivity and other parameters were then evaluated in patients with EOM enlargement.Results. 31/39 patients had one or more enlarged EOM, of whom only 2 patients had clinical EOM dysfunction. Compared to Graves’ disease patients with normal EOM volumes, those with EOM enlargement had significantly higher mean serum TSH (0.020±0.005versus0.007±0.002mIU/L;Pvalue 0.012), free-T4 (52.9±3.3versus41.2±1.7 pmol/L;Pvalue 0.003) and technetium uptake on thyroid scintigraphy (13.51±1.7%versus8.55±1.6%;Pvalue 0.045). There were no differences between the 2 groups in anti-TSH-receptor antibody positivity, the proportion of males, tobacco smokers, or those with active ophthalmopathy.Conclusions. Patients with recently diagnosed Graves’ disease and EOM volume enlargement have higher serum TSH and more severe hyperthyroidism than patients with normal EOM volumes, with no difference in anti-TSH-receptor antibody positivity between the two groups.


Thyroid ◽  
2008 ◽  
Vol 18 (7) ◽  
pp. 695-696 ◽  
Author(s):  
Basil Rapoport ◽  
Sandra M. McLachlan

Author(s):  
Nami Suzuki ◽  
Akiko Kawaguchi ◽  
Jaeduk Yoshimura Noh ◽  
Ran Yoshimura ◽  
Kentaro Mikura ◽  
...  

Abstract Background Thyroid stimulating hormone (TSH) receptor antibody (TRAb) is detected in the serum of patients with Graves’ disease (GD). This study aims to investigate the prevalence of euthyroid individuals showing positive results for TRAb and to clarify the clinical course of thyroid function and TRAb levels in these subjects. Objective Subjects were female patients who newly visited our hospital for a screening test prior to fertility treatment and showed normal thyroid function and volume without nodules between 2014 and 2017. After excluding subjects with a history of thyroid disease, 5,622 subjects were analyzed. Results Forty-seven of the 5,622 subjects showed positive results for TRAb (reference range, &lt; 2.0 IU/L) at the initial visit. Median initial TRAb was 2.9 IU/L (range, 2.0 -14.7 IU/L) and median follow-up was 18.3 months (range, 0- 66.5 months). Six of the 47 subjects (12.8%) developed GD and median duration until development was 6.6 months (range, 1.2 -13.2 months). Median TRAb values initially and at diagnosisof GD for those 6 patients were 3.7 IU/L (range, 2.7 -5.1 IU/L) and 7.2 IU/L (range 3.6 -21.4 IU/L), respectively. TRAb results turned negative for 20 of the 47 subjects, but remained positive despite normal thyroid function in 13 of the 47 subjects. Conclusion GD developed over time in 12.8% of euthyroid young female patients showing positive TRAb within a median of 6.6 months. A positive result for TRAb itself did not mean development of GD, so other factors must be essential for the pathogenesis of GD.


1984 ◽  
Vol 105 (3) ◽  
pp. 330-340 ◽  
Author(s):  
Tjerk W. A. de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol

Abstract. The effect of the anti-TSH receptor antibodies present in the sera of 8 patients with Graves' disease on the affinity constant (Ka) and the number (R) of TSH receptors in autologous human thyroid plasma membranes was investigated. Kinetic analysis of [125I]bTSH binding to human thyroid plasma membranes in the presence of autologous Graves' and normal gammaglobulins was carried out by means of a computer fitting programme. Analysis of the TSH-TSH receptor interaction in the presence of TSH alone yielded curvilinear Scatchard plots, indicating the existence of two independent classes of binding sites (high affinity Ka: 8.5 ± 4.8 × 108 m−1; low affinity Ka: 5.3 ± 2.7 × 106 m−1). Similarly the Scatchard plot for this interaction in the presence of normal gammaglobulins is also curvilinear. Linear Scatchard plots, indicating the existence of only one class of high affinity TSH binding sites (Ka: 3.5 ± 1.8 × 108 m−1), were obtained for both autologous gammaglobulins and pure IgG from 8 patients with Graves' disease. The number of high affinity TSH binding sites in the presence of Graves' gammaglobulins had increased on the average by a factor 3.76 ± 0.74 (sd) with respect to the number found in the presence of normal gammaglobulins. This marked change in the kinetic behaviour of the TSH binding sites provided evidence that there is a direct interaction between anti-TSH receptor antibodies and autologous TSH receptors. Divalency of Graves' IgG or linkage of Fab fragments by anti-Fab antiserum proved to be necessary to produce this specific change in the kinetic behaviour of TSH binding sites. Graves' IgG monovalent Fab and Fc fragments had no effect. We suggest that the mechanism by which anti-TSH receptor antibodies in Graves' disease mimick the biological action of TSH is the IgG-induced cross-linkage of TSH receptors.


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