scholarly journals Hyperthyroid Graves' Disease and Primary Hypothyroidism Caused by TSH Receptor Antibodies in Monozygotic Twins: Case Reports.

1998 ◽  
Vol 45 (1) ◽  
pp. 117-121 ◽  
Author(s):  
JUN-ICHI TANI ◽  
KATSUMI YOSHIDA ◽  
HIROSHI FUKAZAWA ◽  
YOSHINORI KISO ◽  
NORIYO SAYAMA ◽  
...  
Keyword(s):  
Case Reports ◽  
Monozygotic Twins ◽  
Primary Hypothyroidism ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

Anti-TSH antibodies in Graves' disease and their failure to interact with TSH receptor antibodies

1989 ◽  
Vol 120 (6) ◽  
pp. 773-777 ◽  
Author(s):  
Y. Ochi ◽  
T. Nagamune ◽  
Y. Nakajima ◽  
M. Ishida ◽  
Y. Kajita ◽  
...  
Keyword(s):  
Primary Hypothyroidism ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Antibody Technique ◽  
Α Subunit ◽  
Occasional Occurrence ◽  
Assay Methods ◽  
Receptor Antibodies ◽  
Hyperthyroid Patients ◽  
Tsh Receptor Antibodies

Abstract. The occasional occurrence in sera of patients with Graves' disease of negative values in the assay for TSH receptor antibodies led to the discovery of endogenous antibodies to TSH. We examined the sera of approximately 2500 patients with Graves' disease. Eight positive sera were found. The IgG in all 8 sera showed higher binding with both bTSH and porcine TSH (pTSH) than with human TSH (hTSH). This means that autoantibodies to TSH in sera from patients with Graves' disease are rare and often directed towards heterologous bovine and porcine TSH. When hTSH levels were determined in sera of hyperthyroid patients with positive antibodies to hTSH, discrepancies in serum hTSH levels were observed when using different assay methods, i.e. hTSH levels were higher with the double-antibody technique, and lower with immunoradiometric assays. Antibodies in these sera showed higher binding to pTSH-α subunit than to -β subunit. The binding of the two pTSH subunits with antibodies could be displaced by intact bTSH. Neither stimulation in Graves' disease nor blocking in primary hypothyroidism of TSH receptor antibodies interfered with the binding of the anti-TSH antibodies to 125I-labelled pTSH, pTSH-α, and pTSH-β. Consequently, using this type of autoantibodies to TSH we were unable to obtain evidence that the TSH receptor antibodies of patients with Graves' disease was an anti-idiotype antibody against anti-TSH antibodies.

Anti-TSH receptor antibodies in Graves' disease modulate the kinetic behaviour of autologous thyroid TSH receptors. Evidence of the IgG-induced cross-linkage of autologous TSH receptors

1984 ◽  
Vol 105 (3) ◽  
pp. 330-340 ◽  
Author(s):  
Tjerk W. A. de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol
Keyword(s):  
Binding Sites ◽  
Plasma Membranes ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Graves Disease ◽  
Kinetic Behaviour ◽  
High Affinity ◽  
Cross Linkage ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

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.

scholarly journals Graves disease with negative TSH receptor antibodies: a presentation of 5 cases

2020 ◽  
Vol 93 (6) ◽  
pp. 417-419
Author(s):  
Aina Scatti Regàs ◽  
Ricard Pujol Borrell ◽  
Roser Ferrer Costa ◽  
Elsa Puerto Carranza ◽  
María Clemente León
Keyword(s):  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

TSH-RECEPTOR ANTIBODIES IN MOTHERS WITH GRAVES' DISEASE AND OUTCOME IN THEIR OFFSPRING

The Lancet ◽  
1988 ◽  
Vol 331 (8575-8576) ◽  
pp. 14-17 ◽  
Author(s):  
Nobuo Matsuura ◽  
Kenji Fujieda ◽  
Yasuhiro Iida ◽  
Seiichiro Fujimoto ◽  
Junji Konishi ◽  
...  
Keyword(s):  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

The clinical course of endocrine ophthalmopathy in patients presenting with Graves' disease depending on the effect of radioiodine therapy

2011 ◽  
Vol 57 (3) ◽  
pp. 17-20
Author(s):  
M S Sheremeta ◽  
N Iu Sviridenko ◽  
I M Belovalova ◽  
P I Garbuzov
Keyword(s):  
Radioiodine Therapy ◽  
Clinical Course ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Endocrine Ophthalmopathy ◽  
Post Radiation ◽  
Group 2 ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Group 1

The primary objective of the present work was to study the clinical course of endocrine ophthalmopathy (EOP) following radioiodine therapy (RIT) of Graves' disease (GD) and depending on its effect (development of post-radiation hypothyroidism). The secondary objective was to determine risk factors of EOP progression after radioiodine therapy. This prospective study included 38 patients (76 eyes) allocated to two groups. The patients of group 1 (n=19/38 eyes) presented with thyrotoxicosis at each visit and continued to use thyrostatic agents; those in group 2 (n=19/38 eyes) had hypothyroidism at its early stages (3 and 6 months) and were given substitution therapy with levothyroxin. The development of post-radiation hypothyroidism was shown to strongly influence the clinical course of EOP. In the patients of group 1, EOP remained active throughout the entire observation period (12 months) in the absence of appreciable variations of its integral severity index. In group 2, the same index decreased significantly, but active forms of EOP could be detected by the time of onset of hypothyroidism (6 months) (p=0.0000). After 12 months, the level of anti-TSH receptor antibodies in the patients of group 1 was significantly higher than in those of group 2 (10.8±8.3 and 2.9±2.0 respectively, p=0.0003). The regression rate of EOP symptoms following radioiodine therapy (RIT) of Graves' disease was a function of the efficacy of thyroid 131I radioablation. It is concluded that persistence of anti-TSH receptor antibodies was responsible for the deterioration of the clinical picture of endocrine ophthalmopathy after radioiodine therapy.

scholarly journals TSH-receptor autoimmunity in Graves' disease after therapy with anti-thyroid drugs, surgery, or radioiodine: a 5-year prospective randomized study

2008 ◽  
Vol 158 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Peter Laurberg ◽  
Göran Wallin ◽  
Leif Tallstedt ◽  
Mirna Abraham-Nordling ◽  
Göran Lundell ◽  
...  
Keyword(s):  
Medical Therapy ◽  
Radioiodine Therapy ◽  
Randomized Study ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Number Of Patients ◽  
The Common ◽  
Initiation Of Therapy ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies

IntroductionAutoimmunity against the TSH receptor is a key pathogenic element in Graves' disease. The autoimmune aberration may be modified by therapy of the hyperthyroidism.ObjectiveTo compare the effects of the common types of therapy for Graves' hyperthyroidism on TSH-receptor autoimmunity.MethodsPatients with newly diagnosed Graves' hyperthyroidism aged 20–55 years were randomized to medical therapy, thyroid surgery, or radioiodine therapy (radioiodine was only given to patients ≥35 years of age). l-thyroxine (l-T4) was added to therapy as appropriate to keep patients euthyroid. Anti-thyroid drugs were withdrawn after 18 months of therapy. TSH-receptor antibodies (TRAb) in serum were measured before and for 5 years after the initiation of therapy.ResultsMedical therapy (n=48) and surgery (n=47) were followed by a gradual decrease in TRAb in serum, with the disappearance of TRAb in 70–80% of the patients after 18 months. Radioiodine therapy (n=36) led to a 1-year long worsening of autoimmunity against the TSH receptor, and the number of patients entering remission of TSH-receptor autoimmunity with the disappearance of TRAb from serum during the following years was considerably lower than with the other types of therapy.ConclusionThe majority of patients with Graves' disease gradually enter remission of TSH-receptor autoimmunity during medical or after surgical therapy, with no difference between the types of therapy. Remission of TSH-receptor autoimmunity after radioiodine therapy is less common.

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