Clinical course and thyroid stimulating hormone (TSH) receptor antibodies during surgical treatment of Graves' disease

1992 ◽  
Vol 16 (4) ◽  
pp. 647-652 ◽  
Author(s):  
Yoko Mori ◽  
Naoya Matoba ◽  
Shunji Miura ◽  
Nobumitsu Sakai ◽  
Yukio Taira
Keyword(s):  
Surgical Treatment ◽  
Clinical Course ◽  
Thyroid Stimulating Hormone ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Stimulating Hormone

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 Hyperthyroidism in Children

2021 ◽  
Author(s):  
Artur Bossowski ◽  
Karolina Stożek
Keyword(s):  
Surgical Treatment ◽  
Thyroid Hormones ◽  
Clinical Symptoms ◽  
Pediatric Population ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Common Cause ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Immunological Dysfunction

Hyperthyroidism is the state of excessive synthesis and release of the thyroid hormones by thyrocytes. Graves’ disease is the most common cause of hyperthyroidism in children. The condition may occur at any age but the prevalence increases with age. According to the classical paradigm, coexistence of genetic susceptibility, environment triggers and immunological dysfunction are responsible for its development. Diagnosis of Graves’ disease is based on presence of characteristic clinical symptoms, TSH receptor antibodies and excess of thyroid hormones. The management in pediatric population involves mainly pharmacotherapy (thyrostatics, β-adrenolitics), in resistant cases radical radioiodine I131 therapy or surgical treatment is necessary.

A water-soluble fragment of the thyroid-stimulating hormone receptor which binds both thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies

1984 ◽  
Vol 100 (1) ◽  
pp. 113-118 ◽  
Author(s):  
E. Davies Jones ◽  
B. Rees Smith
Keyword(s):  
Hormone Receptor ◽  
Gel Filtration ◽  
Thyroid Stimulating Hormone ◽  
Water Soluble ◽  
Tsh Receptor ◽  
Human Thyroid ◽  
Freezing And Thawing ◽  
Receptor Antibodies ◽  
Tsh Receptor Antibodies ◽  
Stimulating Hormone

ABSTRACT Previous studies have shown that freezing and thawing of human thyroid homogenates releases a water-soluble substance which reversibly binds to TSH-receptor antibodies. This substance has been designated long-acting thyroid stimulator absorbing activity (LAA). We now describe a new method for measuring LAA based on the TSH-receptor assay and application of the technique to the study of LAA. Our results indicate that LAA is a heat-labile glycoprotein which co-elutes with haemoglobin on gel filtration. Furthermore, LAA is retarded by columns of Sepharose–TSH but not by Sepharose coupled to human chorionic gonadotrophin, normal immunoglobulin G or bovine serum albumin, suggesting that LAA contains a binding site for TSH as well as for TSH-receptor antibodies. It would seem therefore that LAA is a water-soluble fragment of the TSH receptor possibly resulting from proteolytic cleavage of the receptor at a site close to the cell surface. J. Endocr. (1984) 100, 113–118

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.

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