Antiidiotypic Blocking of Graves′ Disease Biologic Activity with Autologous Sera But Not Consistently with Homologous Sera: Evidence for Polyclonality of Thyroid Receptor Antibodies (Trab)

1987 ◽  
pp. 389-392
Author(s):  
R. Paschke ◽  
J. Teuber ◽  
U. Schwedes ◽  
K. H. Usadel
Keyword(s):  
Graves Disease ◽  
Biologic Activity ◽  
Thyroid Receptor ◽  
Receptor Antibodies

Extrathyroidal synthesis and biologic action of thyroid receptor antibody (TRAb) in Graves' disease

1987 ◽  
Vol 116 (1_Suppl) ◽  
pp. S352-S354 ◽  
Author(s):  
R. Paschke ◽  
H. G. Heinze ◽  
J. Teuber ◽  
R. Schmeidl ◽  
K. H. Usadel
Keyword(s):  
Nude Mice ◽  
Radioiodine Therapy ◽  
Thyroid Tissue ◽  
Graves Disease ◽  
Receptor Antibody ◽  
Radioligand Assay ◽  
Biologic Activity ◽  
Thyroid Receptor ◽  
Bio Assay

Abstract. In a patient with Graves' disease who underwent thyroidectomy with subsequent radioiodine therapy thyroid receptor antibody could be detected by radioligand assay. No thyroid tissue could be detected by 131I-scintiscanning. Thyroglobulin was repeatedly negative. Biologic activity of this patients serum could be demonstrated in the nude mice bio assay. 131I-incorporation and secretion of human thyroglobulin could be stimulated by injecting thymusdysplastic nude mice with transplants of thyroid tissue from a patient with Graves' disease with the athyroid patients serum. These results demonstrate evidence for extrathyroidal production and biological actiivty of TRAb in vivo.

scholarly journals Macular Rash, Thrombocytopenia, and Hyperbilirubinemia in a Preterm Infant

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Nurin Chatur ◽  
Marina Castro ◽  
Kin Fan Young Tai
Keyword(s):  
Preterm Infant ◽  
Early Identification ◽  
Congenital Infection ◽  
Rare Condition ◽  
Graves Disease ◽  
Macular Rash ◽  
Neonatal Hyperthyroidism ◽  
Thyroid Receptor ◽  
Maternal Thyroid ◽  
Receptor Antibodies

Neonatal hyperthyroidism is usually caused by the passage of maternal thyroid receptor antibodies. This relatively rare condition has various manifestations including cholestasis, prematurity, and cardiomegaly. We present a case of a preterm infant with neonatal Graves’ disease who presented with cholestasis, cardiomegaly, and a macularpapular rash that was thought to be suspicious for congenital infection. This case has been reported to illustrate lessons learnt for early identification of a neonate with Graves’ disease in order to expedite treatment.

Graves’ disease in a patient with Down syndrome: a shift from hyperthyroidism to hypothyroidism

2021 ◽  
Vol 14 (9) ◽  
pp. e242612
Author(s):  
Sara Todo Bom Costa ◽  
Vanessa Albino ◽  
Ana Peres ◽  
Patrícia Ferreira
Keyword(s):  
Down Syndrome ◽  
Rare Condition ◽  
Laboratory Evaluation ◽  
Graves Disease ◽  
Laboratory Studies ◽  
Thyroglobulin Antibodies ◽  
Increased Risk ◽  
Thyroid Receptor ◽  
Receptor Antibodies ◽  
New Onset

Down syndrome (DS) is associated with an increased risk of multisystemic dysfunction, namely endocrine abnormalities. Thyroid dysfunction is the most common endocrinological disorder, and it can manifest as either hypothyroidism or hyperthyroidism. A 16-year-old patient with DS developed hyperthyroidism after a lifetime of alternating between subclinical hypothyroidism and euthyroidism. He presented new onset weight loss, agitation and diarrhoea. Laboratory studies were compatible with hyperthyroidism. Thyroid receptor antibodies (TRAbs) were positive, antithyroid peroxidase antibodies and thyroglobulin antibodies were negative. Antithyroid medication (methimazole) was prescribed and, despite therapy adjustments, laboratory evaluation revealed new onset hypothyroidism with persistently positive TRAbs. He experienced weight gain and remained in a hypothyroid state even with withdrawal of methimazole and administration of levothyroxine. This case illustrates an example of Graves’ disease with coexisting stimulating and inhibiting TRAbs that led to a shift from hyperthyroidism to hypothyroidism, a rare condition in patients with DS.

Anti-thyrotrophin receptor antibodies in Graves' disease as demonstrated directly by immunoprecipitation assay

1983 ◽  
Vol 102 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Tjerk W. A de Bruin ◽  
Daan van der Heide ◽  
Maria C. Krol
Keyword(s):  
Binding Site ◽  
Tsh Receptor ◽  
Graves Disease ◽  
Immunoprecipitation Assay ◽  
Receptor Complexes ◽  
Auto Antibody ◽  
Receptor Antibodies ◽  
Normal Controls

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.

The relationship between thyroid receptor antibody and anti mullerian hormone in Graves' disease

2019 ◽  
Author(s):  
Keziban Demir ◽  
Hakan Kursat ◽  
Sevde Yazici ◽  
Hamide Pişkinpaşa ◽  
Evin Bozkir ◽  
...  
Keyword(s):  
Graves Disease ◽  
Receptor Antibody ◽  
Thyroid Receptor ◽  
The Relationship

scholarly journals Remission Rate of Graves' Disease and the Trend of Changes in Serum TSH Receptor Antibodies in Prolonged Antithyroid Drug Treatment

2020 ◽  
Vol 18 (Suppl) ◽  
Author(s):  
Danilo Villagelin ◽  
Roberto Bernardo Santos ◽  
João Hamilton Romaldini
Keyword(s):  
Drug Treatment ◽  
Remission Rate ◽  
Antithyroid Drug ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Remission Rates ◽  
Thyrotropin Receptor Antibodies ◽  
Antithyroid Drug Treatment ◽  
The Impact ◽  
Receptor Antibodies

Context: Graves’ disease is an autoimmune disease caused by thyrotropin receptor antibodies (TRAb). These antibodies can be measured and used for the diagnosis, prediction of remission, and risk of Graves’ orbitopathy development. There are three treatments for Graves’ disease that have remained unchanged for the last 75 years: Antithyroid drugs, radioiodine, and surgery. Antithyroid drugs are the first treatment option worldwide and are usually used for 12 - 18 months. Recent reports suggest the use of antithyroid drugs for more than 18 months with better outcomes. This review focuses on two aspects of treatment with antithyroid drugs: The impact of using antithyroid drugs for more than 12 - 18 months on remission rates and the trend of TRAb during prolonged antithyroid drug treatment. Evidence Acquisition: A review was performed in Medline on the published work regarding the duration of ATD treatment and remission of Graves' disease and also ATD treatment and TRAb status during the 1990 - 2019 period. Results: Remission rates are variable (30% - 80%), and many clinical and genetic factors serve as predictors. The long-term use of antithyroid drugs appears to increase remission rates. TRAb values usually decline during ATD treatment, but the trend could occur in two ways: Becoming negative or showing a fluctuating pattern. However, approximately 10% of the patients will remain TRAb-positive after five years of treatment with antithyroid drugs. Conclusions: Antithyroid drugs can be used for long periods with an increase in remission rates, and a gradual decrease in TRAb levels, with the disappearance of TRAb in 90% of the patients after 60 months.

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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