scholarly journals Prevalence and clinical relevance of thyroid stimulating hormone receptor-blocking antibodies in autoimmune thyroid disease

2017 ◽  
Vol 189 (3) ◽  
pp. 304-309 ◽  
Author(s):  
T. Diana ◽  
J. Krause ◽  
P. D. Olivo ◽  
J. König ◽  
M. Kanitz ◽  
...  
Keyword(s):  
Thyroid Disease ◽  
Hormone Receptor ◽  
Clinical Relevance ◽  
Autoimmune Thyroid Disease ◽  
Thyroid Stimulating Hormone ◽  
Receptor Blocking ◽  
Autoimmune Thyroid ◽  
Blocking Antibodies ◽  
Stimulating Hormone

The Antibody Response in Human Autoimmune Thyroid Disease

1997 ◽  
Vol 92 (6) ◽  
pp. 529-541 ◽  
Author(s):  
Richard S. McIntosh ◽  
M. Suhail Asghar ◽  
Anthony P. Weetman
Keyword(s):  
Antibody Response ◽  
Thyroid Disease ◽  
Hormone Receptor ◽  
Autoimmune Thyroid Disease ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Autoimmune Thyroid ◽  
Thyroid Autoantigens ◽  
Reactive Antibody ◽  
Stimulating Hormone

1. The analysis of the antibody response in autoimmune thyroid disease has followed several historical trends. It was the investigation of thyroid-reactive antibody that allowed the initial characterization of the three principle thyroid autoantigens, thyroglobulin, thyroid peroxidase and the thyroid stimulating hormone receptor. 2. Analysis can be grouped under two broad areas: analysis of the physiological and pathological effects of the antibody, and analysis of the structure of the antibodies themselves. This review will focus on the latter. 3. Within recent years there has been a great increase in knowledge of thyroid-reactive antibody structure, principally through the adoption of phage display combinatorial library methodologies. While this latter technique has established some general principles for antibodies to thyroglobin and especially thyroid peroxidase, there is still a substantial gap in our knowledge of the antibody response to the thyroid stimulating hormone receptor. 4. Thyroid peroxidase antibodies have a relatively restricted V-region usage, and there is a correlation between the V-regions used and the epitope on thyroid peroxidase bound. In particular the Vκ light chain, Vκl(O12), is associated with reactivity to one epitope. 5. The purpose of this review is to bring together the latest results concerning the molecular analysis of the antibody response in autoimmune thyroid disease, to highlight areas of ignorance and conflict, and to discuss the methods adopted to circumvent the problems associated with analysis of the antibody response.

scholarly journals The development of Graves' disease after long-term hypothyroidism due to Hashimoto's disease

2020 ◽  
Vol 66 (5) ◽  
pp. 24-30
Author(s):  
E. A. Panfilova ◽  
L. P. Kruk ◽  
M. P. Isaeva ◽  
P. O. Osmanova ◽  
F. A. Bostanova ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Clinical Case ◽  
Thyroid Volume ◽  
Thyroid Stimulating Hormone ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Blocking Antibodies ◽  
Stimulating Hormone

The main autoimmune thyroid diseases are Hashimoto's thyroiditis (HT) and Graves' disease (GD). Despite the significant differences in a pathogenesis and a clinical picture between HT and GD, the literature describes the cases of the conversion of one autoimmune disease to another, which, according to one version, is associated with a change in the balance between the levels of a stimulating and blocking antibodies to the thyroid-stimulating hormone receptor. At the same time, there are more frequent observations of the transition of GD to HT, and much less often describe, on the contrary, the development of GD against the background of HT. The article presents a clinical case of the conversion of HT to GD. A detailed algorithm of the conservative management according to the «block-replace» scheme is described, indicating the results of laboratory and instrumental examination. At the time of describing the clinical case, the result of the treatment can be considered successful. The predictors such as a low level of the thyroid-stimulating hormone receptor and thyroid volume before discontinuation of the thyrostatic therapy suggest a low risk of the recrudescence of GD.According to the authors, the phenomenon of the conversion of one autoimmune thyroid disease to another, in addition to the scientific interest, is important for the practitioners, since a timely change in the diagnostic paradigm can significantly change the treatment strategy and the favorably affect the prognosis of disease, preventing the development of complications.

scholarly journals Incidental Identification of a Thyroid Hormone Receptor Beta (THRB) Gene Variant in a Family with Autoimmune Thyroid Disease

Thyroid ◽  
2013 ◽  
Vol 23 (12) ◽  
pp. 1638-1643 ◽  
Author(s):  
Cæcilie C. Larsen ◽  
Alexandra Dumitrescu ◽  
Laura M. Guerra-Argüero ◽  
Cecillia Gállego-Suárez ◽  
Alberto Vazquez-Mellado ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Disease ◽  
Hormone Receptor ◽  
Autoimmune Thyroid Disease ◽  
Thyroid Hormone Receptor ◽  
Gene Variant ◽  
Autoimmune Thyroid ◽  
Receptor Beta

scholarly journals Hashimoto’s Thyroiditis and Graves’ Disease in One Patient: The Extremes of Thyroid Dysfunction Associated with Interferon Treatment

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
R. H. Bishay ◽  
R. C. Y. Chen
Keyword(s):  
Thyroid Disease ◽  
Autoimmune Thyroid Disease ◽  
Pegylated Interferon ◽  
Thyroid Stimulating Hormone ◽  
Tracer Uptake ◽  
Graves Disease ◽  
Interferon Treatment ◽  
Autoimmune Thyroid ◽  
Technetium Scan ◽  
Chronic Hcv

Autoimmune thyroid disease associated with interferon therapy can manifest as destructive thyroiditis, Graves’ Hyperthyroidism, and autoimmune (often subclinical) hypothyroidism, the latter persisting in many patients. There are scare reports of a single patient developing extremes of autoimmune thyroid disease activated by the immunomodulatory effects of interferon. A 60-year-old man received 48 weeks of pegylated interferon and ribavirin therapy for chronic HCV. Six months into treatment, he reported fatigue, weight gain, and slowed cognition. Serum thyroid stimulating hormone (TSH) was 58.8 mIU/L [0.27–4.2], fT4 11.1 pmol/L [12–25], and fT3 4.2 pmol/L [2.5–6.0] with elevated anti-TPO (983 IU/mL [<35]) and anti-TG (733 U/mL [<80]) antibodies. He commenced thyroxine with initial clinical and biochemical resolution but developed symptoms of hyperthyroidism with weight loss and tremor 14 months later. Serum TSH was <0.02 mIU/L, fT4 54.3 pmol/L, and fT3 20.2 pmol/L, with an elevated TSH receptor (TRAb, 4.0 U/L [<1.0]), anti-TPO (1,163 IU/mL) and anti-TG (114 U/mL) antibodies. Technetium scan confirmed Graves’ Disease with bilateral diffuse increased tracer uptake (5.9% [0.5–3.5%]). The patient commenced carbimazole therapy for 6 months. Treatment was ceased following spontaneous clinical and biochemical remission (TSH 3.84 mIU/L, fT4 17pmol/L, fT3 4.5 pmol/L, and TRAb <1 U/L). This raises the need to monitor thyroid function closely in patients both during and following completion of interferon treatment.

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