scholarly journals Graves’ Disease

2021 ◽  
Author(s):  
Vasudha Bakshi ◽  
Gollapalli Rajeev Kumar
Keyword(s):  
Thyroid Gland ◽  
Hormone Receptor ◽  
Treatment Options ◽  
Positive Family History ◽  
Current Treatment ◽  
Thyroid Stimulating Hormone ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Autoimmune Thyroid ◽  
Stimulating Hormone

Graves’ disease (GD) is an autoimmune thyroid disorder where autoantibodies are produced against TSH (Thyroid Stimulating Hormone) receptor causing thyrotoxicosis. It is characterized by goiter, ophthalmopathy, and occasionally pretibial myxedema. The autoimmune mechanism causing disease is not well understood and it is complex. It involves multifactorial etiology involving environmental and genetic factors. Smoking and positive family history contributing to the development of GD. GD can be diagnosed based on the clinical manifestation and demonstrating low concentration of TSHs, high TRab (Thyroid Stimulating Hormone receptor autoantibodies), and high FT4 (Free thyroxine) concentration. Current treatment options aimed at stable restoration of euthyroidism by following different modalities of suppressing thyroid gland using antithyroid drugs, removing/ablating thyroid gland by surgery, and radioactive iodine treatment with iodine- 131.

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 Antithyroid drug therapy for Graves’ disease

2021 ◽  
Vol 64 (10) ◽  
pp. 690-698
Author(s):  
Soo Myoung Shin ◽  
Ka Hee Yi
Keyword(s):  
Hormone Receptor ◽  
Adverse Reactions ◽  
Low Dose ◽  
Radioactive Iodine ◽  
Thyroid Stimulating Hormone ◽  
Reproductive Age ◽  
Antithyroid Drugs ◽  
Graves Disease ◽  
Definitive Therapy ◽  
Stimulating Hormone

Background: Graves’ disease is the most common cause of hyperthyroidism which is caused by stimulating autoantibodies against thyroid-stimulating hormone receptor. There is no etiology-specific treatment for Graves’ disease.Current Concepts: Graves’ disease can be treated with antithyroid drugs (ATDs), radioactive iodine, or thyroidectomy. ATDs are the most preferred first-line therapy, because they do not cause either permanent hypothyroidism or exacerbation of orbitopathy, despite low remission rate. ATDs have serious adverse reactions including agranulocytosis and fulminant hepatic necrosis requiring liver transplantation. Methimazole (MMI) is recommended in every patient starting ATD therapy, except during the first trimester of pregnancy and in cases of thyroid storm, because of relatively lower incidence and severity of serious adverse reactions compared with propylthiouracil. Treatment should be continued for 12 to 18 months, then discontinued if the levels of thyroid-stimulating hormone and thyroid-stimulating hormone receptor antibodies are normalized. In cases of relapse of hyperthyroidism, radioactive iodine or thyroidectomy can be recommended for definitive therapy; however, recent studies support longer-term maintenance of low dose MMI as a favorable alternative therapy. All ATDs may induce congenital anomalies when exposed during early pregnancy. Every female patient of reproductive age should be advised to postpone pregnancy until their thyroid function is maintained within normal range and to stop ATDs when pregnancy is confirmed to avoid the risk of congenital anomalies.Discussion and Conclusion: Longer-term low dose MMI therapy can be a good choice for Graves’ hyperthyroidism with relapse. Before pregnancy, hyperthyroidism should be controlled to stop ATDs during pregnancy.

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 Non-immune thyrotoxicosis caused by thyroid-stimulating hormone receptor activating gene mutation (the first description in Russia)

2009 ◽  
Vol 55 (2) ◽  
pp. 48-50
Author(s):  
V A Peterkova ◽  
O V Vasyukova ◽  
A N Tyul'pakov
Keyword(s):  
Pregnant Women ◽  
Gene Mutation ◽  
Clinical Picture ◽  
Hormone Receptor ◽  
Thyroid Stimulating Hormone ◽  
Maternal Antibodies ◽  
Graves Disease ◽  
Gene Encoding ◽  
Activating Mutations ◽  
Stimulating Hormone

Thyrotoxicosis of newborns, observed in less than 1% of pregnant women with Graves disease, is due to transplacental transfer of stimulating antibodies to the thyroid stimulating hormone receptor (rTSH). The clinical picture manifests itself in the first days of a child’s life, is transient in nature and, as a rule, ends with a full recovery as the maternal antibodies to rTSH disappear from the bloodstream of the newborn. However, in addition to the "classic" autoimmune thyrotoxicosis, cases of congenital and familial non-autoimmune thyrotoxicosis, which are caused by inherited activating mutations of the gene encoding rTSH - TSHR, have been described. This article presents its own observation.

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