scholarly journals Antithyroid drug therapy for Graves’ disease

2021 ◽  
Vol 64 (10) ◽  
pp. 690-698
Author(s):  
Soo Myoung Shin ◽  
Ka Hee Yi

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.

2021 ◽  
Author(s):  
Vasudha Bakshi ◽  
Gollapalli Rajeev Kumar

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.


2009 ◽  
Vol 55 (2) ◽  
pp. 48-50
Author(s):  
V A Peterkova ◽  
O V Vasyukova ◽  
A N Tyul'pakov

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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