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.
Presence of Thyroid-Stimulating Hormone Receptor Antibodies in a Patient with Subacute Thyroiditis followed by Hypothyroidism and Later Graves' Disease with Ophthalmopathy: A Case Report
