Summary
Hyperthyroid Graves’ disease is one of the commonest autoimmune disorders, affecting about 1% of women. It is most frequent in the 4th decade of life. There is a genetic predisposition to Graves’ disease, determined by alleles at the major histocompatibility complex (MHC), cytotoxic T-lymphocyte-associated antigen (CTLA-4), protein tyrosine phosphatase non-receptor 22 (PTPN22), and other less well-defined chromosomal loci. Additional, non-genetic, factors that have an influence are cigarette use, pregnancy, estrogen use, and stressful life events. The hyperthyroidism is caused by thyroid-stimulating hormone (TSH) receptor stimulating autoantibodies that lead to excess thyroid hormone production and thyroid growth. Thyroid peroxidase autoantibodies are also frequently found and may be important in thyrocyte destruction and perpetuation of autoimmunity. Graves’ disease may be treated with thionamide antithyroid drugs, radioiodine or thyroid surgery. No treatment is perfect and each has its pros and cons. The recent isolation of monoclonal human TSH receptor antibodies may lead to more sensitive tests for thyroid-stimulating autoantibodies. A key challenge is to define novel therapies that lead to more certain and safe remission of hyperthyroidism without ablation of thyroid function.
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Pearce, S.H. (2007). Graves’ Disease. In: Weetman, A.P. (eds) Autoimmune Diseases in Endocrinology. Contemporary Endocrinology. Humana Press. https://doi.org/10.1007/978-1-59745-517-6_6
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