Graves' disease

Napier, C; Pearce, SHS

doi:10.1007/978-3-319-45013-1_15

Graves' disease

Lookup NU author(s): Dr Catherine Napier, Professor Simon Pearce ORCiD

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Abstract

© Springer International Publishing AG, part of Springer Nature 2018. Graves’ disease (GD) is a common autoimmune thyroid disorder, affecting 20–30 per 100,000 of the population per year. In keeping with other autoimmune diseases, it exhibits a clear female preponderance (F:M 6–7:1) with approximately 3% of women and 0.5% of men developing GD during their lifetime. GD is a complex genetic condition, with environmental factors precipitating the disease in genetically predisposed individuals who harbor multiple susceptibility alleles. Thyroid-stimulating hormone receptor (TSHR) antibodies are the immunological hallmark of the disease and the key driver for thyrocyte hyperplasia and the resulting hyperthyroidism. Our understanding of the pathogenesis of the condition has developed significantly in recent years, reflecting advances in human genomics, molecular immunology, and the availability of murine models of disease. Clinical features in GD are widespread, with a myriad of typical symptoms and physical findings at presentation. Frequently reported symptoms include tremor, palpitations, heat intolerance, weight loss, and anxiety. Physical examination may reveal warm, tremulous extremities, atrial fibrillation, signs of thyroid orbitopathy, and a goiter with a bruit. A series of extrathyroidal manifestations can accompany GD at presentation or appear during the course of the disease; these are associated with elevated titers of circulating autoantibodies. The commonest extrathyroidal manifestation is thyroid orbitopathy, which can be sight-threatening and requires a detailed and careful approach to management. Recent developments in our understanding of the pathogenesis of these conditions may lead to the development of novel therapies in coming years.