Although most ophthalmologists are familiar with Graves disease, some may be less familiar with the role that immune regulation plays in thyroid disease. Often associated with hyperthyroidism, Graves disease occurs because of antibodies binding to and activating the thyroid-stimulating hormone receptor. The most common cause of hypothyroidism is Hashimoto thyroiditis, which is also the most common autoimmune disease. It is characterized by autoantibodies to thyroid antigens such as thyroperoxidase and thyroglobulin. Together, Hashimoto thyroiditis and Graves disease constitute autoimmune thyroid disease (AITD),1 which occurs more commonly in women than in men. Both genetic and environmental factors affect the development of AITD. Genetic polymorphisms for several human leucocyte antigens, various proteins including cytokines, thyroid-stimulating hormone receptor, and cytotoxic T lymphocyte–associated factor 4 play a role.2 Environmental exposure to toxins may lead to the development of AITD, but even this possibility is not fully understood. For example, while smoking exacerbates Graves disease, multiple studies have suggested that it reduces the risk of developing autoantibodies and hypothyroidism.
Garg SJ. Autoimmune Thyroid Disease and Uveitis. JAMA Ophthalmol. 2017;135(6):599–600. doi:10.1001/jamaophthalmol.2017.0776
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