Graves’ Disease is an autoimmune disorder represented by the overproduction of thyroid hormones (hyperthyroidism). Graves’ Disease is more common among women of reproductive age, and genetic, endogenous, and environmental factors influence the pathogenesis of Graves’ Disease. Graves’ Disease presents with many clinical manifestations, such as tachycardia, fatigue, heat intolerance, palpitations, weight loss, muscle weakness, alterations in menstrual cycles, insomnia, hair loss, goiter, and others. Currently, there are three main treatment routes for Graves’ Disease: antithyroid drugs, radioactive iodine therapy, and thyroidectomy. Antithyroid drug therapy has a high relapse rate. At the same time, both radioactive iodine and thyroidectomy eradicate or surgically remove the tissue of the thyroid and lead to the consequence of developing another disease, hyperthyroidism, that requires a life-long supplementation of the thyroid replacement hormone, levothyroxine. Presently, investigations are focused on finding new therapeutics that can supplement existing treatments as a combination therapy that can lengthen the remission period after cessation of ATDs or conduction of RAI therapy. Future research is exploring treatment options that target different components of the immune system response pathway, the thyroid stimulating hormone receptor or thyrotropin receptor autoantibodies, that have the potential to cure Graves’ Disease.
| Identifer | oai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/47978 |
| Date | 30 January 2024 |
| Creators | Moses, Carissa S. |
| Contributors | Offner, Gwynneth, Symes, Karen |
| Source Sets | Boston University |
| Language | en_US |
| Detected Language | English |
| Type | Thesis/Dissertation |
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