It was first described by the Japanese physician Hakaru Hashimoto in 1912. In 1957, it was recognized as an autoimmune disorder. Signs and symptoms
Many symptoms are attributed to the development of Hashimotos thyroiditis. The most common symptoms include: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and miscarriages.Hashimotos disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly appears in middle age, particularly for men. People who develop Hashimotos disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves.The thyroid gland may become firm, large, and lobulated in Hashimotos thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis, rather than tissue hypertrophy. While their role in the initial destruction of the follicles is unclear, antibodies against thyroid peroxidase   or thyroglobulin are relevant, as they serve as markers for detecting the disease and its severity. They are thought to be the secondary products of the T cell-mediated destruction of the gland.It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma.
Severe hypothyroidism is associated with mutations leading to lower production of IL-4 (Th2 cytokine suppressing cell-mediated autoimmunity), lower secretion of TGF-β (inhibitor of cytokine production), and mutations of FoxP3, an essential regulatory factor for the Tregs development. Development of Hashimotos disease was associated with mutation of the gene for TNF-α (stimulator of the IFN-γ production), causing its higher concentration.Preventable environmental factors, including high iodine intake, selenium deficiency, and infectious diseases and certain drugs, have been implicated in the development of autoimmune thyroid disease in genetically predisposed individuals. Iodine
Excessive iodine intake is a well-established environmental factor for triggering thyroid autoimmunity. A higher prevalence of thyroid autoantibodies is in the areas with higher iodine supply. Several mechanisms by which iodine may promote thyroid autoimmunity have been proposed. Iodine exposure leads to higher iodination of thyroglobulin, increasing its immunogenicity by creating new iodine-containing epitopes or exposing cryptic epitopes. It may facilitate presentation by APC, enhance the binding affinity of the T-cell receptor, and activating specific T-cells.Iodine exposure has been shown to increase the level of reactive oxygen species. They enhance the expression of the intracellular adhesion molecule-1 on the thyroid follicular cells, which could attract the immunocompetent cells into the thyroid gland.Iodine is toxic to thyrocytes since highly reactive oxygen species may bind to membrane lipids and proteins. It causes thyrocyte damage and the release of autoantigens.