Autoimmune diseases most commonly associated to Hashimotos thyroiditis include celiac disease, type 1 diabetes, vitiligo, and alopecia.The genes implicated vary in different ethnic groups and the incidence is increased in people with chromosomal disorders, including Turner, Down, and Klinefelter syndromes usually associated with autoantibodies against thyroglobulin and thyroperoxidase. Progressive depletion of these cells as the cytotoxic immune response leads to higher degrees of primary hypothyroidism, presenting with low T3/T4 levels, and compensatory elevations of TSH. Pathophysiology
Multiple  mechanisms by which the pathology of Hashimotos thyroiditis develops have been suggested. Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors, although a small percentage of people may have none of these antibodies present. As indicated in various twin studies, a percentage of the population may also have these antibodies without developing Hashimotos thyroiditis. Nevertheless, antibody-dependent, cell-mediated cytotoxicity is a substantial factor behind the apoptotic fall-out of Hashimotos thyroiditis. Activation of cytotoxic T-lymphocytes (CD8+ T-cells) in response to cell-mediated immune response affected by helper T-lymphocytes (CD4+ T-cells) is central to thyrocyte destruction. As is characteristic of type IV hypersensitivities, recruitment of macrophages is another effect of the helper T-lymphocyte activation, with Th1 axis lymphocytes producing inflammatory cytokines within thyroid tissue to further macrophage activation and migration into the thyroid gland for direct effect.Gross morphological changes within the thyroid are seen in the general enlargement, which is far more locally nodular and irregular than more diffuse patterns (such as that of hyperthyroidism).
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.