The exact cause is unclear; however, it is believed to involve a combination of genetic and environmental factors. While a theoretical mechanism occurs by which exposure to severe stressors and high levels of subsequent distress such as PTSD (Post traumatic stress disorder) could increase the risk of autoimmune<unk>  and cause an aggravation of the autoimmune response that leads to<unk> , more robust clinical data are needed for a firm conclusion. Genetics A genetic predisposition for<unk>  is seen, with some people more prone to develop TSH receptor activating antibodies due to a genetic cause. Human leukocyte antigen DR (especially DR3) appears to play a role. To date, no clear genetic defect has been found to point to a single-gene cause. Genes believed to be involved include those for thyroglobulin, thyrotropin receptor, protein tyrosine phosphatase nonreceptor type 22 (PTPN22), and cytotoxic T-lymphocyte–associated antigen 4, among others. Infectious trigger Since<unk>  is an autoimmune<unk>  which appears suddenly, often later in life, a viral or bacterial infection may trigger antibodies which cross-react with the human TSH receptor, a phenomenon known as antigenic mimicry. The bacterium Yersinia enterocolitica bears structural similarity with the human thyrotropin receptor and was hypothesized to contribute to the development of thyroid autoimmunity arising for other reasons in genetically susceptible individuals. In the 1990s, it was suggested that Y. enterocolitica may be associated with<unk> . More recently, the role for Y. enterocolitica has been disputed. Epstein–Barr virus (EBV) is another potential trigger.
Graves' disease
Hashimoto's thyroiditis
Autoimmune thyroiditis
Riedel's thyroiditis
Ord's thyroiditis
Cushing's disease
Radiation-induced thyroiditis
Behr syndrome