The exact<unk>  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 disease and<unk>  an aggravation of the autoimmune response that leads to Graves' disease, more robust clinical data are needed for a firm conclusion. Genetics A genetic predisposition for Graves' disease is seen, with some people more prone to develop TSH receptor activating antibodies due to a genetic<unk> . 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<unk> . 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 Graves' disease is an autoimmune disease 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 Graves' disease. More recently, the role for Y. enterocolitica has been disputed. Epstein–Barr virus (EBV) is another potential trigger.
medical cause of Hyperthyroidism
medical cause of Hypothyroidism
medical diagnosis of Hyperparathyroidism
symptom of Hypothyroidism
medical cause of Precocious puberty
symptom of Hashimoto's thyroiditis
medical cause of Hyperparathyroidism
complications of Graves' disease