Graves disease and Hashimoto thyroiditis are common autoimmune diseases (AIDs) in which autoantibodies interfere with the function of the thyroid gland, in the former causing hyperthyroidism and in the latter hypothyroidism. Consequently, the disease mechanisms are different; in Graves disease an antibody (thyroid-stimulating immunoglobulin) mimics the function of thyroid stimulating hormone (TSH), and thus an excessive production of thyroid hormones ensues. The initial phase of Hashimoto thyroiditis is characterized by lymphocytic infiltration into thyroid follicles followed by their gradual destruction; antibodies against thyroid peroxidase or thyroglobulin are often found but whether they contribute to the disease mechanism or are consequences thereof remains unestablished. These diseases are associated with each other and many other AIDs presenting examples of polyautoimmunity. Both of the diseases are much more common in women than in men.

For both diseases genetic and environmental causes are thought to be important. Microbial antigenes may be triggers of these diseases, as well as some dramatic psychosocial events. Autoimmune thyroid diseases also appear as a side-effect of immunotherapy, which has recently become a promising novel therapeutic modality in the treatment of some cancers. Multiple low-to-moderate-risk susceptibility genes for Graves influence effector pathways, such as thyroglobulin, thyrotropin receptor, protein tyrosine phosphatase nonreceptor type 22, and cytotoxic T-lymphocyte–associated antigen ; the latter is also associated with Hashimoto thyroiditis. Familial risk is known for both of these diseases, also between each other and a few other autoimmune diseases.

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Mishita
Jornal co-ordinator
Journal of  Autoimmune Disorders