Hashimoto's disease commonly known as Hashimoto's thyroiditis, is an autoimmune disorder that is the most frequent cause of clinical hypothyroidism. In this disease antibodies bind to the thyroid and prevent the manufacture of sufficient levels of thyroid hormone. In addition to binding to thyroid tissue, these antibodies may also bind to the adrenal glands, pancreas, and acid-producing cells of the stomach (parietal cells).
Hashimoto's thyroiditis is associated with the following signs of autoimmune thyroid disease:
- Serum antibodies against thyroid proteins such as thyrogloblin (TG) or thyroperoxidase (TPO), although 10% to 15% can be antibody-negative.
- Diffuse enlargement of the gland detected by physical examination, ultrasound, or computed tomography (CT scan).
- Diffuse iodine uptake and glandular enlargement on radioiodine uptake scan.
A histologic assessment will typically find cellular infiltration of immune cells, especially lymphocytes.
The variables that predict Hashimoto's disease are family history of thyroid disease of any type and exposure to environmental triggers. Certain toxins are known to be concentrated within the thyroid follicles. Such toxins generate free radicals, which activate immune responses and possibly sensitize immune cells to surrounding thyroid proteins.
Chemicals that are documented to correlate with Hashimoto's disease include:
- Bisphenol A
- Iodine (in excess or when intake increases significantly)
In the majority of cases individuals with autoimmune thyroid disease will progress to hypothyroidism . The presence of Hashimoto's disease raises the risk of having or developing other autoimmune diseases.
In addition, clinical hypothyroidism can be caused by thyroid surgery and postpartum hypothyroidism, which is a transient form of hypothyroidism, affecting 5% to 10% of women.