Thyroid hormones
Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T) and thyroxine (T). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T and T are partially composed of iodine. A deficiency of iodine leads to decreased production of T and T, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T), which has a longer half-life than T. In humans, the ratio of T to T released into the blood is approximately 14:1. T is converted to the active T (three to four times more potent than T) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (Ta) and thyronamine (Ta). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.
Antithyroid autoantibodies
Anti-thyroid peroxidase (anti-TPO) antibodies are specific for the autoantigen TPO, a 105kDa glycoprotein that catalyses iodine oxidation and thyroglobulin tyrosyl iodination reactions in the thyroid gland. Most antibodies produced are directed to conformational epitopes of the immunogenic carboxyl-terminal region of the TPO protein, although antibodies to linear epitopes have been seen. Anti-TPO antibodies are the most common anti-thyroid autoantibody, present in approximately 90% of Hashimoto's thyroiditis, 75% of Graves' disease and 10-20% of nodular goitre or thyroid carcinoma. Also, 10-15% of normal individuals can have high level anti-TPO antibody titres. High serum antibodies are found in active phase chronic autoimmune thyroiditis. Thus, an antibody titer can be used to assess disease activity in patients that have developed such antibodies. The majority of anti-TPO antibodies are produced by thyroid infiltrating lymphocytes, with minor contributions from lymph nodes and the bone marrow. They cause thyroid cell damage by complement activation and antibody dependent cell cytotoxicity. However, anti-TPO antibodies are not believed to contribute to the destruction of the thyroid.