Thyroid and antithyroid drugs
The thyroid gland produces two types of hormones: hormones known as thyroid hormones thyroxine (T4) and triiodothyronin (T3) and calcitonin ( See Calcitonin).
Secretion of thyroid hormones T4 and T3 is controlled by the hypothalamus which secretes TRH, thyreotropin releasing hormone, and the anterior pituitary gland which secretes TSH, thyreostimuline hormone, also called thyrotropin. This one stimulates the secretion of thyroid hormones which by negative feedbach slow down the secretion of TRH and TSH.
In patients with Graves' disease, secretion of thyroid hormones is stimulated by abnormal antibodies which were called LATS (long acting thyroid stimulator) and now TSI (Thyroid Stimulating Immunoglobulins). These antibodies are agonists of the TSH receptors of the thyroid.
Regulation of T3 and T4 secretion
TRH, thyreotropin releasing hormone
TRH is the hypothalamic hormone which stimulates the anterior pituitary to release TSH. TRH is a tripeptide, L-pyroglutamyl-L-histidyl-L-proline amide, present in the hypothalamus, but also in the central nervous system where its effects are not yet well known. It is not used as a therapeutic agent but to test the capacity of the pituitary gland to release TSH. However TRH in parenteral administration has been tested as treatment of certain forms of epilepsies.
TSH, thyroid stimulating hormone
TSH or thyrotropin is a glycoprotein consisting of two polypeptide chains. It is synthesized in and secreted by the anterior pituitary. Its molecular weight is approximately 30 000. It acts on membrane receptors coupled to G proteins of the thyroid epithelial cell by activating adenylcyclase and probably phospholipase C. The stimulation of TSH receptors increases iodine uptake and the synthesis and secretion of thyroid hormones T3 and T4 by activation of the expression of thyroglobulin and thyroid peroxidase. In addition it induces thyrocyte proliferation being able to lead to the formation of a thyroid adenoma.
The secretion of TSH is reduced by thyroid hormones by a negative feedbach mechanism; it is decreased in patients with Graves' disease. The decrease of TSH in plasma is a good marker of hyperthyroidism.
Recombinant human TSH is used in patients after thyroidectomy to improve the localisation of residual thyroid tissue, normal or malignant, by radioactive iodine binding.