Thyroid Growth Factors

The effect of exogenous and endogenous factors on the thyroid is manifested as stimulation or inhibition of the gland's excretory activity and growth regulation of the thyroid tissue itself. External factors affecting thyroid enlargement were known as early as approximately 2000 years B.C. in ancient China, where marine products were administered to inhabitants of the central part of the country. This specific supplementation of iodine-rich products prevented goiter development. [1,2] In modern times, the first country to introduce iodine prophylaxis was Switzerland, followed by the United States. Poland has been implementing a program of common salt iodization since 1986, albeit with an interruption of less than a score of years. We presently know than apart from iodine, there are numerous factors that affect regulation of thyroid secretion and growth. Thyroid homeostasis is thus controlled by several different substances acting on various levels: directly and indirectly by thyrotropin TSH (thyroid stimulating hormone); locally by other growth stimulators, such as the epidermal growth factor (EGF), transforming growth factor alpha (TGF-┙), insulin growth factors (IGFs), fibroblast growth factors (FGFs), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF) and transforming growth factor beta (TGF-┚), as well as through programmed cell death in the mechanism of apoptosis. Hence, changes in thyroid size and hormone demand occur mostly through TSH and complex interactions of local growth factors with expression of specific receptors. It has been also observed recently that paraand autocrine effects of growth factors are also associated with expression of particular oncogenes. Except the embryonal and adolescent periods, the volume of a normal thyroid gland does not increase. Each thyroid follicular cell is programmed to undergo five mitotic cycles during adult life and the final population of thyrocytes demonstrates specific differentiation, manifested by hormone secretion in response to thyrotropin via the mechanism of negative feedback. Thus, participation of the thyroid gland in hemostasis is regulated via hormonal, neural and immune pathways. The first level of thyroid growth and function control occurs via the effect of thyrotropin (TSH). The second level of tissue hemostasis is controlled by local factors. The third level consists of interactions between thyroid cells and connective tissue stroma, while the fourth level includes genetic factors with programmed death cell (apoptosis).