Thyroid Hormones

In the follicles of the thyroid gland, triiodothyronine (T3) and thyroxine (T4) are synthesised through iodination of the amino acid thyronine. The required iodine must be obtained from the diet. T3 and T4 are secreted into the peripheral bloodstream in a ratio of approximately 1:10, where more than 99% of them are bound to serum proteins. However, only the unbound, free forms – fT3 or fT4 – can enter target cells, with fT3 being the metabolically active hormone. While T4 is produced exclusively in the thyroid gland, around 80% of T3 is generated peripherally by conversion from T4. As this deiodination occurs predominantly in the liver, it is understandable why liver dysfunction can impact thyroid hormone metabolism. Reverse T3 (rT3) is a biologically inactive metabolite, primarily formed when the demand for thyroid hormones is low or when a T4-to-T3 conversion disorder occurs. Through rT3 analysis, combined determination of total T3 (TT3) and calculation of the TT3/rT3 ratio provides enhanced sensitivity for advanced thyroid diagnostics. This allows clear indications of a conversion disorder, which can be clinically relevant in non-thyroidal illnesses or ineffective T4 monotherapy. Another important hormone is TSH (thyroid-stimulating hormone, thyrotropin), which is produced by the pituitary gland. It stimulates the growth, iodine uptake, and hormone production of the thyroid gland.

Additionally, the measuring of antibodies involved in thyroid activity can provide diagnostic support. TSH receptor autoantibodies (TRAK) can bind to the TSH receptor and trigger various clinical symptoms. Thyroid peroxidase antibodies (TPO-Ab) are directed against thyroid peroxidase and indicate the presence of autoimmune thyroid diseases.