Thyroxine or T4 is the main secretion product of the thyroid gland. It is likely that all body cells are target for TH. Thyroid hormones have profound effects in the main physiological processes: development, growth and metabolism. The metabolic effects of TH include increment of the basal metabolic rate and increased heat production. In the fat metabolism, TH stimulates fat mobilization, resulting in increased concentrations of fatty acid in the plasma. In the carbohydrate metabolism, TH is involved in enhancement of insulin-dependent entry of glucose into the cells, gluconeogenesis and glycogenolysis. Furthermore, TH plays an important role in normal growth and in development of fetal and neonatal brain.
Also good functioning of the cardiovascular, reproductive and central nervous system depends on TH. Thyroxine therapy is given to treat hypothyroidism. The mechanism of action: thyroxine enters the cells by a carrier-mediated process. Subsequently, thyroxine is transferred to the nucleus and binds to a specific nuclear thyroid hormone receptor and alters gene transcription by binding to DNA. Treatment of hypothyroidism begins with 25-50 μg levothyroxine daily. This amount is increased every 4-6 weeks by 25 μg until the optimal dose is reached. When the TSH levels are normalized, the dosage of levothyroxine can be maintained. If TSH levels remain increased, the dosage of thyroxine should be increased.
I. The plasma half-life of thyroxine is 1 day.
II. Patients with hypothyroidism and hypertension or cardiovascular problems should begin levothyroxine therapy with a low dosage (12,5-25 mg).
Extra info: The thyroxine half-life is 8 days. Over 99% of the thyroxine binds to the plasma thyroglobulin. This explains the relatively long half-life of thyroxine. Levothyroxine therapy increases the risk of angina, arrhythmias, and myocardial infarction in patients that suffer from cardiovascular insufficiency. Therefore, thyroxine therapy should be given in low doses in these patients.