Thyroid Hormone Therapy

Thyroid hormones accelerate metabolism. Their release (A) is regulated by the hypophyseal glycoprotein TSH, whose release, in turn, is controlled by the hypothalamic tripeptide TRH. Secretion of TSH declines as the blood level of thyroid hormones rises; by means of this negative feedback mechanism, hormone production is "automatically" adjusted to demand.

The thyroid releases predominantly thyroxine (T4). However, the active form appears to be triiodothyronine (T3); T4 is converted in part to T3, receptor affinity in target organs being 10-fold higher for T3. The effect of T3 develops more rapidly and has a shorter duration than does that of T4. Plasma elimination t1/2 for T4 is about 7 d; that for T3, however, is only 1.5 d. Conversion of T4 to T3 releases iodide; 150 jig T4 contains 100 jig of iodine.

For therapeutic purposes, T4 is chosen, although T3 is the active form and better absorbed from the gut. However, with T4 administration, more constant blood levels can be achieved because degradation of T4 is so slow. Since absorption of T4 is maximal from an empty stomach, T4 is taken about V2 h before breakfast.

Replacement therapy of hypothyroidism. Whether primary, i.e., caused by thyroid disease, or secondary, i.e., resulting from TSH deficiency, hypothy-roidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocar-dial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 150 jg/d).

Thyroid suppression therapy of euthyroid goiter (B). The cause of goiter (struma) is usually a dietary deficiency of iodine. Due to an increased TSH action, the thyroid is activated to raise utilization of the little iodine avail able to a level at which hypothyroidism is averted. Therefore, the thyroid increases in size. In addition, intrathyroid depletion of iodine stimulates growth.

Because of the negative feedback regulation of thyroid function, thyroid activation can be inhibited by administration of T4 doses equivalent to the endogenous daily output (approx. 150 jg/d). Deprived of stimulation, the inactive thyroid regresses in size.

If a euthyroid goiter has not persisted for too long, increasing iodine supply (potassium iodide tablets) can also be effective in reversing overgrowth of the gland.

In older patients with goiter due to iodine deficiency there is a risk of provoking hyperthyroidism by increasing iodine intake (p. 247): During chronic maximal stimulation, thyroid follicles can become independent of TSH stimulation ("autonomic tissue"). If the iodine supply is increased, thyroid hormone production increases while TSH secretion decreases due to feedback inhibition. The activity of autonomic tissue, however, persists at a high level; thy-roxine is released in excess, resulting in iodine-induced hyperthyroidism.

lodized salt prophylaxis. Goiter is endemic in regions where soils are deficient in iodine. Use of iodized table salt allows iodine requirements (150300 jg/d) to be met and effectively prevents goiter.

Hypothalamus

Hypothalamus

Thyroid

Effect Thyroid Hormornes Cells

L-Thyroxine, Levothyroxine, 3,5,3',5'-Tetraiodothyronine, T4

Liothyronine

3,5,3'-Triiodothyronine, T3

Thyroid

L-Thyroxine, Levothyroxine, 3,5,3',5'-Tetraiodothyronine, T4

Liothyronine

3,5,3'-Triiodothyronine, T3

Effector cell: receptor affinity

Blood Pressure Health

Blood Pressure Health

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