Hyperthyroidism: Finding the Right Drug Therapy

Methimazole

Mechanism of action

The drug methimazole is a thyrostatic (antithyroid) compound that inhibits the production of excessive hormones in a pathologic thyroid gland. The drug inhibits the iodination of thyroglobulin, process that is catalyzed by the enzyme thyroperoxidase (Fumarola, Di Fiore, Dainelli, Grani & Calvanese, 2010). Iodine facilitates the addition of iodide solution to the residues of tyrosine on thyroglobulin, a precursor of the two hormones T3 and T4 (Kittisupamongkol, 2009). As such, the drug inhibits the formation of the thyroid hormones T3 and T4.

Pharmacological effects

In normal circumstances, the drug is easily absorbed in the gastrointestinal tract and metabolized in the liver system. Methimazole also interacts with a number of other drugs to produce adverse effects. For instance, it interacts with anticoagulants such as digoxin, warfarin and theophylline as well as some vitamins. It also inhibits all enzymes with CYP450, meaning that it has the potential to increase the plasma concentration of all drugs metabolized in the liver (Fumarola, et al., 2010).

Place in therapy

Methimazole is an antithyroid drug (thyrostatic) used to inhibit the production of hormones T3 and T4. Therefore, it is used to manage the condition rather than treat the causes.

Propylthiouracil

Mechanism of action

Propylthiouracil (PTU or 6-n-propylthiouracil) is an effective drug for treating hyperthyroidism as well as Grave’s disease. The drug inhibits enzyme thyroperoxidase in order to decrease the production of hormones T3 and T4. It also acts through the inhibition of tetraiodothyronine 5’ deiodinase, an enzyme actively involved in the conversion of T4 to T3 (Siraj, 2008).

Pharmacological effect

Once taken orally, the drug achieves its peak concentration in the serum after one hour. At this point, it is concentrated in the thyroid gland. More than 70% of the drug is bound to proteins but can be transferred across the placenta in pregnant individuals (Kittisupamongkol, 2009). It has a plasma half-life of one hour, but it may last for 8 hours due to the concentration in the glands rather than in the serum (Kittisupamongkol, 2009).

Place in therapy

As described above, the drug is an antithyroid compound used to manage the condition. However, it is more effective than methimazole because it manages Grave’s disease.

Radioiodine (Iodine-131 or 131I)

Mechanism of action

The compound is a radioisotope of iodine with a decay half-life of 8 days (Fumarola, et al., 2010). It acts by destroying or severely restricting the function of the pathologic thyroid glands. It targets and damages the pathologic tissues of these glands and must be given orally on a one-time basis.

Pharmacological effect

Once administered orally, the compound is readily picked by thyroid glands, although this is not exclusive of some other tissues. Specifically, the over-active thyroid cells of the gland absorb the compound. Therefore, the destruction and restriction is a local function (Fumarola, et al., 2010).

Place in therapy

Radioiodine is an important compound for radioactive therapy required to treat the excessive production of thyroid hormones. It also treats and manages Grave’s disease as well.

Iodide

Mechanism of action

Iodine solutions such as potassium iodide-iodine and saturated potassium iodide are some of the iodine compounds used in the management of hyperthyroidism and Grave’s disease. Iodine derived from these compounds actively inhibits the secretion of hormones T3 and T4 in thyroid glands. It also inhibits the synthesis of the thyroid hormone through a temporary inhibition of iodine organification in the glands.

Pharmacological effects

After oral administration, iodine is concentrated in thyroid glands. It targets the pathologic cells of the thyroid, where it is easily picked and accumulated. The inhibition of synthesis of thyroid hormones is transient, with the production resuming after two weeks.

Place in therapy

As indicated above, the compound is used in the management of hyperthyroidism by specifically targeting the pathologic cells of thyroid glands.

References

Fumarola, A., Di Fiore, A., Dainelli, M., Grani, G., & Calvanese, A. (2010). Medical treatment of hyperthyroidism: state of the art. Experimental and clinical endocrinology & diabetes 118(10), 678–84

Kittisupamongkol, W. (2009). Hyperthyroidism or thyrotoxicosis? Cleve Clin J Med, 76(3), 152.

Siraj, E. S. (2008). Update on the Diagnosis and Treatment of Hyperthyroidism. Journal of Clinical Outcomes Management 15(6), 298–307.

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