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Iodine Supplementation in Pregnant Women

In European countries with access to iodized salt, pregnant women and women planning a pregnancy should receive an iodine supplements containing approximately 150 μg/day. However, iodine supplementation should be implemented to prevent a development of maternal thyroid failure during pregnancy, iodine intake must be maintained at a safe level. Both iodine deficiency and iodine excess can cause not only maternal thyroid failure but also transient congenital hypothyroidism in infants. In 2007, WHO Technical Consultation first recommended both a low (250 µg/day) and upper (500 µg/day) limit of iodine intake for pregnant and lactating females. Pregnant and breastfeeding women are recommended to take prenatal vitamin-mineral supplements containing iodine in the form of potassium iodide (KI). Kelp and seaweed-based products, because of unacceptable variability in their iodine content, should be avoided. Prenatal supplement manufacturers should be encouraged to include adequate iodine in their products. Professional organizations should influence evolving EU legislation to ensure optimal doses for iodine in prenatal vitamin-mineral supplements.

Different Iodine Fortification of Salt in Various Countries

The daily iodine intake varies widely throughout the world. US iodized salt contains 46–77 ppm (parts per million), whereas in the UK the iodine content of iodized salt is recommended to be 10–22 ppm. Table salt in Italy is iodized at 30 ppm, which is typical of many European programs. Although iodine consumption is generally lower in Europe, the people in these countries do not usually develop thyroid disease. However, when people with past or present thyroid abnormalities are exposed to unaccustomed, large amounts of iodine (such as moving to North America and increasing their iodine intake), they can develop thyroid disease.

Iodine Supplements in the Treatment of Hypothyroidism

If iodine deficiency isn’t the cause of hypothyroidism, then iodine supplements provide no benefit. Hashimoto’s thyroiditis, also known as chronic autoimmune hypothyroidism, is the most common cause of hypothyroidism in the United States and is not caused by iodine deficiency. More than adequate or excessive iodine intake may lead to iodine-induced hypothyroidism, autoimmune thyroiditis and may increase the severity of existing autoimmune thyroiditis especially for susceptible populations with recurring thyroid disease, the elderly, fetuses, and neonates. Therefore, if there is anybody who shouldn’t take iodine, it is thyroid patients.

Drugs That Suppress TSH or Cause Central Hypothyroidism

A small subset of medications including glucocorticoids, dopamine agonists, somatostatin analogs and rexinoids affect thyroid function through suppression of TSH in the thyrotrope or hypothalamus. This decrease is less pronounced than the TSH suppression that occurs in hyperthyroidism. These medication effects can be difficult to distinguish from the changes of non-thyroidal illness in the setting of severe illness, where many of these medications are frequently used. Fortunately, most of these medications do not cause clinically evident central hypothyroidism. However, a newer class of nuclear hormone receptors agonists, called rexinoids, cause clinically significant central hypothyroidism in most patients and dopamine agonists may exacerbate ‘hypothyroidism’ in patients with non thyroidal illness.

Drugs That May Cause Protein-Binding Site Replacement And Drugs That May Either Increase Or Decrease Serum TBG-Concentration

Levothyroxine has a narrow therapeutic index and being a drug that is administered in chronic form; there is a high risk of its interaction with different drugs that could be simultaneous administration with it when it is under use for the treatment of hypothyroidism. Levothyroxine in different steps of its pharmacokinetic could interact with various drugs.
Because thyroid hormone is highly protein bound, medical conditions that alter the amount of binding hormones and drugs that compete for binding may change the amount of available free thyroid hormone. The thyroid replacement dosage must be changed in response to both alterations in binding status and alterations in amounts of transport proteins.