Iodine deficiency refers to a group of interrelated disorders caused by inadequate iodine intake due to environmental iodine deficiency. These include endemic goiter, cretinism, subclinical cretinism, simple deafness, and other related conditions. Iodine is present in trace amounts in soil, water, plants, and animals, and insufficient iodine intake in the diet is typically a consequence of environmental iodine deficiency. The most significant impact of iodine-deficiency-induced hypothyroidism is on brain development, making fetuses, neonates, and young children the most vulnerable.
Etiology
The root cause of iodine deficiency lies in inadequate iodine content in food and drinking water. Deficient iodine intake leads to impaired synthesis of thyroid hormones, which affects physical growth and brain development.
Clinical Manifestations
The severity of clinical manifestations depends on the degree of iodine deficiency, the duration of deficiency, and the age of the affected individual. Pregnant women with iodine deficiency may experience fetal stillbirths, premature births, and congenital malformations. Iodine deficiency during the neonatal and early childhood stages may lead to hypothyroidism, with severe cases resulting in cretinism. Symptoms of cretinism include delayed mental development, intellectual disability, hearing loss, and growth impairment. In older children, iodine deficiency may cause endemic goiter and endemic hypothyroidism, with primary symptoms including intellectual impairment and growth retardation. Chronic mild iodine deficiency in children may result in subclinical hypothyroidism, often accompanied by delayed physical growth.
Laboratory Findings
Assessment of iodine nutritional status in individuals and populations can be carried out using indicators such as the degree of thyroid enlargement, urinary iodine levels, plasma thyrotropin (TSH), and others. The evaluation of thyroid gland size can be conducted through palpation or ultrasonography, with ultrasonography being the definitive diagnostic method if discrepancies arise between the two approaches.
Urine iodine concentration serves as a reliable indicator for assessing iodine status in populations:
- <20 µg/L: Severe iodine deficiency
- 20–49 µg/L: Moderate iodine deficiency
- 50–99 µg/L: Mild iodine deficiency
- 100–199 µg/L: Normal
- 200–299 µg/L: Above normal range
- ≥300 µg/L: Excessive iodine intake
Whole blood TSH levels are an indirect indicator of iodine nutritional status and can be used to screen for neonatal hypothyroidism. The normal range for TSH in whole blood is <10 mU/L.
Treatment
Iodine Preparations
Iodine preparations are primarily recommended for cases of severe diffuse goiter caused by iodine deficiency with a short disease duration. Compound iodine solution (approximately 3.5 mg of iodine per 1–2 daily drops) or potassium (sodium) iodide (10–15 mg daily) can be administered. A treatment course lasts for two weeks, with a three-month interval between successive courses, and repeated treatment over the course of one year may be necessary. Long-term use of large doses of iodine preparations should be monitored for the potential development of hyperthyroidism.
Thyroid Hormone Preparations
Details on thyroid hormone preparations are discussed under congenital hypothyroidism.
Prevention
The use of iodized salt is a simple, effective, and globally implemented measure for preventing iodine deficiency.
Iodine supplementation among women of childbearing age and pregnant women helps prevent iodine deficiency during fetal development.