Iodine in the urine
Last reviewed: 23.04.2024
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The reference values (norm) of iodine excretion in the urine are 100-500 μg / l.
Iodine is a trace element present in nature in trace amounts. In drinking water, the content of iodine is insignificant, so the bulk of this trace element enters the human body with food. The highest concentration of iodine in seafood (approximately 800 mcg / kg); especially rich in iodine seaweed. A lot of iodine in fish oil. Usually sources of iodine in the body are milk, eggs, meat and grains. The required daily intake of iodine depends on the person's age, amounting to 40 mcg / day in infants and 150 mcg / day for adults. During pregnancy, the need for iodine increases to about 200 μg / day.
Iodine, supplied with food in the body in the form of iodide, is absorbed into the digestive tract. From the blood, it easily penetrates into various organs and tissues, partially deposited in lipids. The most significant part of iodine (up to 10-20%) is selectively absorbed by the thyroid gland. Isolation of iodine from the body is carried out mainly by the kidneys (up to 70-90%).
After entering the blood, inorganic iodine is actively captured by the thyroid gland, where its concentration is 30-40 times higher than that in the blood. The iodide concentrated in the thyroid gland is oxidized to molecular iodine, which quickly binds to the remains of thyroglobulin, forming monoiodotyrosine and diiodotyrosine (iodine phase). During the condensation phase, two diiodotyrosines combine to form T 4 or one mono- and one diiodotyrosine to form T 3. The main factor regulating the synthesis of thyroid hormones is the thyroid-stimulating hormone (TSH). It affects all stages of iodine metabolism: it strengthens the ability of the thyroid gland to concentrate iodine from the blood, accelerates iodination and the formation of hormones from the thyroglobulin molecule, changes iodination sites in thyroglobulin with the predominant formation of T 3 and activates cysteine proteinases and cathepsins that break down thyroglobulin.
With iodine deficiency in the body, the production of thyroid hormones becomes insufficient, which has a multitude of consequences, combined by the term "iodine deficiency states". Such consequences include goitre, hypothyroidism, developmental delay, reproductive disorders, etc.
Up to 90% of the ingested iodine appears in the urine, so the excretion of iodine in the urine correlates with iodine supply. Concentration of iodine in urine can serve as an indicator that adequately reflects its consumption. Numerous studies have shown that the concentration of iodine in a single portion of urine correlates well with the level of iodine in daily urine. Nevertheless, iodine levels in individuals change daily and even during the day and therefore can not reflect the provision of iodine to the population as a whole. The analysis for iodine in urine is suitable only for epidemiological studies. The minimum number of samples should be at least 60. Due to the very uneven distribution of iodine levels in the urine of the subjects, it is better to evaluate the median excretion of iodine in the urine rather than the mean. If the median exceeds 100 mcg / l, there is no iodine deficiency in this population.
The International Committee on iodine deficiency disorders and WHO allocates three severity levels of iodine deficiency median for urine iodine levels: 99-55 μg / l - mild; 49-20 μg / l - moderate; less than 20 μg / l - heavy. When an excess amount of iodine enters the body of a person with normal thyroid function, the synthesis of thyroid hormones decreases transiently (about 48 hours). The acute inhibitory effect of iodine on the synthesis of thyroid hormones is called the Wolf-Chaikoff effect and is associated with an increase in iodine concentration in the thyroid gland itself. Then, despite the continued intake of large amounts of iodine, the synthesis of thyroid hormones is restored, providing an euthyroid state (due to a decrease in the capture of iodide by the gland). Despite the existence of such an adaptive mechanism, an excess of iodine may cause hypothyroidism with or without goitre in susceptible individuals, as well as hyperthyroidism.
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