Overview of Congenital Hypothyroidism | Endocrinology

Congenital Hypothyroidism

What is congenital hypothyroidism?

Congenital hypothyroidism (CHT) is a deficiency or underdeveloped thyroid gland (dysgenesis) or inability to produce thyroid hormone due to a “production line” problem (dyshormonogenesis). Children with CHT cannot make enough thyroid hormones for their bodies ‘ needs. The word “congenital” means condition at birth.

Congenital hypothyroidism, formerly known as creatinine, is a serious deficiency of thyroid hormone in newborns. It causes impaired nerve function, growth retardation, and physical disability. This condition is caused by a problem with the baby’s thyroid gland or a lack of iodine in the mother’s body during pregnancy.

The baby’s body needs iodine to make thyroid hormones. These hormones are essential for healthy growth, brain development, and nervous system development. Between 1 in 2,000 and 1 in 4,000 reliable babies are born with congenital hypothyroidism.

The introduction of iodized salt in the early 1900s made congenital hypothyroidism very rare in the United States and the rest of the Western world. However, severe iodine deficiency is still common in developing countries.

Symptoms of congenital hypothyroidism

Symptoms of congenital hypothyroidism are not usually apparent in the first week of life.

  • Bad nutrition
  • Excessive sleep
  • Weak cry
  • Constipation
  • Chronic jaundice after birth (yellow skin)

In these babies, the doctor may find a larger tongue with a swollen face, muscle strength and abdomen, and a larger tongue than the normal fontanelles (soft spots) on the head.

Causes of congenital hypothyroidism

Congenital hypothyroidism in newborns can be caused by:

  • The missing, malformed, or abnormally small thyroid gland
  • A genetic defect that affects thyroid hormone production.
  • Too little iodine in the mother’s diet during pregnancy.

Use of medications that interfere with the production of thyroid hormones during pregnancy, such as antithyroid medications, sulfonamides, or lithium. Iodine deficiency due to the introduction of iodized salt is not considered a health hazard in the United States. However, it remains the most reliable source of impaired neurological function in the world.

Since our bodies do not make iodine, we need to get it from food. Iodine enters the diet through the soil. The soil in some parts of the world is iodine deficient Globally, iodine deficiency is the most common cause of congenital hypothyroidism, but in the more developed world and in areas with sufficient ambient iodine, cases occur due to a combination of known and unknown causes.

The most common is a defect in the development of the thyroid gland, resulting in atherosclerosis or an underdeveloped (hypoplastic) gland. However, recent studies have shown an increase in the number of cases caused by the sweat gland (called dyshormonogenesis when there is a defect in the production of hormones). The hypoplastic gland also develops mainly on the neck or the back of the tongue. The gland in the wrong place is called ectopic, and the ectopic gland at the base or back of the tongue is a lingual thyroid.

Some of the causes of abnormal gland development are caused by genetic defects and some are “scattered” for no apparent reason. Neonatal hypothyroidism has been reported in infants exposed to lithium, a mood stabilizer used to treat bipolar disorder in utero. In some cases, hypothyroidism detected by screening tests can be unstable. A common cause of this is the presence of maternal antibodies, which can temporarily alter thyroid function for several weeks.

Usually due to iodine deficiency from birth with low iodine levels in soil and local food sources. The term, like many other 19th century medical terms, has pejorative meanings as used in Le Speech. It has now been removed, the ICD-10 uses the “congenital iodine deficiency syndrome” with a variety of additional specifiers.

Diagnosis of congenital hypothyroidism

In the developed world, almost all cases of congenital hypothyroidism are detected by the neonatal screening program. These depend on the level of TSH or thyroxine (T4) in the second or third day of life.

Treatment of congenital hypothyroidism

The goal of neonatal screening programs is to identify and begin treatment within the first 1-2 weeks of life. Treatment consists of a daily dose of thyroxine, which is available as a small tablet. The common name is levothyroxine and there are several brand names available. The tablet is crushed and given to the baby with a small amount of water or milk.

The general recommended dose range is 10 to 15 μg / kg per day, usually 12.5 to 37.5 or 44 44 g. Within a few weeks, T4 and TSH levels are rechecked to make sure treatment brings them back to normal. As the child grows, these levels are checked periodically to maintain the proper dose. The dose increases as the child grow.

Prevention of congenital hypothyroidism

Congenital hypothyroidism is more common in developing countries where iodine deficiency is common. Adults can prevent iodine deficiency by receiving an Institute of Medicine recommended dietary allowance (RDA) of 150 micrograms per day.

Since iodine deficiency during pregnancy is dangerous for the growing baby, pregnant women are advised to take 220 micrograms of iodine daily. The American Thyroid Association recommends that all pregnant or nursing women take a prenatal vitamin that contains at least 150 micrograms of iodine daily.

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