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Thyroid Disorders and Pregnancy Children’s Hospital of Philadelphia

Thyroid Disorders and Pregnancy Children’s Hospital of Philadelphia

These antibodies are immunoglobulin G proteins that can cross the placenta and cause fetal hyperthyroidism.21333In this special scenario, treatment with a block-and-replace strategy may be warranted. Subclinical hyperthyroidism, as well as gestational thyrotoxicosis, do not require treatment during pregnancy, and rather, observation is recommended with periodic monitoring of thyroid function tests every 4 to 6 weeks. In the last few years, the correlation between maternal thyroid dysfunction during pregnancy and adverse obstetric and perinatal outcomes has been largely investigated.

Hyperthyroidism

Inadequacy is also found in levels of physical and intellectual development and response to environmental stimuli compared to children born to women with normal thyroid functioning throughout their pregnancy. Some clinicians used LT4 treatment for mild SCH pregnant women with TPOAb−, although the recent clinical guideline did not recommend it. In the recent ATA guideline in 2017, LT4 treatment is considered for mild SCH pregnant women with TPOAb positive, but LT4 treatment is not recommended for mild SCH pregnant women with TPOAb− 11. Several randomized controlled trials were carried out to investigate the effect of LT4 treatment in women with mild SCH with TPOAb−, none of these studies have identified beneficial effects on preventing adverse pregnancy and offspring outcomes 12–15. Furthermore, Maraka et al. 16 reported that LT4 treatment may increase the risk of adverse pregnancy outcomes (preterm delivery, gestational hypertension and pre-eclampsia) in mild SCH pregnant women, although lacked information about TPOAb status. Zhang et al. 17 observed increased risks of gestational diabetes mellitus (GDM) in LT4 treated mild SCH women with TPOAb− compared to untreated women and the controls.

  • Treatment for subclinical hypothyroidism is generally recognized to be beneficial in preventing adverse events, particularly pregnancy loss.
  • Pregnant women whose last menstrual period was between May 2016 and April 2019 were included in the study.
  • Thyroxine, the hormone produced by the thyroid gland, is responsible for regulating the body’s metabolism.
  • Longitudinal ultrasound measurements of fetal growth indicators can prospectively reflect the intrauterine fetal growth and better capture the effect of thyroid diseases on fetal growth in a time-sensitive manner.

MeSH terms

  • Failure to adapt to physiological changes results in thyroid dysfunction, especially if complicated by the presence of thyroid antibodies.
  • During the early phase of pregnancy, the hCG hormone has a weak stimulatory effect on the thyroid gland 20.
  • If Graves disease has been previously treated outside of pregnancy with thyroidectomy or ablative therapy, there may be persistent thyroid receptor antibodies.
  • In cases where congenital hypothyroidism is thought to be temporary, the baby’s doctor (endocrinologist) may recommend a trial off levothyroxine treatment after age 3 years (after the time of critical brain development).
  • This condition is characterized by excessive production of thyroid hormones, which can have various effects on the mother and the developing baby.

Current evidence from several species indicates that there is substantial transfer of maternal thyroid hormones across the placenta. In addition to the potential risks to the pregnancy, thyroid disorders can also have long-term effects on the baby’s development. Studies have shown that children born to mothers with untreated thyroid disorders during pregnancy may have an increased risk of cognitive impairments and developmental delays. It may lead to preterm birth (before 37 weeks of pregnancy) and low birth weight for the baby.

  • The main diagnostic indicator of thyroid disease is the measurement of serum thyroid-stimulating hormone and free thyroxine levels.
  • Human fetuses acquire the ability to synthesize thyroid hormones at roughly 12 weeks of gestation, and fetuses from other species at developmentally similar times.
  • In the normal individuals, this does not appear to represent much of a load to the thyroid gland, but in females with subclinical hypothyroidism, the extra demands of pregnancy can precipitate clinicial disease.
  • Before the 20th week of pregnancy, brain development primarily relies on the mother’s thyroid hormone.
  • Your doctor will do periodic thyroid function tests so that the dose of medication can be properly adjusted as your child grows.

Iodide is cleared from the kidneys when the maternal glomerular filtration rate increases. This clearance, together with enhanced thyroxine metabolism, leads to a drop in plasma iodide levels. Due to increased placental deiodinases, T4 metabolism is boosted in the second and third trimesters 2,26.

Hypothyroidism during pregnancy is defined as elevated TSH levels above the population and trimester-specific reference range. This can present as overt hypothyroidism, defined as increased trimester-specific TSH andlow free T4 levels, or subclinical hypothyroidism, defined as increased trimester-specific TSH and normal free T4 levels. Hypothyroidism is diagnosed based on a low free T4 or total T4 and high TSH (except for rare cases of central hypothyroidism where TSH will also be low).

The Benefits of Taking Synthroid During Pregnancy

Some symptoms of hyperthyroidism may include palpitations, excessive sweating, heat intolerance, anxiety, insomnia, weight loss, and tremors. Physical examination findings may include tachycardia, lid lag, stare, diaphoresis, and hyperreflexia. Findings specific to Graves disease include diffuse goiter, ophthalmopathy (exophthalmos), and pretibial myxedema. See the American Academy of Pediatrics (AAP) policy statement, Update of Newborn Screening and Thereapy for Congenital Hypothyroidism, for more information.

Hashimoto’s disease, an autoimmune disorder, is one of the most common reasons for primary hypothyroidism in which the thyroid is attacked by its own body’s immune system interfering with the normal functioning of the thyroid hormones 1,12. It needs careful management as this abnormality can hinder mental development and may cause compressive goiter in infants. In morphological thyroid disorders, the problem is usually differentiated thyroid cancer, as its frequency of growth is higher during pregnancy. Its consequences are aggravated and enhanced by the thyroid-stimulating hormone (TSH), like the effect of the human chorionic gonadotropin (hCG) hormone 4,14. About 20 years ago, many endocrinologists brought the effects of maternal thyroid hormone deficiency to public attention 15. In 1999, it was demonstrated that a child’s neurodevelopment might be severely affected if hypothyroidism is left untreated in pregnant women 16.

As the thyroid hormone can cross the placenta in the first trimester, the fetus depends on its mother for hormone transport 19. During the early phase of pregnancy, the hCG hormone has a weak stimulatory effect on the thyroid gland 20. As a result, the maternal serum thyrotropin (TSH) levels decrease, which then subsequently increase. Consequently, maternal serum thyrotropin (TSH) levels fall, followed by a rise in free thyrotropin levels 21,22.

For this reason, thyroid dysfunction is a common condition in preterm infants and can be linked to several factors. First, there are physiological conditions related to prematurity, that include immaturity of the hypothalamic-pituitary-thyroid axis, impairment of thyroid ability to concentrate and synthesize iodine, and immaturity of the metabolic pathways in the thyroid. Then, preterm newborns have greater demand for thyroid hormones for thermogenesis and dealing with diseases related to prematurity. Williams et al showed that typical diseases of preterm, e.g. respiratory distress syndrome (RDS), sepsis, intra ventricular hemorrhage (IVH), may alter thyroid function through inflammatory response.

Figure 1. Screening and the number of articles included in the final review.

Screening and the number of articles included in the final synthroid awp review are summarized in Figure 1. Levothyroxine remains the gold-standard in the treatment of pregnant patients with hypothyroidism worldwide. Fortunately, close and tight management of thyroid disease within the fluctuating physiologic milieu of pregnancy offers opportunities to significantly improve perinatal outcomes.

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