Changes in the function of the thyroid gland during pregnancy
Pregnancy is a period that in the best of times creates great physiological stress, both for the mother and for the fetus. However, if pregnancy is complicated by endocrine disorders, such as hypothyroidism, the potential for adverse outcomes in the mother and fetus can be enormous. Hypothyroidism is widespread among pregnant women, and the detection rate, especially in a developing country, does not lag behind the scale of the problem. Since hypothyroidism is easily treated, timely detection and treatment of the disorder can reduce the burden on unfavorable fruit and maternal outcomes, which are very common.
Thyroid dysfunction during pregnancy is common with a frequency of 2% -4%. Thyroid dysfunction in the mother is associated with an increased risk of various adverse maternal and child outcomes, including miscarriage, intrauterine growth retardation, hypertension, premature birth, and decreased IQ of the child. During pregnancy, profound changes in the physiology of the thyroid gland occur to provide a sufficient level of the thyroid hormone, for both the mother and the fetus. This is especially important during the early pregnancy, because the fetal thyroid begins to produce significant amounts of TSH only from about 20 weeks of pregnancy, until the fetus is highly dependent on the maternal hormone level. This suppression of the synthesis of thyroid hormones in the fetus, as well as an increased concentration of hormone binding proteins (thyroxine-binding globulin) and T4 degradation by placental iodothyronine deiodase 3, require an increase in the production of the maternal thyroid hormone. This requires a healthy thyroid gland in the mother and adequate accessibility of dietary iodine. As a consequence, the concentration of free thyroxines in the blood serum (FT4) increases, and the concentrations of TSH decrease from about the eighth week during the first half of pregnancy, which leads to different control intervals for TSH and T4 compared to the non-pregnant state.
Given these pregnancy-related changes in the physiology of the thyroid and complications associated with thyroid dysfunction, it is important to determine the control intervals for normal thyroid function during pregnancy. This is crucial for identifying women who need treatment or correction of thyroid function.
Non-diagnosed dysfunction of the thyroid gland can be a problem. While much attention has been focused on unfavorable results of the fetus associated with hypothyroidism, attention is also gradually directed to the unfavorable maternal outcomes of this disorder. Quick diagnosis and treatment of hypothyroidism during pregnancy is very important. Subclinical hypothyroidism also needs to be identified and treated to prevent adverse outcomes, especially maternal ones. Since women with hypothyroidism during pregnancy, especially an autoimmune variety, may have an outbreak after childbirth or may continue to require replacement of thyroxine after delivery, adequate monitoring is mandatory. And even if the woman before pregnancy was absolutely healthy and never had thyroid disorders, such problems can appear in her even against the background of a normal pregnancy.
The physiology of the thyroid gland changes markedly during normal pregnancy. These changes occur throughout the entire pregnancy, help prepare the maternal thyroid to cope with the metabolic needs of pregnancy, are reversible after delivery.
The most noticeable change is the increase in thyroxin-binding globulin (TSH). It starts at the beginning of the first trimester, plateau during the mean time and persists until the birth. This is due to the stimulation of the synthesis of TSH by elevated levels of estrogen in mothers and, more importantly, due to a decrease in hepatic clearance of TSH due to estrogen-induced sialing. This increased concentration of TSH leads to a broadening of the pool and leads to increased total levels of T3 and T4 due to an increase in the synthesis of the thyroid hormone in the mother. Synthesis of thyroid hormones in the mother is also increased because of the accelerated renal clearance of iodide as a result of an increase in the rate of filtration of the glomerular tissue.
The increased metabolism of T4 in the second and third trimesters, due to the growth of placental type II and type III deiodinases, which turn T4 into T3 and T4 in the opposite direction of T3 and T2, act as an additional impulse to T4 synthesis. Iodide levels in the plasma are reduced due to an increase in thyroxine metabolism and an increase in the clearance of kidney iodide. All these changes lead to an increase in the size of the thyroid gland in 15% of pregnant women, which returns to normal in the postpartum period.
HCG serum has its own thyrotropic activity, which increases after fertilization and peaks in 10-12 weeks. Consequently, in the first trimester free levels of T3 and T4 increase slightly, and levels of TSH decrease in the first trimester with an adjustment in the second and third trimesters, when the levels of hCG decrease.
How does TSH affect pregnancy? Given that its level is slightly reduced by the principle of feedback in the first trimester, its effect is also slightly reduced. But the synthesis of this hormone persists, and it affects not only the body of a woman, but the thyroid gland of a child who is actively developing.
Fetal thyroid gland develops up to 7 weeks of pregnancy. Fetal gland is capable of catching iodine at week 12 and can synthesize thyroxine at week 14 of pregnancy. However, significant secretion of hormones is not observed until 18-20 weeks of pregnancy. After this, embryonic TSH, T4 and TSH gradually increase to the adult population at 36 weeks of gestation. Transmission of TSH through the placenta is negligible, but transport of T3 and T4 can be significant.
Thus, it can be concluded that the maternal thyroid gland functions as a fetus before a certain period of pregnancy. Therefore, the mother herself may have different thyroid insufficiency, especially if she had hypothyroidism or hyperthyroidism before . The control of thyroid function during pregnancy is very important, because even a clinically insignificant malfunction in the mother of the thyroid gland can cause serious cognitive impairment and developmental disorders in the child.
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Control of thyroid function during pregnancy
Uncovered maternal hypothyroidism can lead to premature birth, low birth weight and respiratory distress in newborns. Over the years, enough evidence has been accumulated about the role of thyroxine in the normal development of the fetal brain. The presence of specific nuclear receptors and thyroid hormones found in the fetal brain at week 8 of pregnancy, free T4, found in coelomic and amniotic fluids, and the demonstration of the transmission of thyroid hormones in the mother through the placenta, emphasize the role of thyroid hormones in the development of the fetal brain. Complex interactions between iodothyronine deiodases D2 and D3 during pregnancy help to accurately adjust the amount of adequate T3 required for normal brain development.
Therefore, not always clinically a woman can manifest hypothyroidism, while there is a lack of hormones. Therefore, in pregnant women, indications for screening of thyroid function deficiency are expanded.
The prevalence of hypothyroidism during pregnancy is estimated at 0.3-0.5% for open hypothyroidism and 2-3% for subclinical hypothyroidism. Autoimmune thyroiditis is the most common cause of hypothyroidism during pregnancy. However, throughout the world, the lack of iodine is still one of the leading causes of hypothyroidism, both explicit and subclinical.
Hypothyroidism during pregnancy is usually asymptomatic, especially with subclinical form. Signs and symptoms that indicate hypothyroidism include inadequate weight gain, cold intolerance, dry skin and a delay in the relaxation of deep tendon reflexes. Other functions, such as constipation, fatigue and drowsiness, are usually attributed to pregnancy.
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How to increase TTG in pregnancy?
Medications known as antithyroid drugs - metamizole are used for this purpose. These drugs act by blocking the ability of the thyroid gland to produce new thyroid hormones. This will reduce the number of peripheral hormones and, on the basis of feedback, increase the TSH level to normal.
TTG in pregnancy twins has some differences from single-pregnancy. The increase in thyroid activity in the first trimester is deeper with twins than with single pregnancy. This is due to the fact that in a double pregnancy the level of chorionic gonadotropin (hCG) increases significantly, and this depresses the production of TSH. Therefore, when double the level of TSH is lower, and the risk of hypothyroidism with such a pregnancy increases, what should be considered when conducting such a pregnancy.
Thyroid disease is the second most common endocrine disorder affecting women during pregnancy. The untimely detection of thyroid gland pathology during pregnancy is associated with an increased risk of miscarriage, placental abruption, hypertensive disorders and restriction of child's growth. Therefore, it is recommended to screen high-risk women, including those with thyroid disease, by determining the level of TSH during pregnancy, even in the absence of a clinic.