Analysis of TSH in pregnancy in 1, 2 and 3 trimester: interpretation of indicators

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Last reviewed: 23.04.2024

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TTG in pregnancy may not be as important as under normal conditions. Thyroid function control is very important for healthy women and women with already existing thyroid dysfunction. After all, the development of the child depends on the function of many organs of the woman, including the function of the thyroid gland.

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Indications for the procedure of the analysis of TTG in pregnancy

Indications for screening for TSH levels are the appearance of symptoms that are characteristic of hypothyroidism: drowsiness, inadequate weight gain, the appearance of tight edema, and trophic skin disorders. If there are such symptoms, then it is a clinical form of hypothyroidism in pregnant women, which means that the examination in such cases is mandatory. But what to do if the course of hypothyroidism is subclinical. In such cases, if a woman wants to give birth to a healthy child, the methods of planning a healthy pregnancy should come first. Examinations before pregnancy at mum in such cases should include and screening of function of a thyroid gland.

TTG in planning pregnancy can become a screening test that will determine whether there are violations in women. Norm TTG when planning pregnancy should be within 0.4-4.0 mIU / l. If a woman has problems with the thyroid gland or she is taking treatment for thyroid pathology, then the TSH level when planning pregnancy should not exceed 2.5 mIU / l. This level will allow to implant the embryo and develop normally.

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Preparation for this analysis has no specific instructions. The day before the survey, it is not recommended to drink alcohol, nicotine and medicines. If a woman uses thyroxine or other drugs to treat the function of the thyroid gland, then for a day you need to stop taking them.

How to take TTG during pregnancy? This is done in the laboratory in the morning on an empty stomach. Venous blood sampling is carried out with subsequent examination for several days.

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Technique of the analysis of TTG in pregnancy

Determination of serum or plasma levels of thyroid-stimulating hormone (TSH) is recognized as a sensitive method in the diagnosis of primary and secondary hypothyroidism. TTG is excreted by the anterior pituitary gland and stimulates the production and release of thyroxine and triiodothyronine of the thyroid gland. Although the concentration of TSH in the blood is extremely low, it is enough to serve the normal function of the thyroid gland. The release of TSH is regulated by TTG-Releasing Hormone (TRH) produced by the hypothalamus. The levels of TTG and TRH are inversely related to the level of thyroid hormones. When there is a high level of thyroid hormones in the blood, a smaller amount of TGH is released by the hypothalamus, so less TSH is released by the pituitary gland. The opposite effect will occur when there is a decrease in the thyroid hormones in the blood. This process is known as a negative feedback mechanism and is responsible for maintaining the proper levels of these hormones in the blood.

Normal performance

Norm TTG during pregnancy in trimester has differences, which is associated with different levels of synthesis of T3 and T4 throughout pregnancy. Different indicators may differ in different laboratories, but there are average recommended levels of TSH levels at different times:

  1. TTG in pregnancy in the first trimester should be in the range of 0.1 - 2.5 mIU / l;
  2. TTG in pregnancy in the second trimester should be within 0,2 - 3,0 mIU / l;
  3. TTG at pregnancy in 3 trimester should be in limits of 0,2 - 3,5 mIU / l.

If there are deviations of any values, then a comprehensive assessment of thyroid function is performed. To do this, examine the levels of TSH, T3 and T4 in pregnancy, which can talk about a particular function of the thyroid gland.

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The device for analysis

The device for performing TSH level analysis uses a monoclonal antibody. A set of ELISA is used to quantify the concentration of thyroid-stimulating hormone (TSH) in human serum. This TTG kit is based on the principle of solid-phase enzyme immunoassay. It uses a unique monoclonal antibody directed against a distintic antigenic determinant on an intact TSH molecule. The mouse monoclonal anti-TTG antibody is used to immobilize the solid phase (wells on a microtiter plate). Goat anti-TTG antibody is in solution of the enzyme conjugate. The test sample reacts simultaneously with these two antibodies, as a result of which the TSH molecules are in a "sandwich" between the solid phase and the enzyme-bound antibodies. After 60 minutes of incubation at room temperature, the wells are washed with water to remove unbound labeled antibodies. A solution of TMB is added and incubated for 20 minutes, which leads to the development of a blue color. Color development is stopped by adding a stop solution to form a yellow color and a measurement is made on a spectrophotometer at a wavelength of 450 nm. Concentration of TTG is directly proportional to the color intensity of the sample. The minimum detectable concentration of TSH by this kit is 0.2 μIU / ml.

Raising and lowering of values

Elevated TSH in pregnancy is one of the laboratory signs of hypothyroidism in women, and hence the insufficiency of the hormone and the child. Elevated TSH with normal concentrations of T4 and T3 is defined as subclinical hypothyroidism. Prevalence of subclinical hypothyroidism during pregnancy is estimated from 2% to 5%. This is almost always asymptomatic. Women with subclinical hypothyroidism more often than women with euthyroidism have a positive activity of antibodies to TPO. Subclinical hypothyroidism is associated with an unfavorable outcome for the mother and offspring, most recommend the replacement of thyroxine in women with subclinical hypothyroidism. Nevertheless, despite the fact that treatment with thyroxine improves obstetric outcome, it has not been proven that it alters long-term neurological development in offspring. The consequences for a high-level child TSH are not limited to low birth weight. A child can be born with signs of congenital hypothyroidism. This pathology is characterized by inadequate development of internal organs, and mainly of connections in the brain. With undiagnosed congenital hypothyroidism, the child develops a deep cognitive neurological deficit.

High TSH and frozen pregnancy can have a direct connection. Since thyroid hormones support pregnancy, stimulating the function of the yellow body, their inadequacy can cause pregnancy to die.

Than to lower TTG at pregnancy if its or his increase is dangerous. First of all, you need to understand that we can not influence the synthesis of TTG directly through the drugs. If the body has elevated TSH, this indicates only that the level of T3 and T4 is below normal. Therefore, it is necessary to increase the concentration of these hormones, and the TSH, respectively, will increase. If the background of high TSH is low T3 and T4, then the treatment requires the hormone thyroxine. The introduction of levothyroxine is a treatment for the choice of maternal hypothyroidism. Pregnant women need large doses because of the rapid increase in TSH levels as a result of physiological elevation of estrogen, increased placental transport and the metabolism of maternal T4 and an increase in the volume of thyroid hormone. During pregnancy, a full dose change of thyroxine is about 2-2.4 μg / kg / day. In severe hypothyroidism, for the first few days, a dose of thyroxine, twice the estimated final daily dose change, can be prescribed to quickly normalize the extrapythroid thyroxine pool before the final replacement dose decreases. Women who already on a thyroxine before pregnancy, as a rule, need to increase their daily dose, on average, 30-50% higher than the dosage before conception. The dose of thyroxine also depends on the etiology of hypothyroidism. Women should be monitored every 4-6 weeks for T4 and TSH values before delivery.

Deficiency of dietary iodine in the mother leads to a violation of the synthesis of the thyroid hormone in the mother and fetus. Low values of thyroid hormones stimulate an increase in production of TGH in the pituitary gland, and elevated TSH stimulates the growth of the thyroid gland, leading to maternal and fetal goiter. Therefore, the cause of elevated TSH can be not so much a low level of T3 and T4, but primarily it may be a deficiency of iodine. In areas with severe iodine deficiency, thyroid nodules may be present in 30% of pregnant women. Serious iodine deficiency in pregnant women is associated with an increase in the frequency of pregnancy loss, stillbirth and increased perinatal and infant mortality.

Normal levels of thyroid hormones are necessary for neuronal migration, myelination and other structural changes in the fetal brain. Since thyroid hormones are necessary throughout pregnancy, iodine deficiency affects both the production of maternal and embryonic thyroid hormones, and inadequate intake of iodine can lead to disastrous consequences. In particular, iodine deficiency in the mother and fetus during pregnancy adversely affects the cognitive function of the offspring. Children whose mothers were severely deficient in iodine during pregnancy may exhibit cretinism, characterized by deep intellectual disabilities, deafness and motor impairment. Iodine deficiency is the main cause of preventable intellectual deficiencies throughout the world.

In such cases, the use of levothyroxine for increasing T3 and T4 levels and for lowering TSH is not advisable, it is first necessary to reconcile the level of iodine deficiency. Iodomarin with elevated TSH during pregnancy is in this case the drug of choice for the treatment of iodine deficiency. All pregnant and lactating women with this problem should take iodomarin, containing 150-200 micrograms of iodine per day.

Hyperthyroidism is less common than hypothyroidism, with an approximate frequency during pregnancy of 0.2%. Low TSH in pregnancy and elevated T4 levels are a laboratory sign of hyperthyroidism in women. Sometimes there is a low TSH with normal T4 during pregnancy, which is typical for subclinical hyperthyroidism. Clinical symptoms of hyperthyroidism include tachycardia, nervousness, tremor, sweating, heat intolerance, weakness of the proximal muscle, frequent bowel movements, decreased exercise tolerance and hypertension.

The reasons for such changes are the formation of an autoimmune process. With this pathology, antibodies (AT) are formed to the TSH receptors, which are increased during pregnancy precisely in the case of hyperthyroidism. These antibodies stimulate the production of TSH in a false way, which in turn stimulates the production of thyroid hormones. These hormones increase in the blood and lead to the activation of all functions of the thyroid gland and other organs and systems of the pregnant woman.

The main problem in women with hyperthyroidism is the potential effect on the fetus. Antibodies to the thyroid receptor should be measured by the end of the second trimester in women with active disease.

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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.

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