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Hypothyroidism in pregnant women
Last reviewed: 23.04.2024
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Epidemiology
Epidemiology of hypothyroidism in pregnant women
In regions with mild iodine deficiency, pregnancy is a rather tough factor in stimulating the thyroid gland. Stimulation of thyroid function in the process of gestation occurs due to the increase in the degree of binding of thyroid hormones to blood proteins, increasing the level of chorionic gonadotropin (HGT), which has a weak "thyrotropic" effect, insufficient supply of the thyroid of the mother with iodine due to increased excretion of iodine in urine during pregnancy and iodine intake by the fetoplacental complex, as well as increased placental deiodination of thyroxine (T4). All these mechanisms have an adaptive physiological character and, in the presence of a sufficient amount of iodine, lead to the fact that the production of thyroid hormones in the first half of pregnancy is increased by 30-50%. The reduced intake of iodine during pregnancy leads to chronic stimulation of the thyroid gland, relative gestational hypothyroxinemia (increase in the production of T4 by only 15-20%) and the formation of goiter, both in the mother and in the fetus.
The frequency of newly diagnosed hypothyroidism during pregnancy (according to different data) varies from 2 to 5%. The carrier of antibodies to thyroid peroxidase in the population of pregnant women is 5-14%. The carrier of antibodies to the thyroid gland (even with normal initial function and thyroid structure) during pregnancy is accompanied by an increased risk of spontaneous abortion at early stages, manifestation of hypothyroidism, development of postpartum thyroiditis.
In this regard, according to modern recommendations, all women living in iodine deficiency zones, at the period of 8-12 weeks of pregnancy (and optimally at the stage of pregnancy planning), it is necessary to determine the level of thyroid-stimulating hormone (TSH), free T4 and antibodies to thyroid peroxidase in the blood serum.
Manifest hypothyroidism in the population occurs in 0.2-1% of cases, subclinical - in 7-10%. According to the data of the appeal to our institute, the causes of pregestational hypothyroidism in pregnant women were: postoperative hypothyroidism in 51.1%, autoimmune thyroiditis (AIT) in 42.2% and congenital hypothyroidism in 6.7% of cases.
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Classification of hypothyroidism in pregnant women
Isolate primary hypothyroidism, due to a decrease in the number of functioning tissue of the thyroid gland, and hypothyroidism of the central genesis (pituitary and hypothalamic).
Danger of hypothyroidism for the mother and fetus
Inadequate treatment of maternal hypothyroidism can lead to complications of pregnancy such as spontaneous miscarriages (19.8%), early toxicosis (33%), the threat of termination of pregnancy at various gestational age (62%), iron deficiency anemia (66%), gestosis (11 , 2%), fetoplacental insufficiency (70%), placental abruption (5%), intrauterine fetal death (2-7%), postpartum hemorrhage (4.2%).
In the fetus, the transplacental passage of the maternal thyroxin in the early stages of pregnancy can play a critical role in the normal development of the brain. Thus, we observed manifestations of perinatal encephalopathy in 19.8% of children. The incidence of ante- and intranatal hypoxia and asphyxia among this neonatal contingent was 19.6%, hypotrophy 13.7%. Even at birth, healthy 50% of children from mothers with insufficiently compensated hypothyroidism can have impaired puberty, decreased intellectual function, and high morbidity. In children born to mothers with elevated levels of antibodies to thyroid peroxidase, even with normal thyroid function, the risk of mental retardation increases.
Diagnostics of the hypothyroidism in pregnant women
Diagnosis of hypothyroidism in pregnant women
In subclinical primary hypothyroidism, an isolated increase in the thyrotropic hormone concentration is detected with a normal free T4 content, with manifest primary hypothyroidism - a combination of elevated TSH and a lower concentration of free T4. With secondary hypothyroidism, the content of both TSH and T4 is reduced.
In almost 90% of cases, the cause of spontaneous hypothyroidism is autoimmune thyroiditis. The basis for the diagnosis of autoimmune thyroiditis, according to the recommendations of the Russian Association of Endocrinologists (2002), is considered to be the following "large" clinical and laboratory signs.
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Treatment of the hypothyroidism in pregnant women
Treatment of hypothyroidism in pregnant women
Treatment of hypothyroidism during pregnancy is reduced to the appointment of replacement therapy with thyroid hormones (levothyroxine sodium), and immediately after the onset of pregnancy the dose of levothyroxine sodium increases by about 50 μg / day.
Treatment of hypothyroidism during pregnancy
Levotiroksin sodium should be taken on an empty stomach for 30-40 minutes before meals. Given that some drugs can significantly reduce the bioavailability of levothyroxine sodium (for example, calcium carbonate, iron preparations), taking any other drugs should be transferred to 4 hours after taking levothyroxine sodium, if possible.
In hypothyroidism, first detected during pregnancy (both manifest and subclinical), or during decompensation of pre-existing hypothyroidism, a complete replacement dose of levothyroxine sodium is administered immediately, i.e. Without gradually increasing it.
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