Ultrasound of the thyroid gland during pregnancy is performed in order to identify various pathological foci in this organ. During the examination, the doctor checks the size and condition of the parathyroid glands. Any deviation from the norm can adversely affect the development of the child.

An ultrasound examination of the thyroid gland is performed at any week of pregnancy, because. it is a safe procedure. Thanks to regular monitoring of the size and structure of this organ, various pathologies, including malignant tumors, can be detected in a timely manner. Any disease of the thyroid gland adversely affects the health of the woman and the development of the fetus.

When is a thyroid ultrasound done for pregnant women?

An organ study is most often prescribed if a pregnant woman has problems with the thyroid gland. For control, you need to regularly donate blood for hormonal composition. But sometimes this is not enough, so the doctor sends the expectant mother for an additional examination.

Ultrasound of the thyroid gland for pregnant women is prescribed in the following cases:

• sudden mood swings;
• weight loss for unknown reasons;
• asthma attacks;
• causeless aggression, increased irritability;
• drowsiness;
• identification of formations or seals of the organ during palpation;
• change in heart rate.

Why is this study needed?

Ultrasound of the thyroid gland during pregnancy allows you to determine the size of the organ and detect changes in the parenchyma. If the organ has increased by no more than 16% of the norm, then its function is not impaired. In this case, the structure of the parenchyma must remain homogeneous.

Identification of seals, foci and other formations in the parenchyma of the gland requires an additional examination. Often during the bearing of a child, there is a problem of hypothyroidism, that is, a lack of thyroid hormones. This leads to complications of pregnancy and the birth of children with developmental anomalies.

The consequences of hypothyroidism for a child include:

• developmental delay;
• low level of intelligence;
• severe thyroid disease.

Due to the timely detection of the disease, it is possible to compensate for the activity of the organ and prevent adverse consequences.

In addition, thyroid diseases lead to various complications. The most dangerous are:

• preeclampsia and fetoplacental insufficiency;
• arterial hypertension;
• heart failure;
• spontaneous abortion or premature birth;
• placental abruption;
• uterine bleeding after childbirth.

Is ultrasound dangerous for the fetus?

Such a study has no contraindications. Ultrasound can also be done during pregnancy, because. it will not cause any harm to the fetus. The examination of the thyroid gland lasts for several minutes, and the impact zone is far from the child.

Preparation

There is no need to prepare for the examination in a special way. If a woman suffers from an increased gag reflex, then ultrasound is performed on an empty stomach, because. pressure on the throat with the transducer may induce vomiting. It is recommended to come in clothes that do not constrain the neck area. The chain must also be removed.

How is a Thyroid Ultrasound Done?

The woman lies back on the couch. The doctor applies a special hydrogel to the neck in the area of ​​the thyroid gland, which is necessary to improve the conductivity of the ultrasound signal from the transducer.

With the help of a device that the doctor runs along the neck, the organ is examined, its contour and dimensions, and the state of the parenchyma are determined. The procedure lasts about 15 minutes.

What does an ultrasound reveal?

Ultrasound of the thyroid gland helps to detect almost all diseases of this organ, and also shows the condition of the soft tissues of the neck, larynx, located nearby lymph nodes. Thanks to the examination, it is possible to detect even minor changes in the gland and start treatment in a timely manner.

What are thyroid problems and what do they lead to?

If a woman suffers from hyperthyroidism during pregnancy, i.e. increased activity of the gland, then she may develop cardiovascular insufficiency or have difficulties during childbirth. In addition, a child after birth is often diagnosed with a congenital disease of the gland.

In hypothyroidism, the thyroid gland slows down its activity, which leads to the production of a small amount of hormones. A woman suffers from fatigue, increased drowsiness, nervousness, etc. The danger of this disease during pregnancy is that the risk of premature birth and the birth of a child with developmental abnormalities increases.

There may also be thyroid nodules. If they are benign, then they are not able to affect the fetus in any way. Nodes of a malignant nature require urgent treatment, especially with elevated hormone levels. This pathology is not grounds for termination of pregnancy. A woman needs to visit an endocrinologist more often to monitor the state of nodal changes.

Thyroid adenoma is a benign formation in which there is an increased synthesis of thyroid hormones. This disease does not affect the course of pregnancy.

The next pathology of the thyroid gland is autoimmune thyroiditis. It occurs under the influence of hormonal disorders occurring in the body. With this disease, the immune system perceives the body's own cells as foreign, which negatively affects the development of the child.

A. V. Kaminsky, Doctor of Medical Sciences, State Institution "National Scientific Center for Radiation Medicine of the National Academy of Medical Sciences of Ukraine"; T. F. Tatarchuk, Corresponding Member of the National Academy of Medical Sciences of Ukraine, Doctor of Medical Sciences, Professor, T. V. Avramenko, Doctor of Medical Sciences, Professor, Institute of Pediatrics, Obstetrics and Gynecology of the National Academy of Medical Sciences of Ukraine; A. V. Popkov, PhD, Verum Medical Center; I.A. Kiseleva, Kiev City Clinical Endocrinology Center

The thyroid gland (TG) is one of the most important organs, the functional state of which determines the possibility of the very conception, bearing and birth of healthy children. Thyroid hormones are needed for the formation of the brain and heart of the unborn child. The trace element iodine is necessary for the synthesis of these hormones, and its lack causes the development of iodine deficiency conditions at any age - in the fetus, children and adults. In addition, iodine deficiency often contributes to a decrease in intelligence in individuals and the nation as a whole.

In Ukraine, the frequency of thyroid pathology is significantly increased. In general, among the population it occurs in 20-30% of adults, and among the victims of the Chernobyl accident - about 50%. The most common problems are nodular goiter and diffuse non-toxic goiter, which are caused by the presence of natural iodine deficiency. Another common pathology is autoimmune thyroiditis associated with a lack of the trace element selenium. Thyroid function disorders (hypothyroidism, hyperthyroidism) are diagnosed infrequently - in 2-5% of the population, but with the highest frequency (up to 12%) - among pregnant women or women who cannot become pregnant, and in those who resort to in vitro fertilization - up to 20%.
In 2001, the World Health Organization (WHO) first introduced the term "iodine deficiency diseases" to refer to all pathological conditions that develop in the population as a result of iodine deficiency, which can be reversible with normalization of iodine intake. These include not only thyroid diseases (nodular goiter, hyperthyroidism, hypothyroidism), but also others: infertility, decreased intelligence, some disorders and malformations (Table 1).

The entire territory of Europe, including Ukraine, is iodine deficient. One can only argue about which region lacks iodine more. Natural deficiency of iodine and some other trace elements (selenium, zinc, etc.), vitamins (groups B, D), poor ecology, chemicalization contribute to the occurrence of thyroid pathology and other disorders that prevent normal conception and bearing healthy offspring.
In some European countries (Switzerland, Germany, Austria, etc.), effective endemic iodine prophylaxis over the past 100 years has made it possible to achieve great success and exclude them from the list of scarce ones. Armenia, Azerbaijan, Turkmenistan, Georgia, Belarus and Kazakhstan managed to almost completely solve the problem of iodine deficiency in the diet of the population through the use of mass iodine prophylaxis in the form of enrichment of edible salt with iodine.

On average, an adult resident of Ukraine receives only 50-80 mcg of iodine per day, which is below the required level - 150 mcg/day (within 100-250 mcg/day). For pregnant and lactating women, the daily requirement for iodine should be higher - 250 mcg, so they and their children are the most vulnerable groups of the population (Table 2).

The average daily dose of iodine 150 mcg corresponds to a median urinary iodine concentration of 100 mcg/l.

Thyroid and pregnancy

Thyroid dysfunction may prevent pregnancy or lead to miscarriage even in the presence of subclinical hypothyroidism (thyroid-stimulating hormone (TSH) levels of 4 mIU/L or higher in non-pregnant women; 3 mIU/L or higher in pregnant women). Fortunately, most thyroid diseases that affect pregnancy are easily diagnosed and corrected. The difficulty lies in the very awareness of the presence of a problem on the part of the thyroid gland. Very often, the symptoms that accompany these disorders are minor, are of a general nature: weakness, fatigue, drowsiness during the day, insomnia at night, sometimes a violation of the stool or menstrual cycle.
With hyperthyroidism, tachycardia, poor heat tolerance are observed, with hypothyroidism - dry skin and / or constipation.
Timely detection of violations of the functional state of the thyroid gland in pregnant women, along with diabetes mellitus, is a very important task, therefore thyroid tests (TSH, ATPO, ATTG, thyroglobulin) and the determination of glycemia (fasting glucose, standard glucose tolerance test, glycated hemoglobin) are mandatory when planning pregnancy, monitoring its development, as well as after childbirth.
In the early stages of pregnancy (up to 3-4 months), the fetus functions only due to the thyroid hormones of its mother. This period, especially the first 4 weeks after conception, is especially critical. During these periods, the greatest number of miscarriages associated with iodine deficiency or hypothyroidism in the mother occurs.
Today in Ukraine a significant number of women are diagnosed with subclinical hypothyroidism, the main cause of which is iodine deficiency. The human body is characterized by high sensitivity to iodine deficiency and significant resistance to excess iodine for a long time. Therefore, according to the WHO recommendation, pregnant women, especially those living in iodine-deficient regions, are required to additionally receive iodine-containing tablets for the entire period. The average iodine requirement in adults is 150 micrograms (100-250 micrograms) daily, according to WHO, and for pregnant women more - 250 micrograms / day. The safe level of iodine for residents of most regions is up to 1000 mcg / day in total. In the conditions of Ukraine, it is almost impossible to achieve it.
Considering that adults in Ukraine actually receive only 50-80 micrograms of iodine per day, the ideal dosage of iodine for pregnant women is 200 micrograms in the form of original potassium iodide tablets taken once daily after meals at a convenient time of the day. The drug is recommended for use throughout the entire period of pregnancy, lactation and a year before the planned conception. At the same time, periodic (every 4-6 months) monitoring of thyroid parameters (TSH and thyroglobulin, sometimes ATPO) is welcome.
After 4 months of intrauterine development, the fetus begins to function its own thyroid gland, which actively captures the iodine absorbed by the mother and synthesizes the amount of thyroid hormones necessary for the body. Therefore, the efficiency of synthesis depends on the daily intake of iodine by the mother.

Diagnosis of thyroid dysfunction

The main function of the thyroid gland is the production of hormones: thyroxine (T4), triiodothyronine (T3), calcitonin. Receptors for them are present in all cells, their effects determine the physiological capabilities of the body. Any deviation of their concentration in the blood from the norm violates the efficiency of the tissues.

The functioning of the thyroid gland is regulated by the hypothalamus and pituitary gland through the release of the latter TSH, which acts as a stimulator of thyrocytes. With a decrease in thyroid function, the pituitary gland increases the secretion of TSH, forcing them to work more intensively, and with excessive production of thyroid hormones, thyroid-stimulating stimulation decreases. Thus, there is an inverse relationship between the concentrations of TSH and thyroid hormones. This feedback mechanism is used in the diagnosis of thyroid dysfunction (Table 3).

Given the dominant role of the pituitary gland in the regulation of thyroid function, which responds to minor changes in the level of thyroid hormones, the determination of TSH concentration is a more sensitive test than free fractions of hormones (FT3, FT4). This is also due to the fact that they, like all biologically active substances, exist in two molecular optical isoforms - active levorotatory and biologically inactive dextrorotatory. Their sum is FT3 and FT4, and the ratio of isoforms (enantomers) may vary depending on the presence of iodine deficiency, inflammation in the thyroid gland, and other reasons. So, for substitution therapy, a highly purified levorotatory isoform of FT4 is used - the drug L-thyroxine.

Features of thyroid dysfunction in pregnant women

When pregnancy occurs, estrogen synthesis increases, which can lead to a decrease in thyroid function and an increase in TSH concentration in approximately 20% of women during the first trimester. At the same time, other women, on the contrary, may experience a decrease in TSH levels due to an increase in the levels of chorionic gonadotropin (which reaches a peak by 10-12 weeks of pregnancy), which in 2% of cases gives a clinic of transient gestational thyrotoxicosis. This condition is characterized by mild manifestations of excess thyroid hormones and uncontrolled vomiting during the first trimester - the so-called toxicosis of pregnant women. Monitoring of TSH in pregnant women who receive thyroxine replacement therapy or have thyroid pathology should be carried out in a stable situation - every 1-2 months. Due to the special risk for the mother and fetus, physiological characteristics for pregnant women, other norms for TSH levels are recommended (Table 4).

Diagnosis of iodine deficiency

Iodine is an important trace element that is needed for the synthesis of thyroid hormones, the normal functioning of the mammary glands, stomach, and other tissues (skin, eyes, brain). Lack of iodine leads to disruption of various physiological processes. From the body, 90% of iodine is excreted in the urine, 10% - in the bile. This factor is used in epidemiological (large-scale) scientific studies to study the level of iodine supply in a particular area. With such a one-time study for 1-2 days, hundreds of thousands of inhabitants collect urine and analyze the concentration of iodine. Despite the rapid change in its content in the body every 3 days, depending on the nature of nutrition, in a large group of observations it is possible to level such a statistical error in the change in ioduria. Therefore, on the recommendation of WHO, the study of ioduria is carried out only in scientific studies in large groups.

For an individual assessment of iodine availability in 1994 and 2007, WHO/UNICEF proposed other indicators of the iodine status of the population - determination of thyroglobulin levels in children, adults and pregnant women, as well as the concentration of TSH in the blood of newborns (neonatal screening on the 4-5th day in full-term ; on days 7-14 in preterm infants).
Thyroglobulin is a protein that is synthesized by the thyroid gland and enters the blood in a small amount. However, with the development of goiter or with a lack of iodine, its concentration increases. Studies have shown that the individual level of thyroglobulin reliably coincides with ioduria. Unlike the latter, the amount of thyroglobulin in the blood changes slowly, over months, so it can be used as a marker of iodine deficiency, as well as track its changes over time during treatment with iodine preparations.
Its blood level of 10 mg / l or more indicates the presence of mild iodine deficiency, 20-40 mg / l - moderate, over 40 mg / l - severe deficiency. Thyroglobulin is also used as a tumor marker when its concentration is 67 mg/l or higher, including in patients with thyroidectomy. It increases in differentiated thyroid cancer (Table 5).

Tactics of treatment and monitoring of pregnant women with hypothyroidism

When a woman is pregnant, her body needs enough thyroid hormones to support the development of the fetus and her own needs. Uncontrolled thyroid hormone deficiency can lead to critical pregnancy complications such as preterm birth, preeclampsia, miscarriage, postpartum hemorrhage, anemia, placental abruption, and death of the baby or mother.
There are several reasons for the development of hypothyroidism. The most common cause of subclinical hypothyroidism is iodine deficiency, manifest hypothyroidism - autoimmune thyroiditis, and in more rare cases - surgical treatment, radiation, drug treatment (amiodarone, lithium preparations). The need for thyroid hormones increases significantly during pregnancy, increasing with each trimester, so hypothyroidism can develop in women with initially normal levels of these hormones in the presence of thyroid disease. After childbirth, the need for them decreases sharply, often to the level preceding pregnancy.
Most women who develop hypothyroidism during pregnancy have little or no symptoms characteristic of it.
The goal of treatment for hypothyroidism is to maintain a normal TSH level, which will indicate the correct balance of thyroid hormones in the blood. The normal TSH level for pregnant women is different from what is allowed in non-pregnant women. Depending on the trimester, the normal range of TSH during pregnancy should be between 0.1-2.5 mIU/L in the 1st trimester to 0.3-3 mIU/L in the 3rd trimester according to US guidelines and similar to European guidelines. The detection of an increase in TSH more than 3-3.5 mIU / l indicates a decrease in thyroid function in a pregnant woman - hypothyroidism, which requires hormone replacement therapy.
Adequate treatment and monitoring of hypothyroidism allows you to completely avoid the possible complications associated with it. The treatment of hypothyroidism consists in hormone replacement therapy with thyroid hormones according to the same principles that exist for non-pregnant women. L-thyroxine for the first time is prescribed in the minimum dose - 25 mcg / day once in the morning, 30 minutes before breakfast, gradually increasing the dose to the required value, which is determined by the level of TSH, which should be within the above-described norm. At the same time, the use of L-thyroxine preparations during pregnancy is absolutely safe if the rules for hormone replacement therapy are taken into account. Most patients with hypothyroidism - both pregnant and non-pregnant - need to select a dose of thyroid hormones that will keep the TSH concentration within the ideal value of 0.5-2.5 mIU / l, which will correspond to the level characteristic of 95% of healthy individuals .

Monitoring of established hypothyroidism is carried out, depending on the clinical task, no more than once every 2 weeks and at least 1 time in 1-2 months, optimally - monthly throughout the entire period of pregnancy and in the first months after childbirth.
Adjustment of the dose of L-thyroxine in pregnant women is made every 2 weeks or every month according to the level of TSH. Once the TSH level returns to normal, less frequent checkups are required. L-thyroxine preparations should be supplemented with iodine preparations (original potassium iodide tablets), usually at a dose of 200 mcg / day, throughout pregnancy until the end of the lactation period, regardless of the type of thyroid disease.
If the problems are chronic, then L-thyroxine and iodine preparations continue to be taken after childbirth (for as long as necessary).

Isolated (euthyroid) hypothyroxinemia in pregnancy

Isolated hypothyroxinemia (pseudohypothyroidism) is characterized by a low concentration of FT4 with a normal TSH level (i.e., euthyroidism). This may be the result of either iodine deficiency or poor laboratory quality (mistake). The use of iodized salt for a long time reduces the likelihood of thyroid diseases and significantly reduces the risk of developing hypothyroxinemia during pregnancy (Fig.).

Approximately 2.5% of healthy women may have an FT4 concentration below the minimum threshold. Nevertheless, they have a high index of pregnancy complications, typical for patients with hypothyroidism. The presence of isolated hypothyroxinemia leads to spontaneous abortions, premature births, complications in childbirth, perinatal mortality, congenital malformations, fetal macrosomia (body weight over 4000 g), deterioration in neuropsychic development in offspring (psychomotor deficit associated with gestational diabetes, neonatal intraventricular hemorrhage).
In such women, it is necessary to investigate the adequacy of iodine supply (thyroglobulin level), if iodine deficiency is detected, replenish with iodine tablets. From a clinical point of view, isolated hypothyroxinemia in pregnant and non-pregnant women does not require L-thyroxine replacement therapy.
Often, the detection of a low level of FT4 with a normal concentration of TSH indicates a laboratory or methodological error, low quality of diagnostic kits. If such a result is detected, it is necessary to repeat the study of FT4 and TSH, preferably in an alternative laboratory. In many cases, reanalysis does not confirm the original result.

Tactics of treatment and monitoring of pregnant women with hyperthyroidism

Hyperthyroidism occurs in 0.1-1% of all pregnancies. It is diagnosed when TSH levels are below normal (less than 0.1 mIU/L) and FT4 and/or FT3 levels are above normal (manifest hyperthyroidism). The most common causes of hyperthyroidism are: diffuse toxic goiter (synonyms: thyrotoxicosis; Graves' disease, Basedow's disease) - 80% of cases, transient hyperthyroidism in autoimmune thyroiditis, toxic thyroid adenoma, thyroid cancer, acute (bacterial) or subacute (viral) thyroiditis. Manifest hyperthyroidism in all cases requires treatment, especially in pregnant women. The risks associated with hyperthyroidism are almost the same as with hypothyroidism, the fetus may additionally experience fetal tachycardia.
In exceptional cases, in women, hyperthyroidism is detected with the development of "ovarian goiter" (struma ovarii), which can develop with ovarian teratoma (2-5% of cases of teratomas), when it contains more than 50% of thyroid tissue cells, or ovarian cystadenoma (1% of all ovarian tumors). These teratomas are usually benign. The symptoms of struma ovarii are similar to those of other ovarian tumors and are nonspecific. Women with struma ovarii may complain of abdominal or pelvic pain and have ascites in 12-17% of cases.
Most women have elevated thyroglobulin levels, and a third have an increased concentration of the CA‑125 marker. The final diagnosis is established by cytological or histological examination. An effective method of treating struma ovarii is surgical.
Subclinical hyperthyroidism is diagnosed when TSH is in the range of 0.10.39 mIU/L (non-pregnant) with normal FT4 and FT3 levels. However, in pregnant women, TSH standards differ (Table 4), which does not require treatment. This is also true for pregnant women with transient hyperthyroidism (TSH
at the level of 0.1-0.3 mIU/l).

Diffuse toxic goiter (thyrotoxicosis) is an autoimmune disease of the thyroid gland, which is always accompanied by excessive synthesis of thyroid hormones due to the action of thyroid-stimulating antibodies (antibodies to the TSH receptor - AT to r-TSH). Among the most common causes of this disease are tobacco smoking, deficiency of trace elements of iodine and/or selenium, in rare cases, long-term (months to years) use of high doses of iodine (more than 1000-5000 mcg/day). Diagnosis of hyperthyroidism includes the determination of blood TSH, FT4, FT3, antibodies to r-TSH (the main differential criterion), sometimes antibodies to thyroid peroxidase and thyroglobulin.

Treatment begins with the cessation of tobacco smoking, if it has taken place, is based on the suppression of the production of thyroid hormones and their effects through the use of thyreostatics (drugs methimazole, thiamazole, carbimazole and propylthiuracil) for 1.5-2 years on average, titrating the dose to the required . In case of unsuccessful treatment, the issue of surgical intervention is considered, the condition for which is to achieve compensation for hyperthyroidism.
Monitoring of treatment in pregnant women is carried out every 2-4-6 weeks, determining the levels of TSH, if desired, FT4, FT3, periodically - the concentration of antibodies to r-TSH, glucose in blood plasma. This approach is also used for women who achieve remission of hyperthyroidism before pregnancy with thyreostatics - they have a low risk of relapse of hyperthyroidism during pregnancy, but a high risk of relapse after delivery. In the middle stages of pregnancy, they are monitored for antibodies to r-TSH.
It is most optimal if a pregnant woman with hyperthyroidism will be jointly supervised by an obstetrician and an endocrinologist.
The specificity of the use of thyreostatics in pregnant women is that methimazole, carbimazole and thiamazole penetrate the placental barrier and can cause a teratogenic effect in the first trimester. Their development is associated with the use of high doses of drugs during the first weeks of pregnancy. Therefore, the American Thyroid Association recommends using propylthiuracil preparations in the first trimester of pregnancy, which are associated with a low teratogenic risk, but are characterized by a risk of developing liver dysfunction; and in the 2nd and 3rd trimester - methimazole preparations.
Untreated hyperthyroidism is a greater threat to the life and health of the mother and fetus than the risks of using thyreostatics. Antithyroid antibodies can cross the placenta and affect the fetal thyroid. If antibody levels are high enough, the fetus may develop hyperthyroidism or neonatal thyrotoxicosis.
Thyreostatics in pregnant women should be used in a balanced manner, at the lowest effective dose, and hormone preparations (L-thyroxine, corticosteroids) are not prescribed additionally (as adjuvant therapy). Of the beta-blockers, propranolol can be used for a short time.
In the postpartum period, women with hyperthyroidism who are breastfeeding and receiving thyreostatics in small doses can continue taking the drugs, which is considered safe and does not affect the thyroid of the child.

Autoimmune thyroiditis

Approximately 11-15% of all women of childbearing age have an increased amount of antibodies to the thyroid gland (ATTG, ATPO). In most cases, the so-called carriage of antibodies takes place. Some of them will develop autoimmune thyroiditis with a gradual increase in titer to diagnostically reliable levels (more than 100 IU), while others will not. When pregnancy occurs, approximately 20-40% of these antibody-positive women will develop hypothyroidism before or immediately after delivery. This risk increases with each trimester. It should be noted that ATPO and ATTH titers gradually decrease as pregnancy progresses, which can lead to false negative findings in late pregnancy. An increase in antibody titers to thyroid components is associated with an increased risk of miscarriage, perinatal mortality, preterm birth, neonatal respiratory distress, and aggressive behavior in children.

Some studies in these women have shown a beneficial effect of L-thyroxine preparations on pregnancy outcomes. However, confirmed autoimmune thyroiditis does not require thyroid drugs in the absence of hypothyroidism.

Postpartum thyroiditis

Postpartum thyroiditis (postpartum thyroid dysfunction) is an autoimmune thyroid disease that resembles autoimmune thyroiditis in its course. It develops in women in the first 12 months after childbirth, more often after 3-4 months. In a third of women, hyperthyroidism is initially observed, which will be replaced by persistent hypothyroidism. Another third have only the hyperthyroid phase or the hypothyroid phase.
According to some members of the American Thyroid Association, this is autoimmune thyroiditis, which was asymptomatic in women with elevated levels of thyroid antibodies (ATPO) even before childbirth, but after childbirth it began to progress rapidly. Given the transient nature of this hyperthyroidism, antithyroid drugs are not used because the thyroid gland is not overactive. When diagnosing hypothyroidism, hormone replacement therapy with L-thyroxine preparations and monitoring according to the standard scheme are used. Subsequently, after 12-18 months, in 50-80% of women, thyroid function is restored to normal, the need for hormone replacement therapy with L-thyroxine preparations disappears.

Tactics of treatment and monitoring of pregnant women with nodular goiter

Due to the fact that Ukraine is an iodine-deficient region, there is an increased prevalence of nodular goiter on its territory. Its frequency is approximately 15-20% among adults, up to 34% among victims of the Chernobyl accident. The American Thyroid Association emphasizes that the most obvious manifestations of iodine deficiency are diffuse non-toxic goiter and nodular goiter.
In most cases, nodular goiter is benign, but in 10% of cases we can talk about thyroid cancer, which in 90% of patients has a predominantly non-aggressive course.
When pregnancy occurs, the nodes that were diagnosed before it tend to gradually increase in size. This is due to an increased need for iodine, an increasing iodine deficiency in those who do not make up for the increased need for it (with the help of original potassium iodide tablets), excessive thyroid-stimulating stimulation associated with them, and other factors. For all pregnant women, regardless of the presence of any pathology of the thyroid gland, WHO recommends replenishing iodine at a dose of 200 mcg using the original potassium iodide tablets, especially in the area of ​​iodine deficiency. This makes it possible to exclude an increase in the volume of the thyroid gland and nodular goiter in such women.
Monitoring of nodular goiter consists in a periodic (every 3-4 months) study of the concentration of TSH, FT4, thyroglobulin in the blood, and also involves a control ultrasound (ultrasound) of the thyroid gland at the same time. If necessary, pregnant women can undergo a fine-needle aspiration biopsy of the thyroid gland, which, like ultrasound, is a safe procedure.
If thyroid cancer is detected during pregnancy, assessing the possible risks, surgical treatment is postponed until the postpartum period. If the cancer is differentiated, the risks associated with it are low. Hormone therapy with L-thyroxine for such women is carried out with a target decrease in TSH to a level of 0.1-1.5 mIU / l. If surgery is still required due to thyroid cancer, the safest time to perform it is during the second trimester of pregnancy.

Recommendations for general screening and prevention of endocrine pathology in pregnant women

Starting from the first trimester of pregnancy until the formation of its own functioning thyroid gland, the body of the fetus is provided with maternal hormones that penetrate the placenta. The blood of a newborn may contain up to 20-40% of maternal thyroid hormones. Low concentrations of thyroid hormones during embryonic development and early childhood are associated with irreversible brain damage, including mental retardation and neurological damage. A meta-analysis of 18 studies found that iodine deficiency (moderate to severe) was associated with a 13.5-point decrease in mean IQ.
The high prevalence among the population of clinically important endocrine pathology in the area of ​​iodine deficiency or environmental risk, which can prevent conception, the normal development of pregnancy and the course of childbirth, affect offspring in the near and long term, forces us to single out some hormonal markers as screening markers, that is, those that are effective in most cases, cost-effective ("price-quality"). The analysis of these markers should be carried out by everyone - healthy and with any concomitant pathology. These include fasting plasma glucose and TSH. Desirable additional markers, the study of which will bring an objective benefit, are the concentration of thyroglobulin, as well as ultrasound of the thyroid gland and parathyroid glands.

Every woman, regardless of whether she is planning a pregnancy, is registered for pregnancy, is diagnosed with infertility, is planning in vitro fertilization, has she had a miscarriage, should be studied levels of glucose in blood plasma and TSH. In 80-90% of women in Ukraine, an increased concentration of thyroglobulin is detected, which indicates the presence of iodine deficiency (Table 5).

The experience of many countries of the world shows that the most effective way to solve the problem of iodine deficiency is to conduct adequate mass, group and individual prophylaxis. According to WHO, all iodine deficiency diseases can be prevented, while the changes caused by iodine deficiency in utero and in early childhood are irreversible and practically untreatable. Therefore, these population groups are primarily at risk of developing the most severe iodine deficiency conditions and require special attention. The highest risk groups are pregnant women and breastfed children.

Iodization is probably the cheapest and most effective way to prevent the development of iodine deficiency diseases. Iodine deficiency cannot be eliminated once and for all. The iodine prophylaxis program should never be terminated because it is carried out in an area where there has always been such a lack of soil and water.
Since iodine is utilized by the body only in a chemically pure state in the form of salts (potassium iodide (KI) and potassium iodate (KIO3) - the main forms of iodine absorbed through the mucosa of the gastrointestinal tract), other forms of iodine, including organically bound iodine, like chemically pure iodine, they are not absorbed by the human body until they turn into these compounds.
As a general prevention, WHO recommends the use of iodized salt (sodium chloride) in everyday life. Salt is poison. Since sodium is toxic, the use of household salt is limited to 5-6 g/day.
In accordance with the international standard, a person should receive 1540 mcg of iodine for every 1 g of salt.
Sea salt contains a low concentration of iodine - 3 micrograms of iodine per 1 g of sea salt. Therefore, it also needs to be enriched with iodine.
Pregnant and lactating mothers, children and adolescents use an active mandatory model of iodine prophylaxis, which consists in prescribing iodine preparations in the form of tablets containing fixed doses of iodide or iodate, and not dietary supplements made from plant materials, which are registered under a simplified system, without multicenter clinical trials.
The existing regulatory documents emphasize that iodine prophylaxis should be carried out daily and continuously in case of living in an area where there is a deficiency of micronutrients (Table 6).

Literature

1. Assessment of the Iodine Deficiency Disorders and monitoring their elemination: a guide for program managers, 3rd ed. / WHO. – Geneva, 2007. – P. 1-98.
2. Zimmermann M.B. Iodine deficiency in industrialized countries // Proc Nutr Soc. - 2009. - No. 8. - P. 1-11.
3. WHO/ICCIDD/UNICEF. Indicators for Assessing Iodine Deficiency Disorders and Their Control Through Salt Iodization. Geneva, Switzerland: World Health Organization; 1994.
4. Rohner F., Zimmermann M., Jooste P. et al. Biomarkers of Nutrition for Development Iodine. Review // J Nutr. - 2014. - Vol. 144(8). - R. 1322S‑1342S.
5. Bath S.C., Rayman M.P. A review of the iodine status of UK pregnant women and its implications for the offspring // Environ Geochem Health. - 2015. - Vol. 37(4). - P. 619-629.

V.V. Fadeev

Federal State Budgetary Institution Endocrinological Research Center of the Ministry of Health and Social Development of Russia, Moscow

V.V. Fadeev - Dr. med. Sci., Professor, Department of Endocrinology, First Moscow State Medical University named after I.I. THEM. Sechenov, Deputy Director of the Federal State Budgetary Institution Endocrinological Research Center of the Ministry of Health and Social Development of the Russian Federation

Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and Postpartum

Federal Endocrinological Research Center, Moscow

(Stagnaro-Green A., Abalovich M, Alexander E. et al. Guidelines of the American thyroid association the diagnosis and management of thyroid disease during pregnancy and postpartum. Thyroid 2011; 21: 1081-1125).

chen is not enough, which is obviously due to ethical restrictions on conducting research involving pregnant women. Many provisions of these recommendations are quite controversial and will be discussed below.

This article provides its own translation of these recommendations and some comments on them. The comments of the author of this publication are in a different font. The translation of the recommendations itself was not made verbatim, but adapted terminologically for better understanding by Russian endocrinologists.

Description

Level A

Level B Level C

Level D

Level I

A strong recommendation indicating that its implementation is associated with an obvious positive effect on the patient's health. Based on high evidence, the benefits far outweigh the risks

For correspondence: Fadeev Valentin Viktorovich - 117036, Moscow, st. Dm. Ulyanova, d. 11. E-mail: [email protected]

Trimester-specific reference ranges for thyroid-stimulating hormone (TSH) levels, which have been developed in a population with normal iodine intake, should be used.

If the laboratory does not have trimester-specific reference ranges for TSH levels, it is recommended to use the following: I trimester 0.1-2.5 mU/l, II trimester 0.2-3 mU/l, III trimester 0.3-3 mU / l.

Level I

A comment. Perhaps the most controversial recommendation, which has actually been discussed for quite a long time. The problem is that it comes into conflict with the 8th recommendation. A natural question arises as to why to approve new reference ranges, if after that clear recommendations are not given on the appointment of replacement therapy. Although the 9th recommendation partly leaves this situation. Note that this recommendation is only rated Level I.

The optimal method for determining the level of free T4 during pregnancy is liquid chromatography - tandem mass spectrometry

If the definition of the level of St. T4 using LC/MS/MS is not possible, it is recommended to do this using available techniques, taking into account their shortcomings. The TSH level is a more reliable test for assessing thyroid function during pregnancy compared to any method for determining the level of f. T4.

Due to the significant variability of the results of the determination of St. T4 using different methods, it is necessary to develop method-specific and tri-mestre-specific reference ranges for the level of St. T4.

Level B.

A comment. The situation with the determination during pregnancy of the level of St. T4, as you know, is even more problematic than with the determination of TSH, which is reflected in recommendations 3-5. It is clear that mass spectrometry for

clinicians are almost inaccessible. If we talk about the usual immunometric methods for determining St. T4, then in general we can say that most of them will underestimate the real level of St. T4 in a woman, while the degree of such an underestimation will progressively increase as the duration of pregnancy increases. As a result, this is what can lead to the so-called isolated gestational hypothyroxinemia, which will be discussed below. Again, it is emphasized that both outside and during pregnancy, the level of TSH should be trusted more than the level of St. T4.

In case of overt hypothyroidism during pregnancy, treatment is necessary. Explicit hypothyroidism should be considered a situation when in women the level of TSH exceeds the trimester-specific reference ranges and a reduced level of F is determined. T4 or when the level of TSH exceeds 10 mU / l, regardless of the level of St. T4.

Isolated hypothyroxinemia during pregnancy does not require treatment.

Level C.

A comment. Isolated gestational hypothyroxinemia is a situation where a patient has a reduced level of F. T4 with normal TSH. This is due to the imperfection of routine methods for determining St. T4. Against the background of a progressive increase in the level of thyroxine-binding globulin, as the duration of pregnancy increases, there will be a gradual artificial underestimation of the real level of St. T4, which in some cases may be lower than the reference (usually about 11 pmol / l). This situation often causes excitement for both the patient and the doctor. As indicated, the appointment of replacement therapy in this situation is not required.

Subclinical hypothyroidism is associated with adverse outcomes for both mother and fetus. However, due to the lack of results from randomized controlled trials, there is currently insufficient evidence to recommend or not recommend levothyroxine (L-T4) therapy in all patients with subclinical hypothyroidism and the absence of circulating antibodies to the thyroid gland. Level I

A comment. In general, it is quite logical - hypothyroidism should have what is called material

substrate, i.e. autoimmune thyroiditis as its main cause. If there are no changes in the thyroid gland according to ultrasound data and there are no circulating antibodies to thyroid peroxidase (AT-TPO), then what is the reason for the increase in the level of TSH? On the other hand, what about the new reference ranges proposed above, according to which subclinical hypothyroidism should be diagnosed with TSH greater than 2.5 mU/L. Unfortunately, this contradiction is still unresolved and it is difficult for practitioners to give more specific recommendations. It should be noted that clinicians in the diagnosis of thyroid diseases during pregnancy are entirely dependent on the quality of the work of the hormonal laboratory.

Women with subclinical hypothyroidism in the presence of circulating TPO antibodies are indicated for L-T4 replacement therapy.

The recommended treatment for hypothyroidism during pregnancy is the administration of L-T4 tablets. The use of any other drugs such as L-Tc or thyroid extracts is strongly discouraged.

The purpose of prescribing L-T4 is to normalize the level of TSH in the mother according to trimester-specific reference ranges (0.1-2.5 mU/l in the first trimester, 0.2-2 mU/l in the second trimester and 0.3- 3 mU / l in the III trimester).

If a woman with subclinical hypothyroidism was not initially prescribed replacement therapy, dynamic monitoring is necessary to detect the progression of hypothyroidism to overt. For this, the level of TSH and St. T4 every 4 weeks up to 16-20 weeks and at least once between the 26th and 32nd week. This approach has not been studied in prospective studies.

Level I

A comment. In my opinion, this recommendation sounds somewhat ominous - there is a feeling that it is easier to prescribe this replacement therapy, and not painstakingly and suspiciously study the function of the thyroid gland in dynamics. Along with frequent visits to the endocrinologist and information about hypothyroidism gleaned from the Internet, this cannot but affect the psychological state of the patient.

If the patient is already receiving replacement therapy for hypothyroidism, when pregnancy occurs, she should immediately increase the dose of L-T4 by 25-30% already with a delay in the menstrual cycle or with a positive home test on the test strip. In fact, this dose increase corresponds to taking nine daily doses of L-T4 per week (29% increase).

The degree of increase in the dose of L-T4, which during pregnancy will maintain normal TSH levels, varies greatly individually: some women need to add only 10-20%, while others may need an 80% increase in dose. This may depend on the etiology of hypothyroidism, as well as on the level of TSH before pregnancy.

Patients with hypothyroidism who are already receiving replacement therapy and planning a pregnancy should optimize replacement therapy before conception so that the TSH level is less than 2.5 mU/L. A low TSH level before conception reduces the risk of its increase in the first trimester of pregnancy.

Level B.

A comment. Interestingly, this recommendation is rated B, although there is a clear contradiction with the previous ones. The question arises: why, if in patients with already diagnosed hypothyroidism on the background of L-X therapy, it is necessary to achieve a TSH level of less than 2.5 mU/l (with a level of evidence B!!!), while if hypothyroidism has not yet been diagnosed (although and there is a recommendation for this 2) and the woman does not receive b-^, then there are no good reasons to reduce TSH, i.e. in general, prescribe b-^ if it is in the range of 2.5-4 mU / l? (see recommendation 8). That is, the “double standard” is obvious: if you have already been prescribed, then lower the TSH below 2.5 mU / l, but there seems to be no good reason for prescribing with TSH more than 2.5 mU / l. Carriage of AB-TPO is proposed as a “saving straw” (recommendation 9). Practitioners, of course, prefer greater clarity, but, alas, there is no such clarity in international recommendations on this issue either.

In women with hypothyroidism receiving L-N replacement therapy, it is recommended to determine the level of TSH once every 4 weeks in the first half of pregnancy.

This is because it is at this time that a change in the dose of the drug is most often required.

In women with hypothyroidism receiving L-Ig replacement therapy, TSH levels between the 26th and 32nd week of pregnancy should be measured at least once.

After delivery, the dose of L-T4 should be reduced to that which the patient took before pregnancy. The level of TSH should be additionally determined 6 weeks after delivery.

In the process of treating patients with adequately compensated hypothyroidism, there is no need to conduct any other studies (such as dynamic fetal ultrasound, antenatal tests and / or determination of any indicators in the umbilical cord blood), if they do not have their own additional indications.

In euthyroid women who do not receive L-N, with the carriage of antibodies to the thyroid gland, it is necessary to monitor its function with the determination of the level of TSH every 4 weeks in the first half of pregnancy and at least once between the 26th and 32nd weeks.

Separate randomized clinical trials have demonstrated a decrease in the likelihood of developing postpartum thyroiditis in women carriers of Ab-TPO during selenium therapy. In the future, no work was performed that would confirm or refute these data. Currently, selenium therapy is not recommended for pregnant women with circulating TPO antibodies.

Level C.

If a suppressed TSH level is detected in the first trimester (less than 0.1 mU / l), it is necessary to determine the St. T4; assessment of the level of total T3

and the level of antibodies to the TSH receptor (AT-rTTH) can help in the differential diagnosis of hyperthyroidism.

There are no sufficient arguments in favor of recommending or not recommending thyroid ultrasound for the differential diagnosis of hyperthyroidism during pregnancy.

Level I

A comment. In general, one cannot but agree with this, since ultrasound is unlikely to be a decisive method for the differential diagnosis of gestational physiological hyperthyroidism and Graves' disease (GD). In the USA, indications for ultrasound are not taken lightly as in Europe and especially in our country.

Radioactive iodine scanning or evaluation of radioactive iodine uptake during pregnancy should not be done.

Sufficient for gestational transient hyperthyroidism and vomiting of pregnancy are supportive measures, prevention of dehydration and, if necessary, hospitalization.

Thyrostatic drugs are not recommended for transient gestational hyperthyroidism.

In women with pre-existing thyrotoxicosis, a euthyroid state should be achieved before pregnancy is planned.

Level A

A comment. The recommendations do not explicitly indicate that if a woman with HD is planning a pregnancy in the very near future, she is indicated for radical treatment. That is, the 27th recommendation can be regarded as allowing for the possibility of achieving euthyroidism while taking thyreostatics and planning pregnancy against their background. In practice, and in some publications, such recommendations are sometimes found, but the author of this article treats them extremely negatively. Indeed, if the pregnancy occurred against the background of GD, the patient is indicated for thyrostatic therapy, which will be described below. But, in my opinion, this should not be taken in reverse. Plan your pregnancy

against the background of thyreostatics means deliberately taking an increased risk for both the mother and the fetus, while the generally good results of treating HD during pregnancy with thyreostatics should not cause euphoria. It should be remembered that the real long-term results of such therapy, by and large, are not known to us. In addition, thyrotoxicosis in any situation should be perceived as a condition that is not completely corrected by the means at our disposal. Finally, there is a rule that the use of any drugs during pregnancy should be avoided as much as possible (b-g does not apply to them, since this is an exact copy of the endogenous hormone). And finally, the conservative therapy of HD in general should be considered as ineffective, with the probability of a true remission of the disease in only about 25% of cases, while the likelihood of recurrence of thyrotoxicosis in the postpartum period in a woman with a history of HD remission is very high. In this regard, in my opinion, there is no more sense in planning a pregnancy while taking thyreostatics than some kind of “pity” for the patient, which, as usual, turns to her own harm. In real clinical practice, different life situations arise, but one way or another, it is better to be guided by the rule according to which pregnancy planning, especially (!!!) with the use of assisted reproductive technologies (ART), is an indication for radical treatment of HD, which eventually either otherwise, at least 80% of the total number of patients with this disease comes.

Propylthiouracil (PTU) is the drug of choice for the treatment of hyperthyroidism in the first trimester of pregnancy. If pregnancy occurs while taking thiamazole, it is advisable to transfer the patient to PTU. At the end of the first trimester, it is again recommended to transfer it to thia-mazol.

Level I

A comment. This is another recommendation that generated the most discussion. The situation has acquired such a turn due to the fact that in the United States, where PTU has traditionally been more widely used (compared to thiamazole, which is more popular in Europe), when analyzing the side effect databases, it was shown that PTU causes a toxic effect somewhat more often than thiamazole. hepatitis. In general, this was known before, while “somewhat more often” is still very rare. Nevertheless, this publication and its discussion led to a cooling of attitudes towards vocational schools. On the other hand, PTU, which penetrates biological barriers worse, is traditionally recommended as the drug of choice in the treatment of thyrotoxicosis during

pregnancy, although there are no clinical studies that would show its advantages over thiamazole in this situation. As a result, we get a certain mix of these two positions: for the first trimester, PTU is recommended, which penetrates the placenta worse, and then thiamazole is recommended, which is less hepatotoxic. There are several contradictions. Firstly, the fetus's own thyroid gland begins to work at 16-18 weeks, i.e. already in the second trimester. In this regard, why recommend vocational school at a time when the fetus has nothing to block yet? Whereas the transition to thiamazole is recommended just when it is worth fearing hypothyroidism in the fetus itself. Secondly, the vast majority of women go to the doctor towards the end of the first trimester. If thyrotoxicosis is detected in this situation, then according to the 28th recommendation of the vocational school, in most cases it will be necessary to prescribe for no more than 2-3 weeks, after which it will be necessary to switch to thiamazole. Does it make sense? Finally, there are no clinical studies that somehow confirm this approach. In this regard, the recommendation received level I, to which it fully complies, since it reflects only the personal opinion of experts, with which we have the right not to agree in everything.

The regimen of combination and thyreostatics (“block and replace”) should not be used during pregnancy, except in rare cases of fetal hyperthyroidism.

Level D

A comment. This refers to rare cases when, due to the transplacental transfer of maternal stimulating antibodies, the fetus develops hyperthyroidism. Accurate diagnosis of this condition is much more difficult. In this case, the woman is prescribed a relatively large dose of thyreostatic, which requires replacement therapy for her (“block and replace”). A thyreostatic with this approach will block the thyroid gland in both the mother and the fetus. How in this situation and on the basis of what to select the dose of thyreostatics remains unclear. Only the great rarity of such a complication saves.

In women receiving thyrostatic therapy during pregnancy, the level of sv. T4 and TSH should be determined approximately 1 time in 2 to 6 weeks. The goal is to maintain the level of St. T4 is slightly above the normal reference range.

Level B.

A comment. The question arises only as to why so often determine the level of TSH - it is obvious that with this approach, when St. T4 is maintained slightly above normal, TSH will be determined all the time as suppressed.

Thyroidectomy during pregnancy is rarely indicated. If it becomes necessary, it is most optimally carried out in the II trimester.

Level A

A comment. I can hardly imagine the indications for thyroidectomy for GD during pregnancy. The inability to control thyrotoxicosis is unlikely to fit here, since thyroidectomy, especially during pregnancy, is necessary only in a euthyroid state achieved against the background of thyreostatics. If this euthyroid state is reached, nothing prevents the continuation of thyreostatics until the end of pregnancy.

In patients with GD, including those with a history, at the 20-24th week of pregnancy, the determination of the level of AT-rTTH is indicated.

An ultrasound examination of the fetus is indicated in a situation where a woman has uncontrolled thyrotoxicosis and / or a high level of AT-rTTH (more than 3 times increased). It is necessary to consult an experienced specialist in the field of perinatal medicine. Monitoring may include ultrasound with an assessment of fetal heart rate, size, amniotic fluid volume, and detection of goiter.

Cordocentesis can be used in extremely rare cases, for example, when a goiter is detected in the fetus and the mother is taking thyreostatics; in this case, it is necessary to decide whether the fetus has hyper- or hypothyroidism? Level I

Thiamazole at a dose of up to 20-30 mg per day is safe for both the nursing mother and the child. PTU at a dose of up to 300 mg per day is the drug of choice, since it has a greater hepatotoxicity. When breastfeeding, the dose of thyreostatic should be divided into several doses.

Level A

4. Pregnancy and iodine prophylaxis

All pregnant and lactating women should consume at least 250 micrograms of iodine per day.

In order to achieve a total daily intake of iodine of 250 mcg, all women living in North America who are planning a pregnancy, pregnant or breastfeeding, it is advisable to additionally take 150 mcg of iodine. It is optimal to prescribe iodine in the form of potassium iodide, since the iodine content in kelp and other forms of algae varies significantly.

In other regions, the strategy for iodine prophylaxis during pregnancy, pregnancy planning and breastfeeding should be determined depending on the local level of iodine intake in the population and on the availability of iodized salt.

The intake of pharmacological doses of iodine during pregnancy is best avoided, except in the context of preparing HD patients for thyroidectomy. Clinicians should weigh the risks and benefits of using drugs or diagnostics containing high doses of iodine.

Regular intake of iodine in excess of 500-1100 micrograms per day should be avoided due to the potential risk of fetal hypothyroidism.

Level C.

5. Spontaneous

abortion, preterm labor, and thyroid antibodies

To date, there is not enough data to recommend or not to recommend screening determination of the level of antibodies to the thyroid gland in all pregnant women in the first trimester.

To date, there is insufficient evidence to recommend or not recommend screening for thyroid antibodies or administration of either immunoglobulin in women with normal thyroid function who have sporadic or recurrent miscarriage or

women undergoing in vitro fertilization (IVF).

To date, there are insufficient data to recommend or not recommend L-T4 therapy during pregnancy for carriers of Ab-TPO in the absence of thyroid dysfunction. Level I

To date, there is not enough data to recommend or not recommend L-T4 therapy during pregnancy for carriers of Ab-TPO in the absence of thyroid dysfunction in the case of planning the use of ART.

To date, there is insufficient evidence for screening for Ab-TPO, as well as for prescribing L-T4 therapy during pregnancy to carriers of Ab-TPO in the absence of thyroid dysfunction in order to prevent preterm labor.

Level I

A comment. All five recommendations in this section sound very similar and all are Level I. By and large, this section in the document could be painlessly omitted, since it essentially only indicates what kind of attempts were made to reduce the likelihood of spontaneous abortion, which is associated with autoimmune thyroiditis, but apparently not with hypothyroidism as such. As a result, as follows from the presented recommendations, “there are no strong arguments either for or against”, i.e. the results of the available studies are contradictory.

6. Nodular goiter and thyroid cancer

The optimal diagnostic strategy for nodular goiter during pregnancy should be based on risk stratification. All women should have a history and physical examination, TSH, and thyroid ultrasound.

The value of measuring calcitonin levels in nodular goiter during pregnancy is unknown. Level I

Needle biopsy of the thyroid gland or lymph nodes during pregnancy does not carry any additional risk. Level A

Nodular goiter, first detected during pregnancy, is the basis for fine-needle aspiration biopsy (FNA) of the thyroid gland in accordance with the 2009 American Thyroid Association guidelines for the diagnosis and treatment of nodular goiter. FNA may be delayed until the postoperative period at the request of the patient. Level I

Radionuclide studies during pregnancy are contraindicated. Accidental, inadvertent administration of radioactive iodine to a patient before 12 weeks of gestation does not lead to destruction of the thyroid gland in the fetus.

Because the prognosis for women with well-differentiated thyroid cancer (HDTC) diagnosed during pregnancy but untreated is similar to that of non-pregnant women, surgical treatment of HDTC can in most cases be deferred until postpartum.

Level B.

A comment. A similar recommendation with various variations in wording has already been repeatedly cited both in the latest recommendations on cancer and in the previous version of these recommendations from 2007. In this case, it was assigned a fairly high level of B. Interestingly, in this case, the appeal is not to there are few retrospective studies comparing the prognosis for patients operated and not operated during pregnancy. First of all, the proposed wording means that pregnancy itself does not contribute to the progression of TDTC, which develops according to its own laws, just as outside of pregnancy. This is followed by the statement that, as a rule (in most cases, generally), the operation can be postponed until the postpartum period, since both during pregnancy and outside it, the postponement of the operation for the period that elapses before the birth will have practically no effect on the an already good prognosis for the patient. Obviously, in some cases there may be exceptions associated both with a specific clinical picture and with the urgent desire of the patient to be operated on as soon as possible.

The effect of pregnancy on the course of medullary thyroid cancer (MTC) is unknown. Operative treatment during pregnancy is recommended in the presence of a large primary tumor or metastases to the lymph nodes.

Level I

A comment. Level I is perfectly legitimate, because, except on some clinical assumptions in the complete absence of the results of any studies, this recommendation is not based. Probably, in the future it makes sense to somehow stratify the risk of MTC using both clinical and molecular genetic methods, and options for such a differentiated approach are already presented in the literature. It is obvious that if during pregnancy with TDTC the overall risk of surgery for the mother and fetus most often exceeds the very low risk of postponing surgery for 4-6 months, then at least in a number of forms of MTC this period may be significant. (Noteworthy in this regard is the 53rd Grade B recommendation.) It should also be noted here that MTC can coexist with pheochromocytoma in the MEN-2 syndrome. In terms of wording, the question arises: what does “large primary tumor” mean?

To date, there is no evidence that surgical treatment of thyroid cancer in the second trimester of pregnancy is accompanied by an increased risk to the mother or fetus.

Level B.

A comment. As they say, choose according to your taste, which recommendation do you like better - the 51st or the 53rd? Both have level B ... I would stop at the 51st, for the reason that, in addition to the physical risk of medical manipulations, during pregnancy, more than ever, the psychological trauma of the patient is expressed. Suffice it to say that from a fairly peaceful obstetric and gynecological circles, the patient smoothly moves into oncology, with a completely different system of units and intonation of the doctors' conversation. The outcome of pregnancy, in the full sense of this concept, including the performance of the unborn child at school, is by and large unpredictable - if it turns out to be unfavorable, then it will be difficult for the patient to explain that there is no causal relationship between him and the surgery undertaken in the second trimester of pregnancy. On the other hand, for some patients, a greater psychological trauma may be the realization that they have (even for several months) a cancerous tumor, for which treatment is not being undertaken. Finally, pregnancy is different: it could be the third pregnancy in a healthy 30-year-old woman, or it could be the first pregnancy.

as a result of the 6th IVF attempt in a woman aged 45 years. Both, of course, are equally valuable, and comparisons are hardly appropriate here, but. The final decision will be made by the patient herself, although it is well known that the doctor will always, even trying to resist this internally, will implicitly incline the patient to the decision that he himself considers the best, and in the case of surgical treatment, to the one that he owns.

If a nodular formation is detected during pregnancy, which, according to FAB, is not a tumor, surgical treatment is not indicated, except in cases of severe compression syndrome.

If the decision is made not to perform surgery until the postpartum period for TDTC during pregnancy, thyroid ultrasound should be performed in each trimester, since rapid and significant growth of the node may require surgical treatment.

Surgical treatment for HDTC can be delayed until the postpartum period without adversely affecting the patient's prognosis. Nevertheless, with a significant growth of the tumor node or the appearance of metastases in the cervical lymph nodes before the onset of the second half of pregnancy, surgical treatment is indicated.

For women who have delayed surgery for TDTC until postpartum, L-I therapy may be given, with the goal of maintaining TSH levels within 0.1-1.5 mU/L. Level I

The reproductive system of a woman is a finely organized system of closely interconnected structural and functional elements. The reproductive function of a woman is provided by a set of mechanisms that are implemented at the level of the reproductive organs (ovaries, vagina, uterus, fallopian tubes) and are under the strict control of the highest regulatory center - the hypothalamic-pituitary system. The whole cascade of processes necessary for follicle maturation, ovulation, fertilization, corpus luteum function, preparation of the endometrium for implantation, adhesion and invasion of the blastocyst, as well as successful prolongation of pregnancy, depends on the preservation of neuroendocrine regulatory pathways in the woman's body, the slightest violation of which can lead to disruption of the functioning of the entire complex mechanism.

The thyroid gland is one of the most important parts of the neuroendocrine system and has a significant impact on reproductive function.

The main function of the thyroid gland is to provide the body with thyroid hormones: thyroxine and triiodothyronine, an integral structural component of which is iodine.

Thyroid hormones regulate the processes of development, maturation, specialization and renewal of almost all tissues and are of exceptional importance for the laying and development of the fetal brain, the formation of the child's intelligence, the growth and maturation of the bone skeleton, the reproductive system, affect sexual development, menstrual function and fertility.

Thyroid diseases, being one of the most common endocrine pathologies in women of reproductive age, can have a negative impact on the physiology of reproduction, affecting the metabolism of sex hormones, menstrual function, fertility, pregnancy, fetal and newborn development. Pregnancy is a period of increased stimulation of the thyroid gland women, which is due to the influence of many factors that directly or indirectly stimulate the thyroid gland: hyperproduction of chorionic hormone, increased production of estrogens and thyroxin-binding globulin; an increase in renal blood flow and glomerular filtration, leading to increased excretion of iodine in the urine; changes in the metabolism of maternal thyroid hormones due to the active functioning of the fetoplacental complex.

These changes are aimed at increasing the pool of thyroid hormones, since the fetal thyroid gland begins to fully function only from the 15-16th week of pregnancy, and in the early stages of pregnancy, the entire embryogenesis and, above all, the development of the central nervous system of the fetus, is provided by the mother's thyroid hormones. In this regard, the need for thyroid hormones in the first trimester of pregnancy increases by 30-50%, and the need for iodine in a pregnant woman increases by 1.5-2 times. Hypothyroxinemia negatively affects the development of the fetus precisely in the early stages of pregnancy, and the central nervous system of the fetus is the most vulnerable to deficiency of thyroid hormones.

Features of the diagnosis of thyroid dysfunction during pregnancy
For pregnant women, the upper reference range for thyroid-stimulating hormone is reduced from 4.0 to 2.5 mU/L.
Standards for thyroid-stimulating hormone by trimester of pregnancy: I trimester: 0.1-2.5 mU/l; II trimester: 0.2-2.5 mU/l; III trimester: 0.3-3.0 honey / l.
The first trimester of pregnancy is characterized by low levels of thyroid-stimulating hormone, which is associated with TSH-like effects of human chorionic hormone.
In the first half of pregnancy after ovulation stimulation or IVF, the level of thyroid-stimulating hormone is normally reduced or suppressed in 20-30% of women and is almost always reduced (suppressed) in multiple pregnancies.
The levels of total fractions T4 and T3 are normally always increased by 1.5 times, which is associated with hyperestrogenism and an increase in the production of thyroxin-binding globulin in the liver. Determination of total T4 and T3 in pregnant women is not advisable.
The level of free T4 gradually decreases from the 1st to the 3rd trimester of pregnancy and in the later stages (> 26-30 weeks) using standard methods is defined as low-normal or borderline-low normal.

IODINE DEFICIENCY DISEASES
Iodine deficiency diseases are all pathological conditions that develop in a population as a result of iodine deficiency, which can be prevented by normalizing iodine intake. Women at the highest risk of developing iodine deficiency diseases include women during pregnancy and breastfeeding and children.

All mechanisms of stimulation of the thyroid gland during pregnancy are physiological in nature, ensuring the adaptation of the woman's endocrine system to pregnancy, and in the presence of adequate amounts of iodine will not have any adverse effects.

Lack of iodine intake in the body leads to the deployment of a chain of successive adaptive processes aimed at maintaining the normal synthesis and secretion of thyroid hormones. But, if the deficiency of these hormones persists long enough, then there is a breakdown of the adaptation mechanisms with the subsequent development of an iodine deficiency disease. The spectrum of iodine deficiency disease is extensive and, in addition to thyroid diseases, it includes a number of obstetric, gynecological and neurological diseases, and the most severe iodine deficiency conditions are associated with reproductive disorders or develop perinatally: congenital fetal anomalies, endemic cretinism, neonatal goiter, hypothyroidism, reduced fertility. The most severe consequence of iodine deficiency in the perinatal period is endemic (neurological) cretinism - an extreme degree of mental and physical developmental delay. Endemic cretinism is usually characteristic of regions with severe iodine deficiency. In regions of moderate iodine deficiency, subclinical disorders of intellectual development are observed. The difference in IQ between the population living in regions with iodine deficiency and normal iodine intake is on average 13.5% points. prevention

To overcome iodine deficiency, the following methods of prevention are used:
- mass iodine prophylaxis - prophylaxis on a population scale, carried out by adding iodine to the most common foods (bread, salt);
- group iodine prophylaxis - prevention on the scale of certain groups at an increased risk of developing iodine deficiency diseases: children, adolescents, pregnant and lactating women. It is carried out by regular long-term use of drugs containing physiological doses of iodine;
- individual iodine prophylaxis - prophylaxis in individuals by long-term administration of preparations containing physiological doses of iodine.

Since pregnancy is the period of the highest risk of developing iodine deficiency conditions, then already at the stage of its planning, throughout pregnancy and in the postpartum period, women are shown individual iodine prophylaxis using potassium iodide preparations (250 μg per day) or multivitamin-mineral complexes containing iodine in equivalent doses.

It is important to note that for individual iodine prophylaxis in pregnant women, it is necessary to avoid the use of iodine-containing dietary supplements. The only contraindication for the appointment of iodine preparations during pregnancy is thyrotoxicosis (Graves' disease). Carrying antibodies to thyroid tissues without thyroid dysfunction is not a contraindication for individual iodine prophylaxis, although it requires dynamic monitoring of thyroid function during pregnancy.

EUTHYROID GOITER
Euthyroid goiter is a visible and / or palpable enlargement of the thyroid gland of the gland without disturbing its function. In most cases, euthyroid goiter is detected during a targeted examination.

Epidemiology
The prevalence of nodular goiter among pregnant women (nodular formations exceeding 1 cm in diameter) is 4%. Approximately 15% of women develop nodules for the first time during pregnancy.

Prevention
The objective of preventive measures is to achieve an optimal level of iodine intake by the population. The development of goiter during pregnancy, both in mother and fetus, directly correlates with the degree of iodine deficiency. Therefore, carrying out iodine prophylaxis from early pregnancy is the most effective method for preventing goiter and hypothyroxinemia, both in the mother and in the fetus.

Diagnostics
To diagnose diffuse euthyroid goiter, it is sufficient to determine the level of thyroid-stimulating hormone and conduct an ultrasound scan of the thyroid gland. Ultrasound of the thyroid gland allows you to determine its volume, structure, the presence or absence of nodular formations and their size. The volume of the thyroid gland is determined by a formula that takes into account the width, length and thickness of each lobe and the correction factor for ellipsoidality:

Thyroid Volume = [(RH W x R L x R T) + (W L x L L x T L)] x 0.479.

In adult women, goiter is diagnosed if the volume of the thyroid gland, according to ultrasound, exceeds 18 ml. If thyroid nodules larger than >1 cm in diameter are detected in a pregnant woman, a fine-needle aspiration biopsy is indicated to exclude a thyroid tumor, which is performed under ultrasound guidance, which minimizes the time of the procedure and reduces the likelihood of obtaining inadequate material. The presence of goiter in a pregnant woman is not a contraindication for pregnancy. The exception is cases of large goiter, squeezing neighboring organs; nodules more than 4 cm in diameter; suspicion of malignancy. In these situations, it is advisable to conduct surgical treatment before a planned pregnancy. The main condition for the onset of pregnancy after surgical treatment is the euthyroid state.

Clinical picture
The picture of clinical manifestations of EZ depends mainly on the degree of enlargement of the thyroid gland, since a violation of its function is not detected for a long time. Stimulation of the thyroid gland during pregnancy in conditions of iodine deficiency leads to an increase in its volume by more than 20% of the original. The consequence of this process is the formation of goiter in 10-20% of women living in conditions of iodine deficiency.

Treatment
The indication for surgical treatment of goiter during pregnancy is the detection of thyroid cancer according to biopsy data, compression of the trachea and other organs with large goiter. The optimal time for the operation is the 2nd trimester of pregnancy - after the completion of placentation processes (16-17 weeks) up to 22 weeks of pregnancy. In the case of thyroidectomy, levothyroxine replacement therapy is indicated immediately after surgical treatment at a daily dose of 2.3 μg/kg of the woman's body weight.

In the presence of diffuse or nodular thyroid goiter during pregnancy, the main task is to maintain a stable euthyroid state. For this, mandatory monitoring of the level of thyroid-stimulating hormone and free T4 is carried out in each trimester of pregnancy. Reducing the size of the thyroid gland is almost impossible to achieve, so it is necessary to prevent excessive growth of goiter or nodules. It is advisable to dynamic ultrasound of the thyroid gland during pregnancy once a trimester.

Treatment of euthyroid goiter during pregnancy is carried out using three therapy options:
- monotherapy with iodine preparations;
- monotherapy with levothyroxine preparations;
- combination therapy with iodine and levothyroxine.

The most optimal in women of reproductive age is potassium iodide monotherapy 200 mcg/day, since it also provides individual iodine prophylaxis. Combination therapy with iodine and levothyroxine is in second place. If a woman received combination therapy before pregnancy, it is not advisable to switch her to monotherapy with iodine preparations. If a woman received levothyroxine monotherapy for EZ, during pregnancy, for the purpose of individual iodine prophylaxis, it is advisable to add 200 μg of potassium iodide.

To monitor therapy, it is necessary to dynamically determine the level of thyroid-stimulating hormone and free T4 every 6-8 weeks.

Indications for the appointment of combination therapy with levothyroxine and iodine in a pregnant woman with goiter are:
- excessive growth of goiter in a pregnant woman in case of ineffectiveness of iodine monotherapy;
- the development of hypothyroxinemia in a pregnant woman - the level of thyroid-stimulating hormone is above 2.5 mU / l.
- the presence of signs of autoimmune thyreolitis (an echographic picture and / or an increase in the level.

Forecast
The presence of goiter or large nodules is not a contraindication for prolongation of pregnancy, in the absence of malignancy according to cytological examination. In most cases, goiter does not require surgical treatment. In the presence of goiter in a pregnant woman, the processes of differentiation of the fetal thyroid gland, changes in its structure, dysfunction can be disrupted, mainly the development of the fetal thyroid gland slows down, which is due to the relative hypothyroxinemia of the mother. This may contribute to hypofunction of the thyroid gland in the postnatal period. Goiter in a pregnant woman is a risk factor for the development of goiter in a newborn.

HYPOTHYROISIS SYNDROME IN PREGNANT WOMEN
Hypothyroidism is a clinical syndrome caused by a persistent deficiency of thyroid hormones in the body.

Epidemiology
Hypothyroidism is one of the most common endocrine diseases. In women, hypothyroidism is diagnosed 6 times more often than in men (6:1). The overall prevalence of primary overt hypothyroidism in the population is 0.2-2%, subclinical - approximately 7-10% in women and 2-3% in men. The prevalence of hypothyroidism during pregnancy: overt - 0.3-0.5%, subclinical - 2-3%.

Classification
Primary hypothyroidism
- due to the destruction or lack of functionally active tissue of the thyroid gland (chronic autoimmune thyroiditis, surgery on the thyroid gland, radioactive iodine therapy, with subacute, postpartum and "silent" (painless) thyroiditis, with agenesis and dysgenesis of the thyroid gland);
- due to a violation of the synthesis of thyroid hormones (congenital defects in the biosynthesis of thyroid hormones; severe deficiency or excess of iodine; drug and toxic effects (thyreostatics, lithium preparations, potassium perchlorate, etc.).

Central (hypothalamic-pituitary, secondary) hypothyroidism:
- destruction or lack of cells producing thyroid-stimulating hormone and / or TSH-RG (tumors of the hypothalamic-pituitary region; traumatic or radiation injuries (surgical operations, proton therapy)); vascular disorders (ischemic and hemorrhagic lesions, aneurysms of the internal carotid artery); infectious and infiltrative processes (abscess, tuberculosis, histiocytosis); chronic lymphocytic hypophysitis; congenital disorders (pituitary hypoplasia, septo-optic dysplasia) .;
- violation of the synthesis of thyroid-stimulating hormone and / or TSH-RG (mutations affecting the synthesis of the TSH-RG receptor, β-subunit of thyroid-stimulating hormone, Pit-1 gene (Pituitary-specific transcription factor 1); drug and toxic effects (dopamine, glucocorticoids, drugs thyroid hormones).

According to the severity of primary hypothyroidism is divided into:
- subclinical - elevated levels of thyroid-stimulating hormone with a normal level of free T4, asymptomatic course or only non-specific symptoms;
- manifest - an increased level of thyroid-stimulating hormone, with a reduced level of free T4, nonspecific symptoms characteristic of hypothyroidism are present, but an asymptomatic course is also possible;
- compensated;
- decompensated;
- complicated - a detailed clinical picture of hypothyroidism, there are severe complications - heart failure, polyserositis, secondary pituitary adenoma, myxedematous coma, etc.

Etiology and pathogenesis
Most often, primary hypothyroidism develops as a result of autoimmune thyroiditis, less often after thyroid surgery and radioactive iodine therapy for various forms of goiter. Primary hypothyroidism in the outcome of autoimmune thyroiditis can be combined with other organ-specific autoimmune endocrine diseases within the autoimmune polyglandular syndrome type 2, the most common variants of which are Schmidt's syndrome (autoimmune thyroiditis in combination with primary hypocorticism) and Carpenter's syndrome (autoimmune thyroiditis). Odit in combination with sugar type I diabetes). Secondary and tertiary hypothyroidism, which develop as a result of thyroid-stimulating hormone deficiency and thyrotropin-releasing hormone, is rarely observed (0.005% -1%), their differential diagnosis in clinical practice presents significant difficulties, and therefore they are often combined with the term "central" (hypothalamic-pituitary) hypothyroidism. Central hypothyroidism, as a rule, occurs with hypopituitarism and is combined with insufficiency of other tropic functions of the adenohypophysis.

The incidence of hypothyroidism ranges from 0.6 to 3.5 per 1000 population per year and increases with age, reaching about 12% in the group of older women. The prevalence of congenital primary hypothyroidism is 1:35004000 newborns. Screening is mandatory for all newborns on the 3-5th day of life.

Clinical picture
Classical clinical manifestations of overt hypothyroidism (weakness, drowsiness, "masklike" face, edematous limbs, periorbital edema, cold intolerance, decreased sweating, weight gain, lower body temperature, slow speech, hoarse voice, drowsiness, lethargy, slow speech, decreased voice timbre , paresthesia, memory loss, hearing loss, brittle hair, thinning hair on the head, dry skin, hyperkeratosis of the skin of the elbows, cold skin, anemia, biliary dyskinesia, bradycardia, diastolic arterial hypertension, constipation, depression, etc.) are diverse, are nonspecific, never occur simultaneously and are not pathognomonic for this disease, have low diagnostic sensitivity. Subclinical hypothyroidism can also present with nonspecific symptoms or be asymptomatic. The clinical symptoms of both overt and subclinical hypothyroidism cannot act as obligate markers for the diagnosis of the disease, therefore, for the diagnosis of hypothyroidism, the data of the clinical picture are of secondary importance. Modern approaches to the diagnosis of thyroid dysfunction do not suggest completely ignoring the clinical stage of diagnosis, but are based on the position that laboratory diagnostics plays a decisive role in the verification of thyroid dysfunction.

Diagnostics
To establish the diagnosis of hypothyroidism, determine the level of damage and assess the degree of its severity, the levels of thyroid-stimulating hormone and free T4 in the blood serum are examined. Primary overt hypothyroidism is characterized by an increase in the level of thyroid-stimulating hormone and a decrease in the level of free T4 (fT4).

Subclinical hypothyroidism is an isolated increase in the content of thyroid-stimulating hormone with a normal concentration of fT4. Secondary or tertiary (central) hypothyroidism is characterized by a normal or reduced content of thyroid-stimulating hormone (rarely a slight increase) and a decrease in the concentration of fT4.

Determination of the concentration of antibodies to thyroglobulin or thyroperoxidase in the blood serum makes it possible to establish the cause of hypothyroidism and predict the transition of subclinical hypothyroidism to manifest (in subclinical hypothyroidism, the presence of AT-TPO serves as a predictor of its transition to manifest hypothyroidism).

Autoimmune thyroiditis is the main cause of spontaneous hypothyroidism. The basis for establishing the diagnosis of autoimmune thyroiditis is the presence of the following "major" clinical and laboratory signs: primary hypothyroidism (manifest or persistent subclinical); the presence of antibodies to thyroid tissue and ultrasound signs of autoimmune pathology (diffuse decrease in echogenicity and heterogeneity of thyroid tissue). In the absence of at least one of these diagnostic features, the diagnosis of autoimmune thyroiditis is probabilistic. Among antibodies to the thyroid gland for the diagnosis of autoimmune thyroiditis, it is advisable to study only the level of Ab-TPO, since the isolated carriage of Ab-TG is rare and has less diagnostic value.

Treatment
Compensated hypothyroidism is not a contraindication for a woman planning a pregnancy. The recommended treatment for hypothyroidism during pregnancy is the administration of levothyroxine tablets.

Patients with hypothyroidism who are already receiving replacement therapy and planning a pregnancy should optimize replacement therapy before conception so that the level of thyroid stimulating hormone is less than 2.5 mU/l. A low level of thyroid-stimulating hormone before conception reduces the risk of its increase in the first trimester of pregnancy. If outside of pregnancy the usual replacement dose of levothyroxine is 1.6-1.8 mcg per kg of body weight, then when pregnancy occurs, the need for levothyroxine increases and its dose should be increased by 25-30% immediately upon confirmation of pregnancy by a positive test. The degree of increase in the dose of levothyroxine, which during pregnancy will ensure the maintenance of a normal level of thyroid-stimulating hormone, varies significantly individually and depends on the etiology of hypothyroidism, as well as on the level of thyroid-stimulating hormone before pregnancy. Adequate compensation for hypothyroidism corresponds to maintaining the level of thyroid-stimulating hormone in a pregnant woman in accordance with the trimester - specific reference ranges: in the first trimester - 0.1-2.5 mU/l; in the II trimester - 0.2-2 mU / l; in the III trimester - 0.3-3 honey / l.

In women with hypothyroidism receiving levothyroxine replacement therapy, the level of thyroid-stimulating hormone is recommended to be determined once every 4 weeks in the first half of pregnancy, since it is at this time that a change in the dose of the drug is most often required. Further monitoring of the adequacy of the dose of levothyroxine is carried out by the level of thyroid-stimulating hormone and fT4 at least once every 30-40 days during pregnancy.

Levothyroxine preparations are taken daily in the morning on an empty stomach 30 minutes before breakfast. Given that some drugs can significantly reduce the bioavailability of levothyroxine (eg, calcium carbonate, iron preparations), the administration of any other drugs should be postponed, if possible, to 4 hours after taking levothyroxine. When determining the content of fT4 in pregnant women who are on levothyroxine replacement therapy, you should not take the drug before taking blood for hormonal analysis, since in this case the results of the study will be overestimated. When examining only the level of thyroid-stimulating hormone, taking levothyroxine does not affect the results of the study.

In overt hypothyroidism first diagnosed during pregnancy (when thyroid-stimulating hormone levels exceed trimester-specific reference ranges and a reduced fT4 level is detected, or when thyroid-stimulating hormone level exceeds 10 mU/l regardless of the level of fT4), the woman is immediately prescribed a full replacement dose of levothyroxine (2, 3 mcg / kg body weight), without its gradual increase, adopted for the treatment of hypothyroidism outside of pregnancy.

Despite the proven association of subclinical hypothyroidism with adverse outcomes for both mother and fetus, due to the lack of results from randomized controlled trials, there is currently insufficient evidence to recommend or not recommend levothyroxine therapy in all patients with subclinical hypothyroidism and the absence of AT. -TPO. If a woman with subclinical hypothyroidism was not initially prescribed replacement therapy, dynamic monitoring is necessary to detect the progression of hypothyroidism to overt. To do this, a dynamic assessment of the level of thyroid-stimulating hormone and fT4 during pregnancy is carried out every 4 weeks until 16-20 weeks and at least once between the 26th and 32nd weeks.

Replacement therapy with levothyroxine is indicated for women with subclinical hypothyroidism in the presence of circulating TPO antibodies. In euthyroid women who do not receive levothyroxine, while carrying AT-TPO, it is necessary to monitor its function with the determination of the level of thyroid-stimulating hormone every 4 weeks in the first half of pregnancy and at least once between the 26th and 32nd weeks. In hypothyroid women receiving levothyroxine replacement therapy, thyroid-stimulating hormone levels between the 26th and 32nd week of pregnancy should be assessed at least once. After delivery, the dose of levothyroxine should be reduced to that which the patient took before pregnancy. The level of thyroid-stimulating hormone should be additionally determined 6 weeks after delivery.

Isolated gestational hypothyroxinemia (low fT4 with normal thyroid-stimulating hormone) does not require treatment during pregnancy. In the process of treating patients with adequately compensated hypothyroidism, there is no need to conduct any other studies, such as dynamic fetal ultrasound, antenatal tests and / or determination of any indicators in the umbilical cord blood, if there are no obstetric indications for them.

Prevention
Timely detection and compensation of hypothyroidism at the stage of pregnancy planning. Screening of pregnant women in risk groups.

Screening
Although there is currently insufficient evidence for or against universal screening with thyroid-stimulating hormone levels in the first trimester of pregnancy, thyroid-stimulating hormone levels in early pregnancy should be performed in the following groups of women at an increased risk of developing hypothyroidism:
- history of thyroid disease, including thyroid surgery;
- age over 30 years;
- symptoms of dysfunction of the thyroid gland or the presence of goiter;
- carriage of AT-TPO;
- type 1 diabetes or other autoimmune diseases;
- history of miscarriages or premature births;
- irradiation of the head and neck in anamnesis;
- family history of thyroid dysfunction;
- morbid obesity (body mass index >40 kg/m2);
- taking amiodarone, lithium or recent administration of iodine-containing contrast agents;
- infertility;
- living in regions of severe and moderate iodine deficiency.

Forecast
Both overt and subclinical hypothyroidism are associated with adverse pregnancy outcomes for both mother and fetus. Pregnant women with hypothyroidism have an increased risk of obstetric and neonatal complications - spontaneous miscarriages, anemia, gestational arterial hypertension, intrauterine fetal death, premature birth, placental abruption and postpartum hemorrhage, low birth weight and neonatal respiratory distress syndrome, disorders of neurocognitive development of newborns , decrease in the coefficient of intellectual development, delays in speech, motor skills and attention in children of primary school age. Pregnant hypothyroidism has an adverse effect on the organogenesis of the fetus, and above all on the development of its central nervous system. Since the thyroid gland of the fetus practically does not function in the first half of pregnancy, with normal function of the thyroid gland of the pregnant woman, the development of the nervous system will be adequately provided for both in a normal fetus and in a fetus with aplasia of the thyroid gland (with congenital hypothyroidism). Pregnant hypothyroidism is more dangerous for the development and functioning of the fetal brain with normal thyroid anlage than congenital fetal hypothyroidism due to thyroid aplasia, with normal thyroid function of the pregnant woman. If a child with congenital hypothyroidism, who was not affected in utero by hypothyroxinemia in the first half of pregnancy, is prescribed levothyroxine replacement therapy immediately after birth, the development of his nervous system may not differ from normal. On the contrary, in case of hypothyroidism in the mother, even in the presence of normal laying of the thyroid gland of the fetus, the consequences of hypothyroxinemia in the first half of pregnancy on the development and functioning of the fetal brain are extremely negative.

THYROTOXICOSIS SYNDROME IN PREGNANT WOMEN
Thyrotoxicosis is a clinical syndrome caused by persistent pathological hypersecretion of thyroid hormones.

Epidemiology
About 80% of all cases of thyrotoxicosis in the population are caused by Graves' disease (Basedow's disease, diffuse toxic goiter). Graves' disease is 5 to 10 times more common in women than in men. As a rule, the disease manifests itself in young and middle age. The prevalence of thyrotoxicosis during pregnancy is 1-2 cases per 1000 pregnancies.

Classification
According to the severity of thyrotoxicosis is divided into:
- subclinical - reduced or suppressed level of thyroid-stimulating hormone with normal levels of free T3 (fT3) and fT4;
- manifest - a decrease in the level of thyroid-stimulating hormone in combination with an increase in the level of fT4 and / or fT3;
- complicated - in the presence of complications (atrial fibrillation, heart failure, tyrogenic relative adrenal insufficiency, dystrophic changes in parenchymal organs, psychosis, severe underweight).

Etiology and pathogenesis
Graves' disease is a systemic autoimmune disease that develops as a result of the production of antibodies to the thyroid-stimulating hormone receptor, clinically manifested by damage to the thyroid gland with the development of thyrotoxicosis syndrome in combination with extrathyroid pathology (endocrine ophthalmopathy, pretibial myxedema, acropathy). The term "diffuse toxic goiter" does not reflect the essence of the pathogenesis of the disease, describing only a change in the structure and function of the thyroid gland. Often, Graves' disease proceeds without enlargement of the thyroid gland or may develop against the background of its previous nodular lesion. The pathogenesis of Graves' disease is based on the production of stimulating autoantibodies to the thyroid-stimulating hormone receptor. The presence of a hereditary predisposition to the disease is indicated by the detection of circulating autoantibodies to the thyroid gland in 50% of relatives of patients with Graves' disease, the frequent detection of the HLA DR3 haplotype (DRB1 * 03 04 alleles - DQB1 * 02 - DQA1 * 05 01) in patients, a frequent combination with other autoimmune diseases. The combination of Graves' disease with autoimmune chronic adrenal insufficiency (Addison's disease), type 1 diabetes mellitus, and other autoimmune endocrinopathies is referred to as type 2 autoimmune polyglandular syndrome.

Clinical picture
In Graves' disease, the symptoms of thyrotoxicosis are more pronounced: shortness of breath, tachycardia, increased appetite, emotional lability, high pulse pressure, weight loss or lack of weight gain during pregnancy. In 50% of women, endocrine ophthalmopathy, pretibial myxedema, increased sweating and dry skin are noted. The main marker of Graves' disease is the detection of autoimmune thyroiditis to the thyroid-stimulating hormone receptor.

Diagnostics
Diagnosis of Graves' disease during pregnancy is based on clinical data and the results of laboratory and instrumental studies.

Differential Diagnosis
It is necessary to carry out a differential diagnosis of Graves' disease and transient gestational hyperthyroidism - a physiological transient suppression of the level of thyroid-stimulating hormone in combination with an increase in the level of fT4, observed in the first half of pregnancy and associated with the structural homology of thyroid-stimulating hormone and human chorionic gonadotropin.

There is a more pronounced increase in the concentrations of fT4 and fT3 and a more significant suppression of the level of thyroid-stimulating hormone, and these changes are persistent. Ultrasound shows an increase in volume and diffuse hypoechogenicity of the thyroid gland, but in some cases goiter may not be detected. On the contrary, with transient gestational hyperthyroidism, the clinical picture is nonspecific and there are symptoms characteristic of pregnancy (general weakness, tachycardia, nausea). Endocrine ophthalmopathy is absent. The level of thyroid-stimulating hormone is not reduced to zero, and the level of fT4 is moderately elevated (with the exception of multiple pregnancies). An elevated level of AT-TPO may be detected, but autoimmune thyroiditis to the thyroid-stimulating hormone receptor is not detected. Transient gestational hyperthyroidism does not require specific therapy; if necessary (uncontrollable vomiting), hospitalization and symptomatic treatment (infusion therapy) are possible. By 16-20 weeks, transient gestational hyperthyroidism is completely stopped.

Screening
Screening in the general population is not economically justified due to the relatively low prevalence of the disease. At the same time, determination of the concentration of thyroid-stimulating hormone in the blood serum during screening for hypothyroidism, which has a high prevalence, makes it possible to identify patients with low levels of thyroid-stimulating hormone.

Treatment
Identification of Graves' disease in a pregnant woman is not an indication for termination of pregnancy. Thyrostatic therapy is the main treatment for Gaves disease during pregnancy. Thyrostatic drugs are currently used, which are not contraindicated during pregnancy and lactation.

In Graves' disease, first diagnosed during pregnancy, conservative treatment is indicated for all patients, regardless of the size of the goiter or any other factors. Even if, according to the clinical picture, the patient is shown radical treatment (surgical removal of the thyroid gland or radioactive iodine therapy), it is transferred to the postpartum period. As the only indication for surgical treatment of thyrotoxicosis during pregnancy (the optimal period is the second half of pregnancy), intolerance to thyreostatics (severe leukopenia, allergic reactions, etc.) is currently considered. If a decision is made on surgical treatment, immediately after removal of the thyroid gland (thyroidectomy or extremely subtotal resection of the thyroid gland), levothyroxine is prescribed at a dose of 2.3 μg / kg of body weight. All thyreostatic drugs cross the placenta and can have a suppressive effect on the fetal thyroid gland . Propylthiouracil penetrates worse from the maternal circulation into the fetal circulation, as well as from the mother's blood into milk. In this regard, propylthiouracil has traditionally been considered the drug of choice for the treatment of thyrotoxicosis in pregnant women, although thiamazole can also be used for this purpose on similar principles and in equivalent doses. According to the latest American Thyroid Association guidelines for the diagnosis and treatment of thyroid disorders during pregnancy and the postpartum period, propylthiouracil is the drug of choice for the treatment of thyrotoxicosis in the first trimester of pregnancy. If pregnancy occurs while taking thiamazole, it is advisable to transfer the patient to taking propylthiouracil, which crosses the placenta to a lesser extent. At the end of the first trimester, it is again recommended to transfer it to thiamazole as a less hepatotoxic drug.

Starting doses of antithyroid drugs depend on the severity and level of hyperthyroxinemia. With moderate thyrotoxicosis, the starting dose of propylthiouracil should not exceed 200 mg per day (50 mg of propylthiouracil 4 times a day); respectively, for thiamazole it is 20 mg (for 1-2 doses). After the decrease in the level of fT4 to the upper limit of the norm, the dose of propylthiouracil is reduced to maintenance (2550 mg / day). Usually after 2-6 weeks the drug is canceled.

The main goal of treatment with thyreostatics during pregnancy is to achieve the level of fT4 at the upper limit of the normal reference values ​​specific for each trimester of pregnancy, or slightly above normal values. To control the ongoing therapy, a monthly study of the level of fT4 is indicated. It is inexpedient to achieve normalization of the level of thyroid-stimulating hormone and to examine it frequently. The administration of levothyroxine (as part of the “block and replace” regimen), which leads to an increase in the need for thyreostatics, is not indicated during pregnancy, since it is not safe for the fetus. With an excessive decrease in the level of fT4 (low normal or below normal), the thyreostatic is temporarily canceled under the monthly control of the level of fT4, if necessary, it can be prescribed again.

Usually, the symptoms of thyrotoxicosis in Graves' disease during treatment with thyreostatics become less pronounced in the first trimester, which makes it possible to reduce the dose of drugs in the II and III trimesters to the minimum maintenance, and in 20-30% of cases, complete withdrawal of drugs after 28-30 weeks of pregnancy is possible. However, with a persistently high titer of antibodies to the thyroid-stimulating hormone receptor, thyreostatic therapy should be continued until delivery.

The improvement in the course of thyrotoxicosis during pregnancy can be explained primarily by the fact that pregnancy is accompanied by physiological immunosuppression and a decrease in the production of antibodies to rTG. In addition, the binding capacity of transport proteins is significantly increased, which leads to a decrease in the levels of fT4 and fT3. In addition, during pregnancy, the balance of the ratio of blocking and stimulating AT-rTTH changes.

Sometimes postpartum aggravation of thyrotoxicosis can be so pronounced that it is necessary to block lactation with dopaminomimetics and prescribe thyreostatic drugs in large doses taken to treat thyrotoxicosis outside of pregnancy.

The problems of treating Graves' disease during pregnancy in some cases are not limited to the elimination of thyrotoxicosis in a woman. Since stimulatory antibodies to the propylthiouracil receptor cross the placental barrier, they can cause transient thyrotoxicosis in the fetus and newborn. Transient neonatal thyrotoxicosis occurs in 1% of children born to women with Graves' disease. It can develop not only in children whose mothers received thyrostatic therapy during pregnancy, but also in children whose mothers have undergone radical treatment for Graves' disease in the past (thyroidectomy, radioactive iodine therapy), since after removal of the thyroid gland, antibodies can continue to be produced on for many years. Conversely, if a woman goes into sustained remission after drug therapy for Graves' disease, the fetus may not develop transient thyrotoxicosis, because remission of the disease indicates the cessation of antibody production. Thus, in women who receive thyrostatic therapy for Gaves disease during pregnancy and in women who have undergone radical treatment in the past (thyroidectomy, radioactive iodine therapy), in the late stages of pregnancy (in the third trimester), an examination of the level of antibodies - rTSH . The detection of their high level makes it possible to attribute the newborn to the group of increased risk of developing transient neonatal thyrotoxicosis, which, in some cases, requires the temporary prescription of thyreostatic drugs to the newborn. If signs of thyrotoxicosis are detected in the fetus before delivery (an enlarged thyroid gland in the fetus according to ultrasound, tachycardia (more than 160 beats / min), growth retardation and increased motor activity), it is advisable for a pregnant woman to prescribe a higher dose of thyreostatic (200-400 mg of propylthiouracil or 20 mg thiamazole), if necessary, in combination with levothyroxine to maintain her euthyroidism. However, most often, transient neonatal thyrotoxicosis develops after childbirth and may present with heart failure, tachycardia, goiter, jaundice, and increased irritability. In all newborns from women with Graves' disease, it is advisable to determine the level of propylthiouracil and T4 in the umbilical cord blood.

Prevention
Timely detection and compensation of thyrotoxicosis at the stage of pregnancy planning.

Forecast
Women with suspected thyrotoxicosis should undergo a complete special laboratory examination and receive adequate treatment, especially at the stage of pregnancy planning, in order to minimize the risk of developing both obstetric complications (arterial hypertension, preeclampsia, placental abruption, premature birth, spontaneous abortion, anemia, heart failure, thyrotoxic crisis) and fetal complications (low body weight, fetal and neonatal thyrotoxicosis, intrauterine growth retardation, fetal malformations and antenatal death).

POSTPARTUM THYROIDITIS
Postpartum thyroiditis is a syndrome of transient or chronic autoimmune thyroid dysfunction that develops during the first year after childbirth.

Etiology and pathogenesis
As a rule, postpartum thyroiditis develops after childbirth or after spontaneous abortion at an earlier date, regardless of the level of iodine supply and genetic predisposition. Postpartum thyroiditis is associated with HLA-DR3 and DR5.

Morphologically, postpartum thyroiditis is manifested by lymphocytic infiltration of the thyroid parenchyma without the formation of giant cells, and clinically by a change in the phases of transient thyrotoxicosis and hypothyroidism. As is known, pregnancy is combined with suppression of the immune system, which is aimed at maximizing tolerance to foreign antigens. During pregnancy, there is a change in the ratio of T-helpers (Th), with a predominance of Th-2, which, due to the production of IL-4, IL-5 and IL-10, contribute to immune suppression and tolerance, and a decrease in the amount of Th-1, which have cytotoxic and cytolytic effect upon activation by interferon γ and interleukin-2 (IL-2). This change in the Th-1/Th-2 ratio occurs due to the effects of maternal hormones that suppress the production of inflammatory cytokines. This is facilitated by catecholamines and glucocorticoids, estrogens and progesterone, vitamin D3, the level of which increases during pregnancy.

The thyroid gland has a unique ability to accumulate a large amount of ready-made thyroid hormones, which would be enough to provide the body for 2-3 months. Thyroid hormones and iodinated thyronins mainly accumulate in the colloid contained in the cavity of the thyroid gland follicles.

Postpartum thyroiditis is a classic variant of destructive thyroiditis, in which there is a massive destruction of the thyroid gland follicles, resulting in an excess of thyroid hormones entering the bloodstream, which leads to the characteristic symptoms and laboratory picture of thyrotoxicosis. Destruction of thyroid follicles in postpartum thyroiditis is caused by transient autoimmune aggression, in the pathogenesis of which the main role belongs to immune reactivation, or the "rebound" phenomenon - a sharp increase in the activity of the immune system after its long physiological suppression during the gestation period, which in those predisposed to postpartum thyroiditis can provoke the development of many autoimmune diseases.

The classic variant of postpartum thyroiditis is characterized by the development of a phase of transient thyrotoxicosis, which is usually followed by a phase of transient hypothyroidism followed by recovery of euthyroidism.

The thyrotoxic phase of postpartum thyroiditis is characterized by the development of transient thyrotoxicosis approximately 8-14 weeks after birth, lasts 1-2 months and is due to the release of ready-made thyroid hormones stored in the thyroid gland into the blood, that is, destructive thyrotoxicosis develops. Then, approximately at the 19th week after birth, the hypothyroid phase develops, which lasts 4-6 months, is accompanied by clinical symptoms of hypothyroidism, which requires the appointment of replacement therapy with levothyroxine. After 6-8 months, the function of the thyroid gland is restored. Very rarely, hypothyroidism precedes thyrotoxicosis. In some women, these two phases develop independently of each other: only the thyrotoxic phase (19-20% of women) or only the hypothyroid phase (45-50% of cases). Approximately 30% of women carriers of TPO antibodies who develop postpartum thyroiditis, the hypothyroid phase passes into persistent hypothyroidism, and requires constant therapy with levothyroxine.

Clinical picture
In most cases, subclinical thyrotoxicosis is detected (an isolated decrease in the level of thyroid-stimulating hormone with a normal level of thyroid hormones), and only 20-30% of women with postpartum thyroiditis have clinical manifestations of thyrotoxicosis (fatigue, tremor, weight loss, tachycardia, nervousness, anxiety and irritability). The hypothyroid phase occurs later and has more symptoms (depression, irritability, dry skin, asthenia, fatigue, headache, reduced ability to concentrate, constipation, muscle and joint pain). This phase coincides with the greatest increase in the level of AT-TPO. The duration of the hypothyroidism phase is variable. Very often, functional changes in the thyroid gland are accompanied by clinical manifestations, while the frequency of the asymptomatic hypothyroid phase is 33%. The mild and prognostically favorable nature of thyroid dysfunction makes it difficult to identify any specific symptoms among the numerous stress symptoms that occur against the background of changes in living conditions after childbirth.

Diagnostics
Determination of the level of AT-rTTH will allow the diagnosis of Graves' disease. The simplest and most accurate diagnostic method is thyroid scintigraphy, which will detect a diffuse increase in the accumulation of the radiopharmaceutical in Graves' disease and a decrease or complete absence of its accumulation in postpartum thyroiditis. Ultrasound of the thyroid gland will help little in carrying out this differential diagnosis - in both cases, nonspecific signs of an autoimmune pathology of the thyroid gland will be determined. However, postpartum thyroiditis is not characterized by a significant increase in the volume of the thyroid gland and endocrine ophthalmopathy.

Differential Diagnosis
Sometimes it is quite difficult to make a differential diagnosis of postpartum thyroiditis and Gaves' disease, since Graves' disease may first be detected in the postpartum period. Often, the diagnosis of Graves' disease or persistent hypothyroidism is quickly established in a situation when it comes to one of the transient phases of postpartum thyroiditis. If a woman is no longer breastfeeding, thyroid scintigraphy will allow you to quickly make a differential diagnosis and determine further tactics. If a nursing woman is diagnosed with severe thyrotoxicosis, she should stop breastfeeding and have a thyroid scintigraphy, since high doses of thyreostatics will be required. With mild or subclinical thyrotoxicosis, there is no need to stop breastfeeding, and differential diagnosis will allow for dynamic monitoring: with Graves' disease, thyrotoxicosis will be persistent and progressive, and with postpartum thyroiditis, a gradual spontaneous normalization of the level of thyroid-stimulating hormone and thyroid hormones will occur. Differential diagnosis of various phases of postpartum thyroiditis and persistent variants of thyroid dysfunction is of great importance, since in the first case the disorders are transient and prognostically favorable, and in the second - hypothyroidism requires lifelong therapy with levothyroxine.

Treatment
Given the destructive nature of thyrotoxicosis in postpartum thyroiditis, thyreostatic drugs are not prescribed in the thyrotoxic phase. With a significant severity of symptoms of thyrotoxicosis, the appointment of β-blockers is indicated. Symptoms of the hypothyroid phase of postpartum thyroiditis are even less specific, since subclinical hypothyroidism most often develops in women with AT-TPO, but sometimes there is a significant increase in the level of thyroid-stimulating hormone (> 40-50 mU/l). The patient is prescribed replacement therapy with levothyroxine at a dose necessary to maintain a normal level of thyroid-stimulating hormone. After 9-12 months, therapy is canceled: with persistent hypothyroidism, an increase in the level of thyroid-stimulating hormone will occur, with transient hypothyroidism, euthyroidism will remain.

THYROID CANCER
Thyroid cancer is the most commonly diagnosed malignant tumor of the endocrine glands, represented by numerous subtypes.

Epidemiology
Thyroid cancer accounts for 0.5-1.5% of all malignant neoplasms. Women get thyroid cancer 3-4 times more often than men.

Classification
The following forms of thyroid cancer are distinguished: papillary (about 80%), follicular (about 14%), medullary (about 5-6%), undifferentiated and aplastic (about 3.5-4%). The problem of thyroid cancer and pregnancy is extremely relevant, since the majority of patients are women of reproductive age.

The issue of the possibility of onset and preservation of pregnancy in women after surgical treatment for thyroid cancer should be decided individually. Modern staged management of patients with thyroid cancer involves thyroidectomy followed by radioactive iodine therapy. The volume of surgical treatment includes the removal of cervical tissue and lymph nodes. Conditions under which pregnancy can be resolved in women who have completed a full course of treatment (radical surgery, radiotherapy) for thyroid cancer.
Highly differentiated thyroid cancer (primarily papillary cancer), with a postoperative period of more than a year, in the absence of relapses of the disease.
In patients who underwent iodine-131 irradiation procedures at doses up to 250 mCi, the interval between radiotherapy and the onset of pregnancy should be at least a year, provided the disease is in remission.
The absence of negative dynamics of the disease based on the periodic determination of the level of thyroglobulin.
Euthyroid state, full compensation of postoperative hypothyroidism.

The tactics of managing pregnancy does not differ from the generally accepted one, however, it is necessary to remember the higher incidence of obstetric complications during pregnancy and childbirth in this category of women.

A dynamic study of the level of thyroglobulin (as is customary in patients who have completed a full course of treatment, especially after subtotal resection of the thyroid gland) during pregnancy is not carried out, since this indicator is not very informative due to the physiological increase in its content during pregnancy.

The process of gestation does not affect the evolution of carcinoma. The risk of cancer recurrence is increased if the first pregnancy ended in a miscarriage or if there are more than four pregnancies in history. If malignancy of the nodes is detected in the first or early second trimester, pregnancy can not be interrupted, but in the second trimester it is advisable to conduct surgical treatment. In a situation where papillary cancer or follicular neoplasia is found in a woman and there is no data for the progression of the process, it is possible to delay surgical treatment until the postpartum period, since most highly differentiated thyroid cancers are characterized by very slow growth and such tactics most likely will not change the prognosis. If malignancy is suspected in the 3rd trimester, it is also advisable to delay treatment until the postpartum period, except in cases of rapidly growing nodes. It must be remembered that radioactive iodine treatment is contraindicated during breastfeeding. Lactation should also be stopped 1-2 months before the planned radiotherapy with iodine due to the possibility of accumulation of the radiopharmaceutical in the breast tissue. There are certain indications for prescribing levothyroxine preparations in doses that provide some suppression of the level of thyroid-stimulating hormone. In this case, the concentration of fT4 should be at the upper limit of the norm for pregnant women. Such therapy is indicated for women who received treatment for well-differentiated thyroid cancer before pregnancy, if material suspicious for thyroid cancer is obtained during pregnancy and / or when surgery for cancer is postponed until the postpartum period.

Forecast
Pregnancy is contraindicated in women treated for undifferentiated carcinoma and medullary thyroid cancer.

Most patients after radical thyroidectomy receive levothyroxine preparations at a daily dose of 2.5 μg per kg of body weight, which must be maintained during pregnancy. In pregnant women who are on hormone replacement therapy after surgical treatment, the question of the adequacy of the dose is decided by the level of thyroid-stimulating hormone and fT4 in the blood. Observation is carried out according to the principles of conducting pregnancy with hypothyroidism.

PLANNING PREGNANCY IN WOMEN WITH THYROID DISEASES

The decision to plan pregnancy in women with thyroid pathology should be made jointly by an endocrinologist and an obstetrician-gynecologist. Pregnancy can be planned in women:
- with compensated primary hypothyroidism, which developed as a result of autoimmune thyroiditis or surgical treatment of non-tumor diseases of the thyroid gland;
- with various forms of euthyroid colloid to varying degrees proliferating goiter (nodular, multinodular, mixed), when there are no direct indications for surgical treatment (compression syndrome);
- in women with a carriage of antibodies to the thyroid gland in the absence of a violation of its function;
- in women who received staged treatment for highly differentiated thyroid cancer (thyroidectomy followed by radioactive iodine therapy), not earlier than after 1 year in the absence of negative dynamics according to periodic determination of thyroglobulin levels.

In women with Graves' disease, pregnancy can be planned:
- at least after 6 months of a stable euthyroid state after the end of thyreostatic therapy carried out for 12-18 months;
- 6-12 months after treatment with radioactive iodine, provided that euthyroidism is maintained;
- immediately after surgical treatment against the background of complete replacement therapy with levothyroxine preparations;
- in women of late reproductive age with infertility, the optimal method of treating Graves' disease is surgical treatment (thyroidectomy), since immediately after the operation, full replacement therapy with levothyroxine preparations is prescribed and, under the condition of euthyroidism, programs can be planned in the near future.

Pregnancy is a special condition for a woman. This condition is physiological (that is, normal), but at the same time it requires a lot of expenses from the body and involves all organs and systems. Today we will talk about how pregnancy proceeds against the background of thyroid diseases and how pregnancy can provoke conditions such as hypothyroidism and thyrotoxicosis.

What is a thyroid gland?

The thyroid gland, despite its small size, is an extremely important organ of internal secretion (hormonal organ). The thyroid gland consists of two lobes and an isthmus, located on the front surface of the neck. The functions of the thyroid gland include the synthesis and secretion of hormones.

Thyroid hormones: thyroxine (T4) and triiodothyronine (T3). The hormone that regulates the production of these hormones is synthesized in a special part of the brain (pituitary gland) and is called TSH (thyroid stimulating hormone).

Thyroid hormones are involved in almost all types of metabolism (especially protein and energy metabolism), the synthesis of vitamins (vitamin A in the liver), and also take part in the regulation of the production of other hormones. All thyroid hormones contain iodine atoms, so iodine appears in many drugs used for treatment (prophylactic administration of potassium iodide preparations, radioactive iodine for the treatment of thyroid tumors).

The effect of pregnancy on the thyroid gland

The thyroid gland during pregnancy increases in size and enhances its functions. Thyroxine is produced by 30 - 50% more compared to the initial level. The physiological function of the thyroid gland begins from the earliest dates, since a sufficient level of thyroid hormones drastically affects the growth and development of the fetus (we will tell you more about the effect of thyroid hormones on the development of the baby below), and the laying of all life systems occurs in the first 12 weeks. Therefore, it is very important to approach pregnancy with a healthy gland, or a compensated state if there is any disease.

In areas endemic for goiter and hypothyroidism, it is necessary to receive iodine prophylaxis even in preparation for pregnancy, and then the entire period of gestation and lactation. An endemic area is an area in which certain diseases predominate, the presence of diseases is not associated with the migration of the population or the introduction of the disease from outside. For example, in our case, endemic regions will be: Krasnoyarsk Territory, the Republic of Sakha, Buryatia, Tyva, Perm and Orenburg regions, Altai, Transbaikalia (iodine deficiency is detected in 80% of the population).

The enlargement of the thyroid gland in size is due to the increased blood supply that is required to provide increased function. In ancient Egypt, a thin silk thread was tied around the neck of a girl who had just entered into marriage and observed. When the thread broke, it was considered a sign of pregnancy.

Thyroid diseases are divided into those that occur with a decrease in function and, conversely, with excessive production of hormones. Separately, oncological diseases of the thyroid gland are taken into account, these are cancer and thyroid cysts.

Diagnosis of thyroid diseases

First of all, a pregnant woman with suspicion of any thyroid disease should be examined by an endocrinologist. He conducts a patient survey to collect characteristic complaints, a general examination (skin color, moisture or, conversely, dry skin and mucous membranes, hand tremor, swelling, size of the palpebral fissure and the degree of its closure, visual enlargement of the thyroid gland and the front of the neck), palpation thyroid gland (an increase in its size, an isolated thickening of the isthmus of the gland, consistency, soreness and mobility, the presence of large nodes).

1. The level of thyroid hormones. TSH (thyroid stimulating hormone) is an indicator that is used to screen for thyroid diseases, if this indicator is normal, then further research is not indicated. This is the earliest marker of all dishormonal thyroid diseases.

The norm of TSH in pregnant women is 0.2 - 3.5 μIU / ml

T4 (thyroxine, tetraiodothyronine) circulates in plasma in two forms: free and bound to plasma proteins. Thyroxine is an inactive hormone, which in the process of metabolism is converted into triiodothyronine, which already has all the effects.

Norm T4 free:

I trimester 10.3 - 24.5 pmol / l
II, III trimester 8.2 - 24.7 pmol / l

T4 general norm:

I trimester 100 - 209 nmol/l
II, III trimesters 117 - 236 nmol / l

The norm of TSH, free T4 and total T4 in pregnant women differ from the general norms for women.

Tz (triiodothyronine) is formed from T4 by splitting off one iodine atom (there were 4 iodine atoms per 1 molecule of the hormone, and now there are 3). Triiodothyronine is the most active thyroid hormone, it is involved in plastic (tissue building) and energy processes. T3 is of great importance for metabolism and energy exchange in the tissues of the brain, heart tissue and bone.

Norm T3 free 2.3 - 6.3 pmol / l
Norm T3 total 1.3 - 2.7 nmol / l

2. The level of antibodies to various components of the thyroid gland. Antibodies are protective proteins that the body produces in response to the ingress of an aggressive agent (virus, bacterium, fungus, foreign body). In the case of thyroid diseases, the body exhibits immune aggression towards its own cells.

For the diagnosis of thyroid diseases, indicators of antibodies to thyroglobulin (AT to TG) and antibodies to thyroperoxidase (AT to TPO) are used.

Norm of AT to TG up to 100 IU / ml
AT norm to TPO up to 30 IU/ml

Of the antibodies for diagnosis, it is advisable to investigate antibodies to thyroid peroxidase or both types of antibodies, since the isolated carriage of antibodies to thyroglobulin is rare and has less diagnostic value. Carriage of antibodies to thyroid peroxidase is a very common situation that does not indicate a specific pathology, but carriers of these antibodies develop postpartum thyroiditis in 50% of cases.

3. Ultrasound of the thyroid gland. Ultrasound examination determines the structure of the gland, the volume of the lobes, the presence of nodes, cysts and other formations. With doplerometry, the blood flow in the gland, in individual nodes, is determined. Ultrasound is performed during primary diagnosis, as well as in dynamics to monitor the size of lobes or individual nodes.

4. Puncture biopsy - this is taking an analysis exactly from the focus (nodule or cyst) with a thin needle under ultrasound control. The resulting fluid is examined microscopically to look for cancer cells.

Radionuclide and radiological methods during pregnancy are strictly prohibited.

Pregnancy due to hypothyroidism

Treatment

Treatment is carried out with thyreostatic drugs of two types, imidazole derivatives (thiamazole, mercasolil) or propylthiouracil (propicil). Propylthiouracil is the drug of choice during pregnancy, as it penetrates the placental barrier to a lesser extent and affects the fetus.

The dose of the drug is selected in such a way as to maintain the level of thyroid hormones at the upper limit of the norm or slightly above it, since in large doses, which lead to normal T4 values, these drugs cross the placenta and can lead to suppression of fetal thyroid function and the formation of goiter at the fetus.

If a pregnant woman receives thyreostatics, then breastfeeding is prohibited, since the drug penetrates into milk and will have a toxic effect on the fetus.

The only indication for surgical treatment (removal of the thyroid gland) is intolerance to thyreostatics. Surgical treatment in the first trimester is contraindicated, according to vital indications, the operation is performed starting from the second trimester. After the operation, the patient is prescribed hormone replacement therapy with levothyroxine for life.

As concomitant therapy, beta-blockers (betaloc-ZOK) are often prescribed with the selection of an individual dose. This drug slows down the heartbeat by blocking adrenaline receptors, and thereby reduces the load on the heart and prevents the development of heart failure and arterial hypertension.

Pregnant women with developed on the background of thyrotoxicosis cardiac pathology are subject to joint management by an obstetrician - gynecologist, endocrinologist and cardiologist.

Prevention

Unfortunately, it is impossible to prevent this condition as an independent disease. But you can protect yourself and your unborn baby as much as possible, minimize the risk of complications if you know about the disease before pregnancy and start treatment in a timely manner.

Tumors of the thyroid gland

Primary detection of thyroid tumors during pregnancy is a rarity. In terms of diagnosis, nothing changes, it is necessary to determine the level of thyroid hormones, perform an ultrasound scan.

Differential diagnosis between gland cysts and malignant neoplasms is performed using a puncture of the formation under ultrasound control. Based on the results of a cytological examination, a diagnosis will be established.

Cysts of the thyroid gland with a normal level of hormones and a negative result of the puncture (that is, no cancer cells were found) are subject to observation.

Tumors of the thyroid gland are subject to observation and treatment by an oncologist. The possibility of prolonging pregnancy against the background of a malignant neoplasm of the thyroid gland is decided at the council, but the final decision is always made by the patient herself.

Hypothyroidism and thyrotoxicosis do not deprive you of the opportunity to give life to the desired baby, but only require you to be much more disciplined in relation to your health. Thyroid diseases are not a categorical contraindication to independent childbirth. Plan your pregnancy ahead of time. Approach her with confidence in your health or a compensated state of chronic diseases, do not miss visits to your obstetrician-gynecologist, endocrinologist and other specialist doctors and follow their recommendations. Look after yourself and be healthy!

Obstetrician-gynecologist Petrova A.V.