Ta'lim innovatsiyasi va integratsiyasi
44-son_3-to’plam_May-2025
ISSN: 3030-3621
329
MODERN VIEWS OF THYROID DISEASES IN PREGNANCY
Bukhara State Medical Institute
named after Abu Ali ibn Sina,
Uzbekistan, Bukhara st. A. Navoi.
Haydarova Nargizaxon Axtamjon qizi
Summary:
The article provides a review of the literature on the characteristics
of pregnancy in women with various types of diseases and endocrine disorders of the
thyroid gland, risk factors for complications from both the mother and the fetus,
principles of treatment depending on the type of pathology of thyroid function and
gestational age. The article provides a review of the literature on modern concepts of
thyroid diseases during pregnancy.
Key words
: pregnancy, thyroid gland, hypothyroidism, woman, fetus.
Relevance
. Diseases of the thyroid gland (TG) are the most common endocrine
pathology, and their prevalence is 10–17 times more common in women than in men.
The thyroid gland is a butterflyshaped gland weighing about 20 g and is located on the
front surface of the neck in the lower third [1]. The function of the thyroid gland is
under the control of the hypothalamic-pituitary system. Thyrotropin-releasing hormone
(TRH) is synthesized in the hypothalamus. TRH, entering the pituitary gland,
stimulates the synthesis of thyroid-stimulating hormone (TSH), which stimulates the
activity of the thyroid gland. The thyroid gland produces two hormones: thyroxine (T4)
and triiodothyronine (T3). The activity of triiodothyronine is 3–5 times higher than the
activity of thyroxine, despite the fact that the thyroid gland secretes 10–20 times more
thyroxine than triiodothyronine. In the blood, most of the thyroid hormones are bound
to the carrier protein thyroglobulin and are inactive, while only a small percentage of
the free fraction of hormones is active [2, 3, 8]. The role of thyroid hormones is
multifaceted. They participate in almost all processes occurring in the human div.
Thyroid hormones influence protein synthesis and cell growth, stimulate RNA
synthesis in the nucleus, activate tissue respiration, play a major role in the process of
growth and differentiation of tissues, affecting all types of metabolism, enhance
metabolic processes, increase the need for various enzymes and, accordingly , in
vitamins necessary for their synthesis [3]. Thyroid hormones affect the gonads by
inhibiting the production of follicle-stimulating hormone and, conversely, increasing
the release of luteinizing hormone from the pituitary gland. In addition, thyroid
hormones increase the sensitivity of the ovaries to gonadotropic hormones and the
endometrium to estrogens. During puberty, they actively influence the div,
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stimulating, together with sex steroids, the final completion of physical, sexual and
mental differentiation and promoting the formation of a normal two-phase cycle in the
female div [12, 13, 14, 15]. During pregnancy, the function of the thyroid gland
changes. Due to an increase in the concentration of thyroxine-binding globulins, caused
by a high level of estrogens, the content of bound forms of thyroid hormones in the
blood increases: total thyroxine and total triiodothyronine, but the free, active fractions
of hormones do not increase. However, as outside pregnancy, it is these free fractions
that provide all the metabolic and biological activity of thyroid hormones. The absence
of elevated levels of total thyroxine and thyroxine-binding globulins is a prognostic
sign of termination of pregnancy. Until 15 weeks of pregnancy, the fetus's needs for
thyroid hormones are met by the mother's thyroid gland. In the first trimester, the
formation and development of the nervous system occurs, which requires thyroid
hormones. Thus, the state of the child’s nervous system depends on the function of the
thyroid gland of the mother with whom she entered into pregnancy, that is, it is
necessary to check and correct the function of the thyroid gland at the pregnancy
planning stage, and if not in time, in the very first weeks [11, 12]. To provide the mother
and fetus with sufficient levels of thyroid hormones, the thyroid gland is stimulated.
The main stimulator of its function is the pregnancy hormone (β-hCG). As a result,
there is an increase in the level of the hormones T4 and T3 (the total level is always
increased, the level of free T4 and T3 sometimes) and, accordingly, a decrease in TSH.
These changes are especially pronounced in the first trimester of pregnancy with the
maximum level of β-hCG. This condition is called gestational hyperthyroidism. It leads
to a change in generally accepted norms in hormonal tests. In multiple pregnancies,
due to high levels of β-hCG, TSH may drop to zero [19, 18]. Taking large doses of
iodine (a favorite folk method: a few drops of iodine in milk) does not lead to
termination of pregnancy, but it damages the function of the fetal thyroid gland [15].
In addition, the removal of iodine from the mother’s div increases and her need for it
increases. In non-pregnant women, the iodine requirement is 150 mcg, in pregnant
women - 200 mcg per day [13, 16, 19]. Hypothyroidism is a condition caused by
decreased function of the thyroid gland and is characterized by a reduced level of
thyroid hormones in the div. The condition, regardless of the specific cause that
caused the decrease in the functional activity of the gland, is usually called primary
hypothyroidism. Severe forms of hypothyroidism are called myxedema; with
athyroidism, the phenomena of cretinism develop. Hypothyroidism in women of
reproductive age, including pregnant women, is detected in 2– 3% of cases. In 90–95%
of cases this is primary hypothyroidism. A decrease in the level of thyroid hormones,
which affect the physiological functions and metabolic processes in the div, leads to
inhibition of all types of metabolism, oxygen utilization by tissues, and a decrease in
the activity of various enzyme systems, gas exchange and basal metabolism. Slowing
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down the synthesis and catabolism of protein, as well as its excretion from the div,
leads to a significant increase in the amount of protein breakdown products in organs
and tissues, skin and muscles [8, 10]. Women with hypothyroidism rarely become
pregnant. Reproductive function in women suffering from hypothyroidism is sharply
depressed. A significant slowdown in metabolic and trophic processes affects the
function of the ovaries: there is a delay in the maturation of primordial follicles,
ovulation and the development of the corpus luteum are disrupted. Untreated or
uncompensated hypothyroidism in women affects conception and increases the
incidence of spontaneous abortions and stillbirths. Impaired conception may be a
consequence of secondary hyperprolactinemia, causing anovulatory menstrual cycles.
Uncompensated hypothyroidism leads to infertility, premature termination of
pregnancy, and in the case of full-term pregnancy, defective children are born [11, 13,
14]. Clinical signs and symptoms of hypothyroidism in pregnant women. Because
thyroid hormone receptors are present in virtually all tissues, the symptoms of
hypothyroidism are many and varied. Their severity depends on the degree and
duration of thyroid hormone deficiency. The most typical clinical signs of
hypothyroidism are: general weakness, lethargy, drowsiness, memory loss, dry skin,
hair loss, brittle nails, constipation, chilliness, muscle pain, bleeding gums, tooth decay,
pale skin, swelling, slow speech, sluggishness movements, hoarse voice, heart rate 52–
60 beats. per minute against the background of a decrease in TSH levels with low or
normal levels of thyroid hormones [8, 14, 17]. As the duration of pregnancy increases,
the symptoms of hypothyroidism in patients constantly taking medications decrease:
in the second half of pregnancy, symptoms of hyperfunction of the thyroid gland
appear, primarily tachycardia. This is a consequence of a compensatory increase in the
function of the fetal thyroid gland and the flow of thyroid hormones from the fetus to
the mother [17, 23, 22]. Typical complications in pregnant women with
hypothyroidism are: eclampsia, intrauterine fetal death, profound developmental
anomalies in newborns, miscarriage, premature birth, persistent weakness of labor, and
the development of iron and folate deficiency anemia. According to modern concepts,
the vast majority of women with thyroid pathology, after appropriate treatment under
the supervision of an endocrinologist, can plan a pregnancy, which, with adequate
control, will not be associated with a significant increase in the risk of obstetric and
gynecological complications and the development of pathology in the fetus [1, 5].
Pregnancy without delay (in the absence of other contraindications) can be planned in
women: with compensated primary hypothyroidism that developed as a result of AIT
or surgical treatment of non-tumor thyroid diseases; various forms of euthyroid goiter
(nodular, multinodular, mixed), when there are no direct indications for surgical
treatment (significant size of nodular goiter, compression syndrome); identified
carriage of antibodies to the thyroid gland in the absence of impairment of its function.
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During pregnancy, all women belonging to the listed groups require a dynamic
assessment of thyroid function, which involves determining the level of TSH and
thyroid hormone. T4 in every trimester of pregnancy. In addition, women with goiter
should undergo dynamic ultrasound [8]. Women with uncompensated hypothyroidism
as a result of AIT or after surgical treatment of non-tumor thyroid pathology can plan
pregnancy after achieving euthyroidism against the background of L-thyroxine
replacement therapy. Patients with thyrotoxicosis, after achieving stable remission, can
plan pregnancy after two years. If radioactive iodine therapy was carried out,
pregnancy should be postponed for one year [22]. It is fundamentally important to have
trained specialists in this field of endocrinology and to adhere to programs for
screening, diagnosing and treating thyroid dysfunction in pregnant women.
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