EFFECTS OF THYROID PATHOLOGY ON PREGNANCY COURSE

Educational Research in Universal Sciences ISSN: 2181-3515 VOLUME 4 | ISSUE 15 | 2025 https://t.me/Erus_uz Multidisciplinary Scientific Journal November, 2025 113 DOI: https://10.5281/zenodo.17781297 EFFECTS OF THYROID PATHOLOGY ON PREGNANCY COURSE Salimova Dildora Erkinovna assistant department of Endocrinology of Samarkand State Medical University Abbas Rizvi student of faculty General medicine of Samarkand State Medical University ABSTRACT The thyroid gland is a vital component of the neuroendocrine system. Its functional state significantly impacts reproductive function. The close connection between the thyroid and reproductive systems is confirmed by changes in thyroid function during pregnancy and lactation. The high prevalence of endocrine pathology, the trend toward a further increase in morbidity in women of childbearing age, and the associated adverse outcomes for the woman and her offspring are of great medical and social significance. It is known that the maternal endocrine system significantly influences the growth and development of the fetus and the child after birth. Maternal endocrine pathology can be accompanied by disruption of the maternal-placental-fetalnewborn system. Most often, this is associated with dyshormonogenesis in the pregnant woman, which increases the likelihood of disturbances in the formation and differentiation of organs and tissues, the development of their functions, and the neuroendocrine regulation of the fetus and newborn. The research results also indicate a high risk of developing health problems in later life in children whose mothers suffer from endocrine pathology. In this regard, it is necessary to monitor women of reproductive age with thyroid pathology, timely correction of the endocrine status in order to prevent the development of complications [3]. The most common endocrine pathology is iodine deficiency diseases, the development of which leads to a lack of iodine in the environment. It is known that more than 1 billion people in the world live in areas with iodine deficiency. Thyroid diseases, accompanied by impaired function, often lead to menstrual disorders and decreased fertility. Women with thyroid pathology have a high probability of developing complications during pregnancy and childbirth: early toxicosis, gestosis, intrauterine hypoxia of the fetus, threatened termination of pregnancy, premature birth. Educational Research in Universal Sciences ISSN: 2181-3515 VOLUME 4 | ISSUE 15 | 2025 https://t.me/Erus_uz Multidisciplinary Scientific Journal November, 2025 114 Keywords: early toxicosis, gestosis, human chorionic gonadotropin, TSH, free T4, iodine deficiency. During pregnancy, the body’s entire metabolism, including thyroid function, changes to meet the growing needs of the developing fetus. Changes in thyroid function occur already in the first weeks of pregnancy and are manifested by an increase in its size and production of thyroid hormones by 30-50%. This condition is considered physiological hyperthyroidism. The most powerful stimulator of the thyroid gland in the first half of pregnancy is human chorionic gonadotropin (hCG), similar in structure to TSH due to its shared-subunits and, in large quantities, is capable of exerting a TSH-like effect. An increase in the production of thyroid hormones via a negative feedback mechanism causes the suppression of TSH production, which is normally reduced in 20% of women in the first half of pregnancy. In multiple pregnancies, when the level of hCG in the blood is significantly elevated, TSH production is suppressed in 100% of cases. Then, as the pregnancy progresses, the amount of hCG decreases, and the TSH level returns to normal values, while the level of thyroid hormones remains elevated until the end of pregnancy and decreases immediately before delivery [8]. As pregnancy progresses, there is also an increase in estrogen production. They stimulate the formation of TSH in the liver [8], the level of which doubles during the 16th-20th weeks of pregnancy. This leads to the binding of an additional amount of free thyroid hormones. In addition, TSH binds to sialic acids in increased amounts, which significantly reduces its clearance. An increase in TSH levels, along with an increase in circulating plasma volume, which occurs throughout pregnancy until delivery, leads to a slight increase in total T4 levels and a decrease in the level of free, biologically active hormone. This, in turn, is accompanied by an increase in TSH levels and additional stimulation of the thyroid gland. With a sufficient amount of the main substrate for the synthesis of thyroid hormones, i.e. iodine, these changes are easily compensated for. Thyroid hormones during fetal development are the most important regulators of the formation and maturation of the brain, while the level of free T4 remains unchanged. With iodine deficiency, the level of free thyroxine remains reduced by 10-15% of that outside of pregnancy. One of the compensatory mechanisms of relative hypothyroxinemia is an increase in the synthesis of biologically more active T3 and thus an increase in the T3/T4 ratio. The thyroid gland is formed in the fetus at 4-5 weeks of intrauterine development. By 10-12 weeks, it acquires the ability to accumulate iodine and synthesize iodothyronines. By 16-17 weeks, the fetal thyroid gland is fully differentiated and Educational Research in Universal Sciences ISSN: 2181-3515 VOLUME 4 | ISSUE 15 | 2025 https://t.me/Erus_uz Multidisciplinary Scientific Journal November, 2025 115 actively functioning. In the second half of pregnancy, an additional factor in thyroid hyperstimulation is changes in thyroid hormone metabolism caused by the formation and functioning of the placenta. According to current concepts, iodine and thyrotropinreleasing hormone easily penetrate the placenta, but TSH does not. The placenta is permeable to a limited amount of T3 and T4. The most obvious manifestation of iodine deficiency and insufficient iodine intake is euthyroid diffuse (nontoxic) goiter—diffuse enlargement of the thyroid gland without impairment of its function. The term "endemic goiter" is also used to describe goiter caused by iodine deficiency. Thyroid enlargement due to iodine deficiency is a compensatory response to ensure the synthesis of sufficient thyroid hormones in conditions of iodine deficiency. The second most common manifestation of iodine deficiency in adults is the development of nodular goiter. Typically, nodular goiter is initially not caused by changes in thyroid function. However, with a sharp increase in iodine intake (for example, when taking certain iodine-containing medications), this can lead to the development of iodine-induced thyrotoxicosis. Furthermore, under conditions of iodine deficiency, thyroid cells can acquire partial or complete autonomy from the regulatory influence of TSH, leading to the development of functional autonomy in the gland and, subsequently, to the development of thyrotoxicosis. As a rule, autonomous thyroid nodules and iodine-induced thyrotoxicosis occur in people over 50 years of age. With extreme iodine deficiency, hypothyroidism can develop, caused by a severe shortage of thyroid hormones in the body. Iodine deficiency, in addition to thyroid enlargement, leads to a number of other pathological conditions. The spectrum of iodine deficiency diseases is broad and depends on the period of life at which iodine deficiency affects the body. Iodine deficiency during pregnancy and embryonic development contributes to a high rate of spontaneous abortions, especially in the first trimester, high perinatal and infant mortality, congenital malformations, and congenital hypothyroidism with delayed physical and mental development. In adulthood, iodine deficiency causes varying degrees of thyroid enlargement. Iodine deficiency is especially dangerous during pregnancy, when inadequate iodine intake is further exacerbated by the increased thyroid needs of both mother and fetus. Under these conditions, there is a high risk of miscarriage, congenital fetal abnormalities, and hypothyroidism and mental retardation in newborns. During embryonic development, thyroid hormones support neurogenesis, neurocyte migration, and cochlear differentiation, which is the formation of hearing and the cerebral structures responsible for human motor functions. In regions with severe iodine deficiency, neurological cretinism predominates, characterized, in addition to significant Educational Research in Universal Sciences ISSN: 2181-3515 VOLUME 4 | ISSUE 15 | 2025 https://t.me/Erus_uz Multidisciplinary Scientific Journal November, 2025 116 intellectual disability, by sensorineural deafness, muteness, and severe motor impairments. Less severe hormone deficiency during this period leads to the development of milder psychomotor disorders, hearing loss, and dysarthria (neurological subcretinism). However, even a mild thyroid hormone deficiency, while not causing serious mental impairment, can still hinder the realization of a child’s genetically determined intellectual potential. CONCLUSION This, determining thyroid hormone levels in the serum of pregnant women with thyroid pathology is a qualitative and quantitative indicator of the functioning of the entire endocrine system of both mother and fetus. Timely diagnosis and treatment of thyroid pathology leads to a significant reduction in the incidence of complications during pregnancy and childbirth, and, consequently, to an improved pregnancy and the birth of a physically and intellectually healthy child. REFERENCES: 1. Balabolkin, M.I. Endocrinology: textbook / M.I. Balabolkin. – M.: Medicine, 1989. – 416 p. 2. The influence of iodine deficiency on the level of thyroid hormones in the blood serum of pregnant women and in the placenta / L.A. Donchenko [et al.] // 3. Salimova D. E. Tosharova MA qizi, Keldiyorova NN qizi, Mahmudova IA qizi. OBESITY AS A RISK FOR TYPE 2 DIABETES MELLITUS //World of Scientific news in Science. – 2024. – Т. 2. – №. 1. – С. 552-558. 4. Shukhratovna N. G. et al. Diabetes mellitus, ischemic heart disease and arterial hypertension //Pedagog. – 2022. – Т. 5. – №. 5. – С. 381-6. 5. Negmatova G.Sh., Salimova, D. E., Oybekovma, X. S., Qamariddinovna, X. A., & Amin o‘g‘li, B. J. (2022). Endocrine glands. STRUCTURE, AGE FEATURES, FUNCTIONS. PEDAGOG, 1(2), 341-345. 6. Rakhmatova F. U., Salimova D. E. DIAGNOSIS OF 21-HYDROXYLASE DEFICIENCY IN CONGENITAL ADRENAL HYPERPLASIA IN UZBEKISTAN //Educational Research in Universal Sciences. – 2025. – Т. 4. – №. 1. – С. 186-188.