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Diseases of the thyroid gland and pathology of the reproductive system

In the system of peripheral endocrine organs, the thyroid gland, along with the ovaries and adrenal glands, plays an important role in the functioning of the female reproductive system. Various forms of thyroid gland pathology (thyroid gland) can cause puberty disorders, primary and secondary amenorrhea, anovulatory cycles, miscarriage and infertility. The influence of the thyroid gland on the reproductive system is realized both through the peripheral endocrine glands (gonads and adrenal glands) and through the central structures (neurotransmitter and hypothalamic-pituitary systems). An increased or decreased content of thyroid hormones changes the processes of steroidogenesis, acting directly on the gonads, as well as through the hypothalamic-pituitary system, thereby violating the mechanism of their relationship, primarily the principle of negative feedback. The influence of thyroid pathology on menstrual and reproductive functions is also explained by metabolic disorders (especially a decrease in metabolic processes in hypothyroidism), which change the sensitivity of receptor systems to hormonal effects at various levels of regulation. A special kind of pathology of menstrual and reproductive functions with thyroid hypofunction is known as secondary galactorrhea-amenorrhea. In diseases of the thyroid gland with impaired thyroid-stimulating function of the pituitary gland, the production and synchrony of the release of thyroliberin of one of the regulators of pulsatory excretion of gonadoliberins changes. Thus, the multilateral mechanism of the influence of thyroid pathology on the menstrual and reproductive functions of women is clearly defined. Along with this, there are differences in reproductive system disorders depending on the form of thyroid pathology. There are a decrease in its function (hypothyroidism), an increase (hyperthyroidism) and various forms of thyroiditis (acute, subacute, chronic, lymphoid and autoimmune) with various functional conditions of the thyroid gland.

Clinical hypothyroidism is described under the name myxedema and cretinism. These are varieties of a deep thyroid pathology with severe violations of the menstrual and generative functions, which are easily established. In obstetric and gynecological practice, subclinical forms of this pathology are of particular importance. Hypothyroidism can be primary (congenital and acquired - after surgical interventions on the thyroid gland) and secondary cerebral-pituitary origin. Primary hypothyroidism develops in connection with thyroid hypoplasia (of congenital origin, including those caused by genetic defects of enzyme systems), autoimmune disorders, iodine deficiency, damage to radioactive iodine, an overdose of thyrostatics and inflammation (thyroiditis). Currently, spontaneous hypothyroidism is more often associated with autoimmune thyroid lesions. On the territory of the Republic of Belarus in recent years, its frequency has increased tenfold. Secondary hypothyroidism is usually a consequence of the inflammatory processes of the hypothalamus with impaired production and pulsation of thyroliberin or pituitary gland with dysynchronosis of the synthesis and secretion of TSH. There are no significant clinical differences between primary and secondary hypothyroidism. Its moderate and severe forms are characterized by a number of symptoms and syndromes (metabolic-hypothermic with a violation of thermoregulation and a decrease in cold tolerance, skin and edema changes, hypotension and bradycardia, cerebral disorders - memory impairment, drowsiness, apathy, etc.). In diagnostics, along with the clinical picture, hormonal (increased TSH, decreased T3 and T4) and biochemical (hyperglycemia, hypercholesterolemia) shifts are important, and a test with thyroliberin allows you to differentiate primary hypothyroidism from secondary. With primary hypothyroidism, a menstrual function pathology is noted (more than 50%), including amenorrhea (10%). With congenital hypothyroidism, puberty is impaired, the formation of secondary sexual characteristics is more often delayed, primary amenorrhea (Van Wick — Ross – Genes syndrome) occurs. With hypothyroidism, which developed in adulthood, anovulatory cycles, secondary amenorrhea, infertility or miscarriage are observed. The pathology of the generative system in hypothyroidism is most often manifested by hyperprolactinemia, which is a consequence of changes in neurotransmitter mechanisms, especially the level of dopamine, which is an inhibitor of prolactin biosynthesis. A shift in prolactinizing mechanisms leads to increased prolactin production, in which the gonadotropic function of the pituitary gland and steroidogenesis are disrupted. If pregnancy occurs in patients with hypothyroidism, then this is fraught with inferior fetal development, the formation of defects and a decrease in mental development in children, and the frequency of this correlates with the severity of the disease.

Thus, in hypothyroidism, the pathology of fertility is more often caused by damage to many regulatory structures: increased secretion of thyroliberin by the hypothalamus promotes hyperplasia of the pituitary lactophores and the development of hyperprolactinemia, and this leads to a violation of the pituitary gonadotropic function and a decrease in steroidogenesis, which results in anovulation, hypoleuria or. This is due to the similarity of the chemical structure of the pituitary glycoprotein tropic hormones (LH, FSH, TSH) and the embryological community of the origin of the thyroid gland (from the pharyngeal structure) and the adenohypophysis (from the buccal epithelium). The severity of hyperprolactinemia to a greater extent depends on the inhibition of inhibition of the function of pituitary lactophores by an inhibiting factor (dopamine). The immediate cause of anovulation or amenorrhea is a violation of the neurotransmitter dopaminergic control of the production and secretion of luliberin by the hypothalamus, and hyperprolactinemia is their consequence and is accompanied by galactorrhea. Secondary prolactinomas can develop in the process of hypothyroidism, and an excess of prolactin leads to a violation of folliculogenesis, atrophy, amenorrhea and infertility. The Van-Wick — Ross — Gennes syndrome indicated earlier is also associated with an increase in the level of ACTH, which suggests the autoimmune genesis of the disease.

Thyrotoxicosis is also often (20-50%) accompanied by menstrual dysfunction, including amenorrhea (6-8%). With thyrotoxicosis, the content of T3 and T4 is increased, which is accompanied by an increase in FSH and especially LH, and this suppresses the ovulatory peak of hormones due to impaired sensitivity of gonads to tropic hormones and causes anovulation, infertility or amenorrhea. In general, if hypothyroidism shows a decrease in the level of gonadotropic hormones with a subsequent decrease in the number of sex steroid hormones and atrophic changes in the endometrium, then with hyperthyroidism there is an increase in gonadotropins (especially LH) with activation of steroidogenesis. However, when the pituitary gland is hypersensitive to gonadoliberins, ovarian resistance to gonadotropic hormones is noted, which is associated with impaired reproductive function and amenorrhea. Hyperprolactinemia is also characteristic of thyrotoxicosis, the severity of which correlates with the severity of hyperthyroidism.

Clinically, hyperthyroidism is manifested by vegetovascular disorders (pulse mobility, blood pressure), neuropsychiatric disorders (irritability, irritability, tearfulness), weight loss. With a mild form of thyrotoxicosis, tachycardia is noted while maintaining operability and the absence of other changes in the cardiovascular system, as well as metabolic disorders. The average form of thyrotoxicosis is characterized by an increase in heart rate up to 100-120 in 1 min, fatigue and decreased performance, moderate weight loss. Severe thyrotoxicosis is manifested by a pronounced pulse rate (more than 120 in 1 min), atrial fibrillation, weight loss, adrenal insufficiency. The severity of ocular symptoms (Moebius, Gref) and increased tendon reflexes are proportional to the severity of the disease.

Thyroiditis distinguishes between acute, subacute (Kerven's disease), chronic, lymphoid and autoimmune (Hashimoto's disease). Regardless of the form of thyroiditis, the disease can occur with the phenomena of hypothyroidism, hyperthyroidism, or with normal thyroid function. In acute thyroiditis, there are symptoms of the inflammatory process (fever, leukocytosis, accelerated ESR), pain in the thyroid gland, entire neck. Subacute thyroiditis occurs after influenza, tonsillitis and is characterized by specific viral antibodies, which is associated with autoimmune processes in the body. Inflammation and often signs of hypothyroidism are noted. In chronic autoimmune thyroiditis caused by congenital disorders of immunological control, hyperplastic processes develop in the thyroid gland (struma), but with hypothyroidism. With all forms of thyroiditis, various disorders of menstrual function and amenorrhea are noted, which are associated with a pathology of the thyroid function.

We should also dwell on autoimmune thyroiditis due to radiation exposure, especially in the territories of the Republic of Belarus, both contaminated with radionuclides and conditionally “clean”. In addition to the traditional symptoms characteristic of this disease, girls often have asthenoneurotic syndrome due to the traumatic situation that developed after the Chernobyl accident. Violations of the reproductive system and menstrual function in this pathology were studied by TA Leonova (1988). When examining girls with this pathology, anemia, dysproteinemia, heterogeneity of the structure and tuberosity of the thyroid gland with an increase in regional lymph nodes are noted. More often they have hypothyroidism with symptoms of chilliness, sluggishness, dry skin, and constipation. Changes in homeostasis were characterized by a decrease in total T-lymphocytes, an increase in the number of T-suppressors and immunoglobulins G. The higher the individual dose absorbed by the thyroid gland, the more pronounced in autoimmune thyroiditis is the decrease in the absolute and relative amounts of T-helper cells and B-lymphocytes, M immunoglobulins and phagocytic index. The presence of high titers of specific antibodies to thyroglobulin and microsomal antigen of thyrocytes is characteristic.
In patients, the content of T3 is reduced, and TSH and TG are increased

In 10-15% of girls with autoimmune thyroiditis, regular menstruation is not established within three years after the menarche, algomenorrhea was observed in 30-40%. In patients with autoimmune thyroiditis more often than healthy, other disorders of the menstrual cycle were noted. With the help of ultrasound, they revealed ovaries enlarged in size, often with cystic degeneration. In parallel with an increased level of TSH, they noted an increase in the level of gonadotropic hormones, the LH index: FSH and PRL, which suggests a violation of the sensitivity of the ovarian receptor apparatus. Thus, already in the puberty with autoimmune thyroiditis (radiation genesis) in girls, marked violations of the reproductive system and menstrual cycle are noted.

Diagnosis of thyroid pathology with menstrual irregularities is based on clinical data, examination of the thyroid gland (examination, ultrasound, scan), assessment of the functional state of the thyroid-pituitary system (levels T3, T4, TG, TSH, TSH), blood biochemical parameters (especially levels cholesterol and sugar), hormonal tests. A test with styroliberin allows you to differentiate the subclinical form of primary hypothyroidism from the secondary. The drug is administered intravenously in the morning on an empty stomach in a dose of 200 mcg (rifotirones, reflex) in physiological saline. The content of TSH and PRL in the blood plasma is determined before the introduction of thyroliberin and after 30, 60 and 120 minutes. Normally, in healthy women of childbearing age, a rise in TSH and PRL of 3 times or more is already observed 30 minutes after the introduction of tyroliberin, and after 120 minutes their level returns to the original level. In the subclinical form of primary hypothyroidism, the TSH level rises tenfold, and returns to the initial level after 2 hours (slow). In secondary hypothyroidism, after administration of thyroliberin, the level of TSH decreases, and the concentration of PRL increases.

Table 9.

The main clinical changes in diseases of the thyroid gland

(differential diagnosis)

It can be concluded that the following disorders of the reproductive system and menstrual cycle are noted in thyroid pathology: puberty pathologies, hypo- and hypermenstrual syndrome, primary and secondary amenorrhea, DMC, amenorrhea-galactorrhea, functional and organic hyperprolactinemia, infertility and miscarriage (tab. 9).

Treatment of thyroid pathology with menstrual irregularities is carried out taking into account the individual characteristics, form and severity of the disease. Treatment of the underlying disease and correction of disorders of the neuroendocrine system for regulating menstrual and, where shown, reproductive functions are provided.

The pathogenetic therapy of thyrotoxicosis is based on the thyroid hormone biosynthesis blockade. For this purpose thyreostatics are used. The most effective derivatives of thiouracil and mercaptoimidazole. More often, mercazolil is applied at 10–20 mg / day for 2–3 weeks, followed by a dose reduction to 5–10 mg / day and continued treatment for 1–2 years. Initial doses of the drug can be large, depending on the severity of the disease. Transfer to maintenance doses is achieved when remission is achieved. In case of intolerance to mercazolil or developed leukopenia, diiodotyrosine of 0.15 g / day is used in 2-3 doses or in combination with mercazolil (courses of 20 days with 10-day intervals for 3-4 months). If such therapy is ineffective, preparations of organic and inorganic iodine are prescribed (Lugol's solution 3-5 drops a day, antistramine 1-2 tablets 2-3 times a week). In severe forms of thyrotoxicosis, glucocorticoids are used (hydrocortisone at 50-100 mg / day or prednisone at 5-10 mg / day). Perhaps combined treatment with propylthiouracil (150 mg / day) with potassium iodide and glucocorticoids. The use of? -Adrenergic blockers is advisable, especially with changes in the cardiovascular system (anaprilin, starting from 30-40 mg / day with a gradual increase in dose to 80 mg / day or more). With severe weight loss, peritol is prescribed 1 tablet 2-3 times a day (8-12 mg). Since with thyrotoxicosis there are violations of the indicators of the cellular and humoral parts of the immune system and antibodies to thyroid antigens are detected, then their titer is used to judge both the severity of the disease and the effectiveness of therapy. With an overdose of drugs, symptoms of hypothyroidism may occur. In this case, a temporary cessation of treatment or a reduction in the dose of drugs is indicated. The therapy is carried out to normalize the menstrual cycle (correction of DMK, amenorrhea). In DMC, hemostasis is initially corrected, if necessary, with the use of hormones. Cyclical estrogen therapy with progestogens is indicated for the treatment of amenorrhea or cycle regulation in DMC. In cases of endometrial hyperplastic processes, gestagens are prescribed in the second phase of the cycle for 2-3 months. If it is necessary to rehabilitate the reproductive function after normalizing the menstrual cycle, ovulation with clomiphene is stimulated according to the traditional scheme.

The treatment of hypothyroidism in both primary and secondary is essentially the same and involves the use of thyroid hormones, although there are certain differences. The dose of thyroid hormones is selected individually. Widely used are L-thyroxine and triiodothyronine. The use of L-thyroxine is based on the fact that the peripheral conversion of T4 to T3 occurs, and taking into account its pharmacokinetics, the drug is prescribed once a day. With severe hypothyroidism, L-thyroxine is recommended at 100-200 mcg / day. The initial dose of the drug is 10-25 mcg / day, and then it is gradually increased. Since triiodothyronine acts faster, the combination of thyroxin with triiodothyronine (in the ratio of 5: 1 or 10: 1) is first introduced, taking into account the clinical picture of the disease. Combined drugs are used: thyrecomb (70 μg of levothyroxine, 10 μg of lyothyronine and 150 μg of potassium iodide), thyreotome (40 μg of levothyroxine and 10 μg of lyothyronine), thyreotome (120 μg and 30 μg, respectively), triiodothyronine (50 μg, lyothiron) L-thyroxine (50 or 100 μg of levothyroxine). In severe forms of thyrotoxicosis, thyroid drugs are combined with hypocorticoids. With congenital hypothyroidism for normal development of the baby, treatment begins immediately after birth, preferably with a thyroxine of an average of 50 mcg / day (based on 8 mcg / kg per day at the age of 1–4 years, 7 mcg / kg at 4–6 years , 6 mcg / kg - at 6-10 and 5 mcg / kg per day at the age of 10-15 years).

For the quickest compensation of patients, thyroid drugs are combined with? -Adrenoblockers. Especially carefully, in small doses with a subsequent increase, thyroid preparations should be administered to patients with cardiovascular disorders. Thyroid drugs are often combined with cardiac glycosides and coronary-expanding agents.

Often with primary and especially secondary hypothyroidism, hyperprolactinemia and galactorrhea-amenorrhea develop. Perhaps even a combination of the intrasellar pituitary tumor (secondary adenoma, from TSH-producing cells) with primary hypothyroidism. Считается, что тиролиберин является стимулятором секреции пролактина. Заместительная гормональная терапия тиреоидными гормонами при первичном гипотиреозе с галактореей-аменореей способствует прекращению галактореи, восстанавливает двухфазный менструальный цикл и приводит к наступлению беременности. Однако нередко в таких ситуациях приходится прибегать к применению парлодела (по 5—10 мг в сутки в 1—2 приема) и циклической гормональной терапии эстрогенами с гестагенами. При реабилитации генеративной функции у женщин с гипотиреозом следует помнить о частых ВПР и снижении интеллекта у новорожденных от таких матерей.

Лечение больных вторичным гипотиреозом спо-мощью ТТГ и ТТГРГ не получило особого распространения из-за технических сложностей их пульсаторного введения, а также в связи с аллергическими реакциями на них и образованием антител к тиреоглобулину. Поэтому терапию женщин со вторичным гипотиреозом и нарушением менструальной функции проводят так же, как и с первичным. Показано также воздействие на гипоталамо-гипофизарную систему (психотерапия, фенозепам по таблетке, ноотропил по 1 таблетке 2 раза в день), витамины В6, В12, А, а также применение диуретиков (верошпирон по 100 мг/сут). При необходимости показана циклическая гормональная терапия эстрогенами с гестагенами и стимуляция овуляции до восстановления генеративной функции.

Передозировка тиреоидных препаратов сопровождаются явлениями гипертиреоза, что требует снижения их доз или временного прекращения лечения.

Лечение тиреоидитов также проводится с учетом формы болезни. При острых и подострых тиреоидитах назначаются глюкокортикоиды в сочетании с салицилатами (преднизалон по 10 мг/сут в течение 1—2 месяцев, ацетилсалициловая кислота по 1,0 г 3 раза в сутки с уменьшением дозы по мере улучшения состояния). При повышенной СОЭ и обострениях болезни лечение возможно продолжать до 3—5 месяцев. Назначение тиреоидных гормонов проводится по показаниям сучетом переносимости, нередко их сочетают с ?-адреноблокаторами. При хронических аутоиммунных тиреоидитах также показаны глюкокортикоидные препараты (преднизалон по 20—40 мг/сут, дексаметазон по 2—3 мг в сутки), хотя целесообразность их применения длительное время оспаривалась. Основным методом лечения хронических аутоиммунных тиреоидитов является назначение тиреоидных препаратов. Терапия аутоиммунных тиреоидитов, связанных с радиационным воздействием, предусматривает назначение тиреоидных препаратов по показаниям, иммуномодуляторов, а также циклической гормональной терапии эстрогенами с прогестероном для коррекции нарушений полового развития и менструальной функции.

При всех формах патологии щитовидной железы по показаниям (диффузия и узловатая гиперплазия) проводится хирургическое лечение.
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Заболевания щитовидной железы и патология репродуктивной системы

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