Hyperthyroidism in pregnancy is an increase in the content of thyroid hormones that occurred before conception or associated with gestation. It is manifested by weakness, fatigue, sweating, nausea, vomiting, increased appetite, increased defecation, irritability, insomnia, tremor of the hands, palpitations, in some patients — an increase in the thyroid gland, exophthalmos, infiltrative dermatopathy of the lower extremities. It is diagnosed on the basis of analysis data on the content of T3, T4, TSH. Thyrostatics, beta-blockers are used for treatment, with a resistant course, bilateral subtotal resection of the thyroid gland is performed.
According to research in the field of endocrinology, the prevalence of hyperthyroidism reaches 1%, in more than half of cases the disorder occurs subclinically. The frequency of thyrotoxicosis at gestation is 0.05-0.4%. In 85-90%, the disorder occurs before the onset of pregnancy and is caused by basal disease. However, in some women, hyperthyroidism is gestational, formed either in the first trimester as a result of compensatory hormonal restructuring of the body, or after childbirth due to the development of autoimmune processes. The urgency of timely detection of pathology is associated with a high risk of complications in severe thyrotoxicosis.
There are several groups of pathological conditions that are manifested by increased synthesis and release of thyroid hormones in pregnant women. Only 8-10% of patients have hyperthyroidism associated with physiological processes occurring during gestation and after childbirth. In other cases, the level of thyroxine and triiodothyronine increases due to diseases that occurred before pregnancy. The main etiological factors are:
- Hyperstimulation of thyrotropin receptors. The thyroid gland produces an excessive amount of hormones with thyrotropinomas — pituitary adenomas that secrete TSH, the stimulating effect of autoimmune complexes in basal disease, an increase in the sensitivity of thyroid-stimulating receptors due to mutations in toxic multi-node goiter or solitary node. At 8-14 weeks of pregnancy, hormone synthesis potentiates chorionic gonadotropin, similar in structure to thyrotropin.
- Destruction of the thyroid gland. With subacute granulomatous thyroiditis, Hashimoto’s thyroiditis, postpartum autoimmune thyroiditis, which occurs in some women in the first months after childbirth, the thyroid tissue is destroyed, and the hormones contained in it enter the blood. At the initial stages of inflammation, hyperthyroidism develops, which may later be replaced by hypothyroidism. Similar processes are possible with the appointment of α-interferon, amiodarone, and in some cases, lithium preparations.
- High levels of iodine in the blood. Sometimes hyperthyroidism is observed against the background of increased activity of functionally autonomous areas of the thyroid gland that use excess iodine to produce hormones. Usually the condition is transient and normalizes after the removal of the trace element from the body. Its causes may be the intake of iodine preparations (cordarone, expectorants), radiation studies with iodine—containing contrast, less often – the use of iodine-rich products.
Extremely rarely, hyperthyroidism in pregnancy is provoked by pulmonary metastases of follicular thyroid cancer and ovarian teratomas containing a sufficient amount of thyroid tissue. The occurrence of transient drug thyrotoxicosis is possible after accidental or intentional intake of thyroid hormones in an increased dosage.
The key point in the development of hyperthyroidism is the strengthening of the secreting function of TSH-sensitive or functionally autonomous thyroid cells or the release of hormones from the destroyed thyroid tissue. The emergence or intensification of these processes is facilitated by changes occurring during gestation. At the beginning of pregnancy, the activity of the gland increases physiologically, which is associated with the importance of thyroid hormones for the normal functioning of the corpus luteum, which preserves pregnancy in the early stages. Estrogens, whose level is gradually increasing, potentiate the production of thyroxine-binding globulin (TSG) in the liver.
Compensatory enhancement of thyrotropin synthesis contributes to maintaining the normal level of biologically active free fractions of thyroid hormones with an increase in their total content. Since the fetal thyroid gland begins to secrete hormones only from the 12th week of pregnancy, in the 1st trimester, the child’s needs for triiodothyronine and thyroxine are met due to their temporary hyperproduction in the pregnant woman’s body under the action of hCG. Immune restructuring after childbirth may be accompanied by the formation of antibodies to thyroid tissue and the development of transient inflammation with signs of hyperthyroidism, which is subsequently often replaced by a decrease in thyroid function.
Hyperthyroidism in pregnancy is systematized taking into account the same criteria as outside the gestational period — the etiological factor and the severity of clinical manifestations. For reasons, there are primary thyrotoxicosis caused by hyperproduction of thyroid hormones by the thyroid gland, secondary, which occurred against the background of pituitary disorders, and tertiary, provoked by hypothalamic dysfunction. Separately, there are variants of the disorder that are caused by the secretory activity of thyroid tissue outside the thyroid gland, associated with its destruction or an overdose of hormonal drugs. Depending on the severity , the following variants of hyperthyroidism are distinguished:
- Subclinical. It is asymptomatic. With a slightly reduced level of thyrotropin, a normal thyroxine content is noted. The risk of obstetric and extragenital complications is minimal.
- Manifest. There is a characteristic clinical picture. There is a significant decrease in the concentration of thyroid-stimulating hormone and an increase in the level of thyroxine. The likelihood of pregnancy complications increases.
- Complicated. Thyroid hormones have a toxic effect on the body. Atrial fibrillation, dystrophy of parenchymal organs, adrenal, heart failure, and other life-threatening disorders develop.
The clinical symptoms of hyperthyroidism in pregnancy usually do not depend on the causes that caused it. With the latent course of hyperthyroidism, symptoms indicating an acceleration of metabolism can be determined — insufficient weight gain, warm skin, increased sweating, fatigue, muscle weakness. With manifest course, pregnant women complain of heat intolerance, nausea, vomiting, increased appetite, increased urge to defecate, insomnia, trembling fingers, palpitations in the precardial region, neck, head, abdominal cavity. Some patients have subfebrility.
The woman looks fussy, touchy, irritable, whiny. With diffuse hyperplasia of the thyroid tissue, a thickening of the lower part of the neck becomes noticeable. Sometimes nodular formations are detected in the thyroid gland. Characteristic signs of hyperthyroidism in Graves’ disease are infiltrative ophthalmopathy and dermatopathy. 60% of pregnant women with toxic goiter have pain in the eye sockets, lacrimation, redness of the conjunctiva, sclera, photophobia, bug-eyed (exophthalmos), double vision when viewing objects. Thyroid dermatopathy is manifested by itching, redness of the anterior surface of the shins, the formation of nodes, extensive non-inflammatory infiltrates. The skin of the toes is less often affected.
With transient hyperthyroidism, which occurs in the first trimester, early toxicosis with indomitable vomiting of pregnant women is more often detected. According to the observations of specialists in the field of obstetrics, the complicated course of gestation is usually found in patients who suffer from toxic goiter. A significant increase in the concentration of thyroid hormones affects the implantation processes and disrupts embryogenesis, which leads to spontaneous miscarriage. With thyrotoxicosis, the risk of premature birth, stillbirth, gestosis with severe hypertensive syndrome, placental abruption, coagulopathic bleeding increases. The course of the disease can be complicated by a thyrotoxic crisis, heart failure.
Against the background of disorders of cardiovascular activity characteristic of hyperthyroidism, fetoplacental insufficiency is more often formed, leading to a delay in fetal development. Toxic effects of thyroid hormones increase the likelihood of anatomical developmental abnormalities, including those incompatible with life. In 2-3% of pregnant women with hyperthyroidism, the transplacental transition of autoantibodies to thyroid-stimulating receptors contributes to the occurrence of intrauterine and neonatal thyrotoxicosis with fetal hypotrophy, increased neuromuscular excitability, disorders of the psychomotor development of the newborn.
If there is anamnestic information about thyroid diseases with an increase in its secretory activity, diagnosis is not difficult. If the development or manifestation of thyrotoxicosis is suspected during gestation, tests are prescribed to detect hormonal imbalance. Laboratory markers of hyperthyroidism in pregnancy are:
- The content of thyroid hormones. In patients with a subclinical course, the indicator may remain normal. With the manifestation of the disease, the concentration of triiodothyronine (T3) and thyroxine (T4), especially free forms, increases.
- Thyrotropin level. The TSH content decreases in both subclinical and manifest primary hyperthyroidism. Such a violation is associated with the suppressive effect of thyroid hormones that circulate in the blood of a pregnant woman.
- Definition of AT RTG. Specific immunoglobulins interact with thyroid tissue receptors, stimulating its secretory function. Detection of antibodies serves as a marker of autoimmune thyroid disease.
To clarify the causes of hyperthyroidism in pregnancy, the level of thyroxine-binding globulin is additionally assessed, a test of extinguished thyroid hormones is performed, ultrasound and thyroid dopplerography are performed. Radiation research methods during pregnancy are not recommended because of the possible damaging effects on the fetus. An important task of the examination is the differential diagnosis between transient gestational hyperthyroidism and an increase in the level of thyroid hormones due to thyroid tissue damage or other causes. In addition to an obstetrician-gynecologist and endocrinologist, the patient is advised by a neurosurgeon, oncologist, immunologist, toxicologist, cardiologist, ophthalmologist, dermatologist.
Dynamic monitoring with regular laboratory monitoring is recommended for women with transient subclinical thyrotoxicosis. The appointment of active methods of treatment is justified in the manifest and complicated course of the disease. With therapeutically resistant hyperthyroidism, artificial termination of pregnancy is carried out for medical reasons for up to 12 weeks. The choice of drugs for the treatment of thyrotoxicosis is determined by the causes that caused the disorder. The main difficulty of therapy is the inability to use drugs containing radioactive iodine during pregnancy. With diffuse toxic goiter, which is most often detected with an increased content of T3 and T4 in pregnant women, prescribe:
- Antithyroid drugs. By blocking thyroid peroxidase, thyrostatics prevent the organification of iodides and the condensation of iodothyrosines, inhibit the peripheral conversion of thyroxine to triiodothyronine. They can quickly improve the condition of 20-50% of patients.
- β-blockers. They are indicated to eliminate the effects of adrenergic stimulation that occurred against the background of hyperthyroidism. Effectively reduce hand tremor, tachycardia, rhythm disturbances, emotional disorders, heat intolerance, relaxation of the stool, proximal myopathy.
- Iodine preparations. During pregnancy, they are rarely used because of possible toxic effects (conjunctivitis, rash, inflammation of the salivary glands). They make it possible to quickly inhibit the release of thyroid hormones and the organification of iodine. They are recommended for thyrotoxic crises and for preoperative preparation.
Usually, drug therapy is carried out in the 1st trimester, when the course of the basal disease is aggravated by physiological changes during pregnancy. Patients with severe hyperthyroidism, intolerance to thyrostatics, ineffectiveness of conservative treatment, compression of neighboring organs with goiter, suspected thyroid cancer require surgery. The intervention is performed in the 2nd trimester, when the risk of spontaneous abortion is minimal. The volume of resection is determined by the severity of the disorder. As a rule, a bilateral subtotal strumectomy is performed.
The preferred method of delivery is natural childbirth against the background of euthyroidism with adequate analgesia, monitoring of fetal condition and hemodynamic parameters. Usually, the birth process proceeds quickly, its duration in primiparous does not exceed 10 hours. Cesarean section is performed in the presence of obstetric indications (incorrect fetal position, narrow pelvis, umbilical cord entanglement, placenta previa, etc.). With exacerbation of hyperthyroidism in the postpartum period, lactation suppression and the appointment of thyrostatic drugs are recommended.
Prognosis and prevention
Timely diagnosis of hyperthyroidism and selection of an adequate treatment regimen allows most patients to carry out pregnancy normally. From 24-28 weeks, the severity of the disorder decreases, spontaneous remission of thyroid disease may occur. Pregnancy in women with pathologies accompanied by thyrotoxicosis should be planned taking into account the recommendations of an endocrinologist. The optimal time of conception is a period of persistent remission with euthyroidism 3 months or more after the end of drug treatment. For preventive purposes, early registration in a women’s clinic is indicated.