Hypothyroidism in pregnancy is a pathological condition caused by a low content of thyroid hormones and occurred before, during or after gestation. It often proceeds asymptomatically, may manifest weakness, fatigue, decreased mental and physical performance, nausea, constipation, hypothermia, dry skin, brittle nails, hair loss, hoarseness of voice, characteristic swelling of the extremities. It is diagnosed on the basis of laboratory data on the content of thyrotropin, thyroid hormones, autoantibodies to thyroperoxidase. Hormone replacement therapy and iodine preparations are used for treatment.
ICD 10
E03.8 Other specified hypothyroidism
General information
According to research in the field of obstetrics, the prevalence of hypothyroidism in pregnancy reaches 1.8-2.5%, while in the general population this indicator is 0.5-2.0%. Antibodies to thyroid enzymes are detected in more than 40% of these patients, and hypotrophy of the organ is sonographically confirmed in 15%. A separate risk group consists of 10-15% of patients with clinically significant content of antibodies to TPO (thyroperoxidase) and normal levels of thyroid hormones. By the time of delivery, 20% of them have thyroid-stimulating hormone levels that rise to indicators characteristic of subclinical hypothyroidism. The urgency of timely diagnosis of thyroid hypofunction is due to the high risk of miscarriage and the development of other obstetric complications.
Causes
Thyroid hormone deficiency that occurred before gestation is most often caused by autoimmune thyroiditis (Hashimoto’s disease), a disease with a hereditary predisposition in which autoantibodies to thyroid tissues are formed. With this pathology, the phase of hyperthyroidism, characteristic of the initial stages of the inflammatory-destructive process, is soon replaced by hormonal insufficiency. Other causes of hypothyroidism in women of reproductive age are hypothalamic-pituitary dysfunction, hypoplasia or aplasia of the thyroid gland, its resection in tumors, diffuse toxic goiter, destruction of thyroid tissue in trauma, radiotherapy. Hormone deficiency may be associated with an overdose of thyrostatic drugs, iodine deficiency in food and water, frequent pregnancies with a long lactation period. During gestation, there are a number of specific factors that contribute to the development of hypothyroid states:
- Immune restructuring after childbirth. Physiological suppression of immunity in a pregnant woman is aimed at reducing the risk of rejection of the fetus and termination of gestation. Against the background of postpartum immune reactivation, transient autoimmune aggression may occur. At the same time, in predisposed women with the presence of autoantibodies to thyroid peroxidase (AT-TPO), the probability of postpartum thyroiditis reaches 30-50%, and in patients with insulin-dependent diabetes mellitus and other autoimmune disorders, the prevalence of pathology is 3 times higher than in the general population.
- Iodine deficiency associated with gestation. The need of a pregnant woman for iodine increases significantly, due to the use of this trace element to ensure the normal operation of the fetoplacental complex and metabolic and plastic processes in the fetus. The situation is aggravated by increased renal clearance of iodine during pregnancy. An additional factor causing relative hypothyroxinemia in the absence of iodine prophylaxis is the activation of type 3 deiodinase, under the action of which thyroxine (T4) is transformed into biologically inactive reversible triiodothyronine (gT3).
- Functional overload of the thyroid gland. In the first trimester, under the influence of estrogens and chorionic gonadotropin, physiological hyperthyroidism develops, aimed at meeting the needs of the fetus in thyroid hormones. With insufficient functional reserve of the organ, the overloads experienced during gestation can serve as a trigger for the formation of a simple non-toxic goiter, the transition of asymptomatic autoimmune thyroiditis to the manifest stage, the occurrence of other thyroid disorders in predisposed patients.
Sometimes hypothyroidism, formed after pregnancy, becomes a manifestation of Sheehan syndrome — necrosis of pituitary tissue due to massive blood loss, infectious and toxic shock, DIC syndrome after complicated abortion or severe childbirth. In such cases, the lack of thyroid hormones develops against the background of multiple endocrine insufficiency.
Pathogenesis
The mechanism of hypothyroidism formation during pregnancy is determined by the causes that caused the disorder. An important link in the pathogenesis is a hereditary predisposition, which is manifested by a tendency to autoimmune reactions and a low functional reserve of thyroid tissue. Physiological hyperstimulation of the thyroid gland, increased excretion of iodine in the urine and its transplacental transfer lead to a relative iodine deficiency, which contributes to the manifestation of subclinical hypothyroidism. In the postpartum period, an additional role is played by the depletion of the cellular reserve of thyrocytes as a result of their destruction by autoaggressive antibodies.
With a low content of thyroxine and triiodothyronine, metabolism slows down significantly, and body temperature decreases. Glycosaminoglycans accumulate in organs and tissues — highly hydrophilic protein metabolites that can retain fluid in the skin, mucous membranes, and internal organs. As a result, widespread mucoid edema develops. In the long-term period, a woman with hypothyroidism manifested after childbirth suffers from positive ovarian-pituitary feedback, the menstrual cycle is disrupted, anovulation, hypomenorrhea, amenorrhea occur.
Classification
When systematizing the clinical forms of the disorder, etiological factors and the clinical severity of the pathology are taken into account. More than 90% of cases are diagnosed with primary hypothyroidism associated with dysgenesis, resection, inflammatory or radiation destruction, infiltrative diseases of the thyroid gland or a violation of hormone biosynthesis due to genetic abnormalities, deficiency or excess of iodine, the action of antithyroid factors. Secondary variants are caused by disorders at the hypothalamic and pituitary levels of endocrine regulation. Separately, there is a disorder caused by generalized resistance to thyroid hormones. Depending on the severity of clinical manifestations , hypothyroidism is distinguished:
- Subclinical. There are no symptoms. The level of thyrotropin is elevated in the blood, the thyroxine content is normal. It is determined in most patients with hypofunction of the thyroid gland. Pregnancy is possible with monitoring of laboratory parameters and minimal doses of hormones.
- Manifest. Clinical symptoms of hypothyroidism are observed. The content of thyroid—stimulating hormone is increased, thyroid hormones are reduced. It is rarely detected, mainly in the second half of pregnancy. Continuation of gestation is allowed only against the background of hormone replacement therapy.
Symptoms
With a subclinical course, the signs of the disease are not determined. In the decompensated state, there are complaints of lethargy, low efficiency, fatigue, drowsiness, chilliness, loss of appetite, nausea, constipation. A pregnant woman becomes forgetful, inattentive, apathetic, and quickly gains weight. Hypothermia, a rare pulse, pallor, dryness and peeling of the skin, hair and nail loss, brittle nails, myxedematous edema of the extremities, hoarseness of the voice, snoring during sleep are characteristic. Possible headaches, muscle, joint pain, numbness of the hands. Vision and hearing often deteriorate, ringing in the ears appears.
Complications
Due to fertility disorders in patients suffering from clinically pronounced hypothyroidism, pregnancy rarely occurs, often has a complicated course and in 35-50% of cases ends with spontaneous abortion or premature birth. Every third pregnant woman has early toxicosis. Up to 3.3% of fetuses have developmental abnormalities, including those caused by structural and quantitative chromosomal aberrations. Gestational hypertension and preeclampsia are observed in 15-22% of patients, fetal hypotrophy — in 8,7-16,6%, stillbirth — in 1,7-6,6%. Fetoplacental insufficiency develops in 70% of cases. There may be over-gestation, weakness of labor, premature detachment of the normally located placenta. In 3.5-6.6% of maternity patients, coagulopathic postpartum bleeding occurs. Hypogalactia is characteristic.
Children born to women with untreated hypothyroxinemia are more likely to have low IQ, other intellectual and mnestic disorders. According to the observations of specialists in the field of endocrinology, carrying a child also affects the development of the disorder that caused hypothyroidism – during pregnancy, the likelihood of clinical manifestations of asymptomatic (euthyroid) autoimmune thyroiditis increases, the formation of progressive postpartum thyroiditis associated with depression in women with circulating AT-TPO. A severe complication of hypothyroidism during gestation is myxedematous coma.
Diagnostics
Subclinical hypothyroidism due to an asymptomatic course is extremely rare. The basis for the appointment of laboratory tests to verify the violation is anamnestic information about the autoimmune diseases of the patient, her parents, siblings. In the presence of complaints and physical examination data indicating a possible violation of thyroid function, the patient is recommended:
- Determination of the TSH level. The analysis is a marker for primary hypothyroidism. In the subclinical variant of the disorder, the concentration of thyroid-stimulating hormone is increased to 4-10 mMU / l, in the manifest case, the indicator is over 10.0 mMU / l or more.
- Analysis of the content of thyroid hormones. In pregnant women with subclinical hypothyroidism, normal indicators of T4, T3 are determined. After manifestation, the concentration of free triiodothyronine does not exceed 4 pmol / l, free thyroxine — 10 pmol / L.
- Detection of antibodies to thyroperoxidase. Since most cases of hypothyroidism are associated with an autoimmune thyroid lesion, the study reveals autoaggression. The indicator from 34 IU/ml is diagnostically significant.
To determine the volume of thyroid tissue, to detect possible structural changes, an ultrasound of the thyroid gland is performed. A puncture biopsy of the organ is performed in doubtful cases with suspected neoplasia. ECG and ultrasound of the heart are shown as additional methods. Characteristic changes are detected in the general blood test: 60-70% of patients have lymphocytosis, increased ESR. In pregnant women suffering from hypothyroidism, anemia is usually more pronounced, cholesterol levels are elevated, and signs of hypercoagulation are noted.
Differential diagnosis is carried out between various diseases in which the production of thyroid hormones decreases. When making a diagnosis, it is necessary to exclude coronary heart disease, chronic nephritis, nephrotic syndrome, thyroid cancer. In addition to the obstetrician-gynecologist and endocrinologist, the patient is advised by a cardiologist, urologist, neurologist, neurosurgeon, dermatologist, oncologist.
Treatment
The main tasks of managing a patient with hypothyroxinemia are complete medical compensation of the disorder, correction of possible concomitant disorders, elimination of prerequisites that can aggravate the pathological condition. Prolongation of pregnancy in the manifest form of hypothyroidism is allowed only with the appointment of hormone replacement therapy. The standard treatment regimen includes medications such as:
- Thyroid hormones. The dose of the synthetic levorotatory isomer T4 is selected gradually with the control of the content of thyrotropin and thyroxine in the blood serum once every 14 days. The correct choice of dosage is indicated by the normalization of the concentration of thyroid-stimulating hormone at the level of 1.5-2 mMu / l. Hormone therapy is indicated for pregnant women not only with obvious hypothyroidism, but also with a subclinical form of the disorder.
- Iodine-containing medicines. Iodine therapy, carried out in violation of the secretion of T3, T4 against the background of iodine deficiency, allows you to reduce the dose of hormonal drugs, and sometimes completely abandon their use. In order to avoid overdose, when developing a scheme for taking medications with iodine, the severity of clinical symptoms and the preservation of thyroid tissue in destructive processes are taken into account.
In the presence of organ disorders caused by hypothyroxinemia, symptomatic treatment with cardioprotectors, stimulators of tissue metabolism, antiarrhythmic agents, nootropics, vitamin and mineral complexes, immunostimulants is used. Natural childbirth is recommended for patients with compensated hypothyroidism. Caesarean section is performed according to obstetric indications.
Prognosis and prevention
Hormonal correction of hypothyroidism minimizes the likelihood of complications for the mother and fetus. Women with thyroid diseases are recommended to plan pregnancy taking into account the opinion of an endocrinologist, after conception, register in a women’s consultation before the 12-week period, regularly visit an obstetrician-gynecologist. To reduce the risk of hypothyroidism in pregnancy, according to indications, iodine prophylaxis is carried out, the diet is supplemented with products saturated with iodine (sea fish, algae, iodized salt). It is necessary to exclude significant physical and psycho-emotional stress.
