Iodine deficiency during pregnancy is a group of pathological conditions caused by iodine deficiency and occurring in the gestational period. With normal thyroidogenesis, they are manifested by an increase in the circumference of the neck, difficulty swallowing and breathing, periodic coughing, decreased performance, headaches and precardial pains. In patients with impaired thyroid function, signs of hypothyroidism or hyperthyroidism are additionally determined. It is diagnosed based on data on the iodine content in urine samples, T4, T3, TSH levels, and the results of thyroid tissue ultrasound. For treatment, iodine-containing drugs, L—thyroxine are used, less often antithyroid drugs and beta-blockers.
ICD 10
E01 Thyroid diseases associated with iodine deficiency and similar conditions
General information
Iodine belongs to the category of essential trace elements, is a mandatory component of thyroid hormones. For the normal development and maintenance of metabolism, a healthy person needs 100-150 micrograms of iodine per day. During pregnancy, the daily requirement increases to 200 micrograms. The territory of USA, like other states, is endemic for iodine-deficient pathological conditions caused by a lack of trace elements in water and products of the natural diet. In most regions, in the absence of iodine prophylaxis, the daily intake of iodine does not exceed 50-80 micrograms. Therefore, iodine deficiency is diagnosed in almost 80% of pregnant women. The urgency of timely detection and correction of iodine deficiency is associated with a high risk of loss of the intellectual potential of the nation due to impaired embryogenesis of the nervous system with moderate and severe iodine deficiency.
Causes
Iodine deficiency during gestation is provoked by a deficiency of trace elements in food and its increased consumption due to the peculiarities of the physiological state of the body. In the absence of planned iodine prophylaxis and irrational nutrition, the pregnant woman initially does not receive this trace element. At the same time, during pregnancy, a woman’s body significantly increases iodine intake. The reasons for the increased need of a pregnant woman for iodine are:
- Hormonal restructuring of the body. Estrogens and chorionic gonadotropin in the 1st trimester of gestational age have a stimulating effect on the thyroid gland. The resulting physiological hyperthyroidism is accompanied by an increased consumption of trace elements, which is necessary for the synthesis of thyroid hormones, and an aggravation of the existing alimentary iodine deficiency.
- Ensuring the needs of the child. In the 1st half of pregnancy, iodine is consumed for increased secretion of thyroid hormones necessary for the functioning of a woman’s body, fetal development and placental complex. From the 15th week, thyroid hormones begin to be secreted by the thyroid gland of the child, which contributes to the additional consumption of trace elements.
- Increased renal clearance of iodine. During pregnancy, renal blood flow and glomerular filtration rate gradually increase by 30-50%, reaching maximum values by 20-26 weeks of gestational age and decreasing by 10-15% by the 36th week. Against the background of constant tubular reabsorption, this provokes increased losses of iodine in the urine, especially significant in 1-2 trimesters.
The occurrence of iodine deficiency during pregnancy is facilitated by the intake of penicillin, cordarone, sulfonamides, bromine, aspirin, glucocorticosteroids and other drugs that prevent the absorption of trace elements in the gastrointestinal tract or accelerate its excretion, diseases of the digestive tract, worm infestations, dysbiosis, chronic infectious and inflammatory diseases. The assimilation of the trace element is disrupted with a low content of selenium, zinc, manganese, molybdenum in products, and the use of chlorinated water.
Pathogenesis
With iodine deficiency in a pregnant woman, first of all, the exchange of thyrogormones is disrupted. The serum level of total and free thyroxine decreases, the content of thyroglobulin and thyrotropin (TSH) increases. Compensatory hyperplasia of the thyroid tissue occurs, the size of the organ increases by 16-31%, active foci (nodes) may appear in it. Since hormones produced by the thyroid gland of a woman provide the metabolic and plastic processes of the fetus up to 15 weeks, with iodine deficiency, the normal development of the child’s central nervous system, formed during this period, is disrupted.
Due to insufficient expression of genes involved in the synthesis of neurogranin and other specific proteins, neuronal migration, axonal and dendritic growth, myelination of nerve fibers, synaptogenesis slows down, which often leads to general underdevelopment of brain tissue and disruption of its histological structure. The lack of thyroid hormones, which arose against the background of iodine deficiency, also negatively affects the formation of skeletal cartilage, the growth and development of fetal bone tissue – when the thyroid gland is disrupted, the division of osteoblasts necessary for the formation of bone matter slows down, the processes of mineralization of the matrix with calcium and phosphorus salts are disrupted.
Classification
When systematizing iodine deficiency conditions in pregnant women, the severity of iodine deficiency and the functionality of thyrocytes are taken into account. This approach is most justified when choosing the optimal tactics for accompanying gestation. To assess the degree of iodine deficiency, an indicator of the excretion of trace elements in urine is used: iodine deficiency is considered mild with its content in urine from 50 to 99.9 mcg / l, average — from 20 to 49.9 mcg / l, severe — less than 20 mcg / l. Iodine deficiency may be accompanied by a change in the size, structure, and functionality of the thyroid gland. Specialists in the field of obstetrics and endocrinology distinguish the following types of iodine deficiency conditions during gestation:
- Non-toxic (euthyroid) goiter. It becomes the result of hyperplasia of the organ with iodine deficiency. It can be diffuse (endemic) and focal. The most common thyroid disease in Europeans, detected in 23.5-25% of women with mild iodine deficiency. To continue gestation, iodine prophylaxis is necessary.
- Hypothyroidism during pregnancy. Insufficient iodine intake in women with subclinical enzyme deficiency (presence of autoantibodies to thyroperoxidase) can provoke the manifestation of autoimmune thyroiditis. Hypothyroidism is detected in 1.8-2.5% of pregnant women. Usually, the disorder occurs with moderate or severe iodine deficiency, complicating the course of gestation.
- FA of the thyroid gland. Functional autonomy of the thyroid gland is a rare and least favorable prognostic variant of the iodine deficiency state, which occurs against the background of prolonged hyperstimulation of thyrocytes with thyroid-stimulating hormone in conditions of mild and moderate iodine deficiency. It is manifested by severe hyperthyroidism with frequent obstetric complications.
Symptoms
The clinical picture of iodine deficiency depends on the functional viability of thyroid tissue. With euthyroid variants of iodine deficiency, the circumference of the lower part of the neck increases in a pregnant woman, breathing and swallowing are periodically difficult, working capacity decreases, dry compulsive coughing appears. Headaches, dizziness, dry skin are possible. A pregnant woman may complain of weakness, fatigue, discomfort in the precardial region. With focal goiter, compacted areas can be felt in the tissues.
When iodine deficiency is combined with thyroid insufficiency, signs of hypothyroidism appear during pregnancy: lethargy, apathy, drowsiness, dyspeptic disorders, hypothermia, forgetfulness, pallor, characteristic swelling of the extremities, the severity of which depends on the degree of hypothyroxinemia. For decompensated hyperthyroid state provoked by iodine deficiency, weight loss, complaints of muscle weakness, interruptions and palpitations, emotional lability, insomnia, sweating, poor heat tolerance, sometimes subfebrility, headaches, hypertension are typical.
Complications
The complicated course of pregnancy with iodine deficiency is more often observed in patients suffering from thyroidogenesis disorders. A decrease in the level of thyroid hormones against the background of iodine deficiency leads to a violation of the formation of the fetal brain, which subsequently manifests itself as intellectual and mnestic disorders in children. The risk of other developmental abnormalities increases by up to 25%. Perinatal encephalopathy is detected in 19.8% of newborns. With severe iodine deficiency in the first trimester of pregnancy, the likelihood of developing cretinism in a child with severe mental retardation, delayed physical development, spastic diplegia, speech disorders, deaf-mute increases. With mild and moderate endemic iodine deficiency, 10% of newborns are diagnosed with congenital (neonatal) goiter with an increase in the volume of the thyroid gland by 30-39%.
Pregnancy in women suffering from iodine deficiency is more often complicated by the threat of termination, gestosis, anemia, fetoplacental insufficiency. Early and late miscarriages are observed in 18-20% of cases. The probability of premature birth increases almost 2 times (up to 10%). In the II-III trimesters, intrauterine fetal hypoxia is observed in 37.5% of cases. Childbirth is complicated in 43.7% of cases of iodine deficiency. The most common disorders are premature discharge of amniotic fluid, detachment of the normally located placenta, weakness of labor forces, intimate attachment of the placenta, hypotonic and atonic bleeding. Hypogalactia is possible in the postpartum period.
With significant hyperthyroidism against the background of iodine deficiency, implantation and embryogenesis are disrupted, which leads to early spontaneous termination of pregnancy. Such patients have a higher probability of fetoplacental insufficiency, premature birth, gestosis with significant arterial hypertension, coagulopathic bleeding, DIC syndrome, stillbirth. A long-term consequence of iodine deficiency during gestation is an increase in thyroid pathology in women of reproductive age. Diffuse goiter that developed during pregnancy does not regress in all cases, and with pre-existing hyperplasia, the size of the gland, the number and volume of nodes increase in patients.
Diagnostics
Iodine deficiency in euthyroid disorders is characterized by a non-specific clinical picture. Therefore, due to the high probability of hypothyroidism developing against its background, all patients living in endemic regions and presenting characteristic complaints should be examined to exclude iodine deficiency lesions of thyroid tissue. The most informative are:
- Determination of iodine content in urine. The analysis is considered a marker for assessing the iodine saturation of the body. A decrease in the level of trace element less than 100 mcg / l indicates the development of an iodine deficiency condition. The study allows monitoring the effectiveness of iodine prophylaxis and treatment.
- Analysis of the concentration of thyroid hormones. A decrease or increase in the content of T4, T3 indicates a manifest violation of thyroidogenesis. Positive test results are sufficient grounds for prescribing hormonal-correcting drugs to a pregnant woman.
- Determination of the level of thyroid-stimulating hormone. Violation of TSH concentration at normal concentrations of thyroxine and triiodothyronine is characteristic of subclinical thyroid dysfunction. The analysis is recommended as a screening for the early diagnosis of hyperthyroidism and hypothyroidism.
- Sonography of the thyroid gland. During ultrasound of the thyroid gland, the size of the organ, its shape, structure, contours are visualized. The nature of changes in thyroid tissue (diffuse hyperplasia, focal formations) is evaluated. The method allows you to determine the number and features of nodes.
To carry out differential diagnosis and assessment of the child’s condition, the patient may be prescribed tests that detect AT TPO, AT RTG, fine needle node biopsy, determination of estradiol levels, HCG, ultrasound of pelvic organs, CTG, fetal phonocardiography. During pregnancy, the disorder is differentiated with hypothyroid and hyperthyroid conditions of another genesis (autoimmune thyroiditis, thyrotoxicosis), follicular neoplasia, Gürtle-Ashkenazi carcinoma, and other types of thyroid cancer. If necessary, the patient is referred for consultation to an endocrinologist, oncologist.
Treatment
When choosing a medical tactic, an obstetrician-gynecologist takes into account the degree of iodine deficiency and secretory activity of thyroid tissue. Non-drug methods of correcting iodine deficiency involve supplementing the diet with iodine-containing seafood, feijoa, dates, currants, persimmons, prunes, baked potatoes, apples, buckwheat, millet, beef, cheese, milk, eggs. In the diet, it is necessary to limit goitre products of plant origin that violate the absorption of an essential trace element — various types of cabbage, peanut and pine nuts, turnips, radishes, legumes (soy, beans), peaches.
Treatment is usually carried out on an outpatient basis, indications for hospitalization are the detection of increasing signs of the threat of termination of gestation, grade III increased uterine tone during pregnancy, other severe obstetric and extragenital complications. Depending on the levels of thyroxine, triiodothyronine, two main therapeutic regimens are recommended for iodine deficiency:
- Monotherapy with iodine preparations. The use of iodine-containing drugs is justified in euthyroid forms of goiter, which occurred during gestation on the background of mild, less often moderate iodine deficiency. The dosage of the drugs corresponds to the patient’s daily need for trace elements.
- Combined iodine replacement therapy. If hypothyroidism is detected, it is recommended to supplement the intake of iodine preparations with the appointment of L-thyroxine. Hormone-containing replacement agent, the dose of which is selected under the control of serum levels of TSH, T4, allows you to make up for thyroideficiency.
A contraindication to the appointment of iodine preparations is hyperfunction of the thyroid gland due to iodine deficiency. When decompensating the hyperthyroid state, the patient is recommended thyrostatics in combination with beta-blockers that eliminate the effects of adrenergic stimulation. The decision on surgical treatment of nodular forms of pathology is usually postponed until the end of gestation. Pregnancy with iodine deficiency is completed by natural childbirth. Caesarean section is performed only when obstetric and extragenital indications are detected.
Prognosis and prevention
The outcome of pregnancy is determined by the degree of iodine deficiency and the functional viability of the thyroid gland. The timely start of iodine prophylaxis for women with habitual miscarriage allows to reduce the frequency of miscarriages by 1.3 times, premature birth — by 1.8 times, fetoplacental insufficiency — by 1.7 times, abnormal labor — by 2.6 times, intranatal fetal hypoxia — by 3 times. Preventive iodine intake in a daily dose of 200 mcg is recommended to begin 3-6 months before conception. Although a fairly effective method of iodine prophylaxis in endemic territories is the replacement of ordinary table salt with iodized salt, the appointment of iodine-containing drugs makes it possible to more effectively control the dose of trace element that a pregnant woman receives. To preserve lactation and ensure the physiological development of the child, iodine prophylaxis should be continued after childbirth.
