Hyperthyroidism in pregnant women

The prevalence of hyperthyroidism in the U.S. is approximately 1% (up 0.4% clinical and 0.6% – subclinical). The most common cause of hyperthyroidism is graves ‘ disease, which is 5-10 times more common in women with a peak incidence in the reproductive age.

Hyperthyroidism during pregnancy is not uncommon, and its prevalence is 0.1 to 0.4%, with graves ‘ disease accounts for up to 85% of cases. Single toxic adenoma, toxic nodular goiter and thyroiditis responsible for the vast majority of all cases of hyperthyroidism during pregnancy, but severe gestational hyperthyroidism and iatrogenic thyrotoxicosis are much less common reasons.

As with other autoimmune diseases, the level of activity in graves ‘ disease may fluctuate during gestation, with exacerbation during the first trimester and gradual improvement in large stages of pregnancy. Half of the women with graves ‘ disease worsening occurs shortly after birth. In rare cases, childbirth, cesarean section and infection can worsen the symptoms of hyperthyroidism and even lead to thyrotoxic crisis.

Autoimmune thyroiditis occurs in 10% of women of childbearing age. In General, the result is hypothyroidism, although it also happens gipertireoze phase of Hashimoto’s disease and silent thyroiditis. Postpartum thyroiditis occurs in 10% of pregnant women and can pass through a phase of hyperthyroidism, usually in the first month or the second.

Since the beginning of postpartum thyroiditis most often falls on the interval from 6 weeks to 6 months after birth and sometimes up to 1 year after childbirth, is not uncommon the beginning of this disease with subsequent pregnancy. In addition, a triggering factor “postpartum” thyroiditis may be a miscarriage in the period of about 6 weeks of pregnancy, and often following pregnancy in these women is coming in the next few months.

Because gipertireoze phase of thyroiditis and later is accompanied by the hypothyroid, and also due to the fact that hypothyroidism is a significant risk factor for the development of the fetus, careful monitoring to detect and treat the hypothyroid phase of the disease.

Women with gestational hyperthyroidism usually go to the doctor in the middle or at the end of the first trimester, usually with excessive vomiting. Usually the symptoms of hyperthyroidism are reasonable or minimal, with the exception of loss of weight, which is the result of vomiting and poor nutrition. In such cases, a differential diagnosis of graves disease and gestational thyrotoxicosis, which allows to determine the feasibility of thyreostatics.

The function of the thyroid gland (TG) of the fetus

Thyroid of the fetus begins to capture iodine at 10-12 weeks of gestation, and the regulation of its function of pituitary TSH is observed around 20 weeks of pregnancy. The levels of TSH, TBG, free T4 and free T3 in the serum of the fetus increase with increasing gestational age and reaches typical adult figures are about 36 weeks pregnant. TSH through the placenta does not penetrate, but clinically significant amounts of maternal T4 cross the placenta.

In newborns with congenital hypothyroidism, the penetration of maternal thyroid hormones across the placenta prevents stigmata of hypothyroidism, the concentration of thyroid hormones in the blood of the umbilical cord is about 50% of normal. In addition, through the placenta penetrate thyroliberin (TRH), iodine, receptor antibodies (TSH-R) and antithyroid drugs.

Fruit and neonatal risks of maternal hyperthyroidism due to the nature of the disease and / or medication. Inadequate treatment of hyperthyroidism in the mother is associated with the risk of medical induction of premature birth, intrauterine growth retardation, preeclampsia, congestive heart failure and intrauterine fetal death. In addition, excessive use thioamide mother can lead to iatrogenic hypothyroidism in the fetus.

According to the materials of the women’s magazine Mamapedia.com.ua