Increased maternal/fetal demand for thyroxine (TH) during pregnancy. This can lead to an increase in hypothyroidism or to the development of subclinical hypothyroidism into clinical hypothyroidism. There is also a tendency to develop hypothyroidism in those with positive peroxidase antibodies (TPOAb). Maternal hypothyroidism during pregnancy is associated with spontaneous abortion, gestational hypertension, placental abruption, fetal distress, preterm delivery, and the occurrence of low birth weight infants. Maternal clinical hypothyroidism has been shown to cause incomplete differentiation and development of the fetal cerebral cortex, which is responsible for speech, hearing and intelligence. Maternal subclinical hypothyroidism or isolated hypo-T4emia during gestation may also result in mild impairment of mental and motor abilities in the offspring.
The diagnosis of clinical hypothyroidism and subclinical hypothyroidism in pregnancy is the same as in the general population.
Clinical hypothyroidism has clinical manifestations such as edema, fear of cold, weight gain, drowsiness, and unresponsiveness; laboratory tests show increased serum TSH and decreased FT4 and TT4. Subclinical hypothyroidism has no obvious clinical symptoms, and laboratory tests show increased serum TSH and normal FT4 and TT4. It should be emphasized that due to the physiological changes of pregnancy, the range of reference values of thyroid function indicators during pregnancy changes and pregnancy-specific reference ranges need to be used. TSH 2.5 mlU/L is currently recommended as a conservative upper limit in early pregnancy, beyond which the diagnosis of hypothyroidism in pregnancy can be considered. TT4 concentration increases during pregnancy and is approximately 1.5 times the normal value in non-pregnancy. If TSH is normal during pregnancy (0.3 to 2.5 mIU/L) and only TT4 is below 100 nmoL (7.8 μg/dl), hypothyroidism can be diagnosed.
Once hypothyroidism is diagnosed, exogenous thyroxine (L-T4) should be supplemented in a timely and adequate manner.
The earlier the treatment is initiated, the better, preferably at the beginning of pregnancy when serum TSH <2.5 mIU/L is achieved; serum FT4 is maintained at the upper 1/3 level of the normal range for non-pregnant adults; serum TT4 is maintained at 1.5 times the level of the normal value for non-pregnant adults. To ensure adequate supply of thyroid hormone during the first period of rapid fetal brain development, i.e., the 4th to 6th months of gestation. Usually the LT4 dose is increased by 30% to 50% during pregnancy compared to the non-pregnant requirement. The amount of increase in dose depends on the degree of TSH increase and the cause of maternal hypothyroidism. Autoimmune thyroid disease (AITD) requires a 35%-40% increase in dose; hypothyroidism after thyroid surgery and 131I treatment requires a 70%-75% increase in dose. The mental development of children will not be affected by appropriate thyroxine replacement therapy in pregnant women with hypothyroidism.
Women with AITD before pregnancy but with normal thyroid function are susceptible to suboptimal hypothyroidism and hypothyroidism.
TSH should be checked before pregnancy, and pregnancy should be considered after TSH is below 2.5 mlU/L. The treatment strategy for women with TSH between 2.5 and 5.0 mlU/L is either to give a small dose of L-T4 so that the pregnant woman’s TSH is less than 2.5 mIU/L; or to monitor TSH. during pregnancy, if the dose of L-T4 is stable, it is recommended that TSH be measured every 6 to 8 weeks. if the dose of L-T4 is adjusted After delivery, thyroxine dosage can be slowly reduced to pre-pregnancy levels, and TSH monitoring is also required during the reduction. l-T4 should be avoided in conjunction with iron- and calcium-containing preparations and soy foods, and should be taken at intervals of at least 4 hours. Thyroid hormone preparations applied during pregnancy and lactation do not have any toxic effects on the fetus or cause malformations as long as they are taken in appropriate doses.
Maternal subclinical hypothyroidism, hypo-T4emia and positive TPOAb can have adverse effects on fetal brain development.
The principles of hypothyroidism treatment in pregnancy are early initiation, attainment of targets as soon as possible, and maintenance throughout pregnancy. Some patients with clinical hypothyroidism may be diagnosed later in early gestation, when their fetuses are likely to have irreversible impairment of mental and cognitive abilities. In such cases, the American College of Endocrinology recommends that the pregnancy be maintained and that thyroid replacement therapy be initiated immediately to rapidly normalize thyroid hormone levels.
Pre-pregnancy screening should be done for those at high risk of developing hypothyroidism. People at high risk for hypothyroidism include.
1. Those with hyperthyroidism, hypothyroidism, or lobectomy of the thyroid gland.
2, with a family history of thyroid disease.
3, goiter.
4. Positive autoantibodies to the thyroid gland.
5, Clinical indication of high or low thyroid function, including anemia, hyponatremia, hypercholesterolemia.
6, Type 1 diabetes.
7, Other autoimmune diseases.
8.Check for infertility and measure TSH at the same time.
9.History of head and neck radiation treatment.
10.People with a history of miscarriage and premature birth. Once diagnosed with clinical hypothyroidism, L-T4 treatment is given; if the thyroid function is normal, regular follow-up observation is recommended.
Pregnant women with Hashimoto’s thyroiditis should be monitored more closely after delivery.
Usually after six months, the thyroid gland becomes enlarged again or even larger than during pregnancy, and anti-thyroid antibodies are significantly elevated. Those with pre-pregnancy hypothyroidism have a greater chance of developing hypothyroidism again after delivery. Therefore, postpartum treatment and follow-up are necessary. Newborns born to women with Hashimoto’s thyroiditis may have hyperthyroidism or hypothyroidism and should be checked for thyroid function. There is a genetic predisposition to thyroid disease, but it does not mean that the offspring will definitely develop thyroid disease, i.e., the offspring will have a greater chance of developing thyroid disease than the normal offspring.