Chapter 53 Thyroid disease in pregnancy
Incidence. In developed countries, 2 in 1000 pregnancies are complicated by hyperthyroidism and 9 in 1000 pregnancies are complicated by hypothyroidism.
Thyroid physiology and pregnancy
• During normal pregnancy, the thyroid gland grows in size due to gland hyperplasia and increased vascularity.
• Circulating levels of iodine are reduced in pregnancy. This may be secondary to reduced renal tubular absorption, maternal–fetal transfer and fetal storage. There is a daily requirement of inorganic iodine 250 μg. This is increased from the non-pregnant state of 150 μg. Iodine is absorbed from foods such as salt, milk, dairy products, seafoods and eggs. Miscarriage rates are increased in iodine-deficient women. Iodine supplementation is recommended for all women except those with Graves’ disease or a past history of hyperthyroidism.
• Thyroid-binding globulin production rises throughout pregnancy as a result of increased oestrogen and remains raised postpartum. Because of this, more T3 and T4 are protein-bound, thus raising total T3 and T4 levels.
• There may be a reduction in free T3 and T4 as pregnancy progresses. In late pregnancy, this may be in the non-pregnant hypothyroid range. Therefore, when low free T3/T4 levels are present in pregnancy, thyroid-stimulating hormone (TSH) is required for a diagnosis of hypothyroidism. Free thyroxine concentrations correlate to thyroid function.
• TSH levels fall in the first trimester. Free thyroid hormones are raised in about 70%–75% of women with hyperemesis, suggesting a relationship between high human chorionic gonadotrophin (hCG) levels and thyroid stimulation (hCG and TSH have the same alpha subunit with different beta subunits; hCG may be a TSH agonist).
• Fetal thyroid commences functioning at 10–12 weeks gestation; however, it is the maternal thyroxine mostly supplying fetal needs until the third trimester when the fetal thyroid is sufficiently mature to be independent. In this trimester, the placenta acts as a barrier to maternal TSH, T4 and T3, and the fetal axis acts independently of the mother. The placenta freely transports iodine and thyrotrophin-releasing hormone. Fetal blood sampling correlates to fetal status most reliably. After birth, fetal TSH levels rise markedly due to a thyrotrophin-releasing hormone surge and decrease to normal over 3 days. The fetal dependence on maternal iodine continues during breastfeeding.
Maternal–fetal interactions
• Thyroid antibodies: microsomal and thyroglobulin antibodies cross the placenta, but are not cytotoxic to fetal thyroid cells.
Hypothyroidism
• Autoimmune thyroid disease is diagnosed by destructive antibodies (antithyroid perroxidase antibodies and antithyroglobulin antibodies). The underlying thyroiditis is known as Hashimoto’s disease. Prevalence is unknown, although antibodies may be present in 5% of women of childbearing age.
• It is possible that women with normal thyroid function when not pregnant are at risk of developing hypothyroidism in early pregnancy when the thyroid gland cannot increase the required production for pregnancy.
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