Thyroid disease in pregnancy

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Chapter 53 Thyroid disease in pregnancy

Michael Flynn

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.
• TSH receptor antibodies are immunoglobulin G-type antibodies and therefore cross the placenta with a risk of neonatal complications.
• Antithyroid antibodies, if present, can increase the risk of miscarriage.

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.
• Always use TSH, free thyroxine (T4) for diagnosis and this should be monitored approximately every 6 weeks:

• Raised TSH, decreased free T4 and positive thyroid autoantibodies are diagnostic of hypothyroidism.
• Mild elevation TSH and normal free T4 are diagnostic of subclinical hypothyroidism likely to become hypothyroid as pregnancy progresses.
• The presence of antithyroid antibodies and normal TSH and free T4 is controversial, but requires frequent monitoring in pregnancy.

• Treat with thyroxine to maintain TSH in the low–normal range. Most pregnant women will increase their thyroxine dose to approximately 50% of preconception dose. In the postpartum, thyroxine requirements decrease.

Congenital hypothyroidism

Incidence. It occurs in 1 in 4000 live births.

It constitutes part of the neonatal screening test.

Hyperthyroidism

Incidence. It affects 2 in 1000 pregnancies.

Causes

• Graves’ disease (the commonest cause in pregnancy)
• gestational trophoblastic disease
• toxic nodular goitre
• Hashimoto’s disease
• subacute thyroiditis
• rare: hyperemesis gravidarum, hydatidiform mole, struma ovarii

Effects on pregnancy

There is an increase in low birthweight infants and a small rise in the neonatal mortality rate.

Graves’ disease

This is caused by thyroid hyperactivity due to TSH receptor-stimulating antibody.

Maternal effects during pregnancy

• In 80% of cases, the woman remains euthyroid throughout pregnancy.
• Episodes of thyrotoxicosis can occur in the first trimester and postpartum, and treatment is required during these times.
• In 20% of cases, thyrotoxicosis remains stable during pregnancy and requires treatment throughout.

Fetal/neonatal effects

• Fetal thyrotoxicosis may occur, as the antibody readily crosses the placenta.
• Goitre may be seen on ultrasound. Fetal blood sampling can be performed.
• Even after treatment of the mother with thyroidectomy, there may be persisting antibodies.
• There is an increased risk of intrauterine growth restriction (IUGR) and premature labour.
• Fetuses at risk can be evaluated by assessment of maternal antibody concentrations and fetal heart rate. Fetal tachycardia begins from about 25 weeks gestation.
• Neonatal Graves’ disease is seen in 10%–20% of neonates of mothers with Graves’ disease. These babies suffer from tachycardia, poor weight gain and accelerated bone ossification.

Management of thyrotoxicosis in pregnancy

Failure to treat is associated with an increased risk of pre-eclampsia, premature labour, thyroid storm, congestive cardiac failure and perinatal mortality. The aim is to achieve the euthyroid state as early as possible (i.e. preconception) to minimise risks. The symptomatic woman requires treatment throughout pregnancy.

Investigations

Investigations include increased serum free T4 and decreased TSH.

Medical management

• Propranolol is used in acute events. The small risk of IUGR is outweighed by control of maternal tachycardia, tremor and anxiety.
• Both propylthiouracil (PTU) and carbimazole cross the placenta and there is no difference in placental transfer or teratogenicity of either. Both these drugs block thyroid hormone synthesis and produce immunosuppression. PTU is preferable in lactation, with less fetal transfer and is indicated in maternal doses of <150 mg a day. The fetal risks of both drugs are fetal goitre and transient hypothyroidism. Both drugs can cause maternal agranulocytosis.
• If treated with antithyroid drugs, monitor thyroid function tests for fetal status, but the risk is low.
• If treated with surgery or radioiodine therapy, measure TSH receptor antibodies early; if high, then repeat in the last trimester.
• If still under treatment with antithyroid drugs, then repeat TSH receptor antibodies in the last trimester.
• Radioactive iodine is contraindicated in pregnancy.
• Surgical management: if possible, delay this until the second trimester.
• Antenatal management: includes combined management with endocrinology clinic.
• Check thyroid function tests monthly and adjust medications to keep serum T4 at upper limit of normal.
• Fetal monitoring is indicated in the third trimester for assessment of fetal growth and fetal hyperthyroidism.

Labour and delivery

Notify the paediatrician, as the neonate requires monitoring for hyperthyroidism.

Postpartum thyroiditis

Incidence. About 10% of women develop subclinical postpartum thyroiditis.

Clinical presentation

• Symptoms typically develop 1–3 months postpartum.
• It often commences with symptoms of mild hyperthyroidism and then mild hypothyroidism at about 3–6 months postpartum, which then resolves.
• If symptoms persist, Hashimoto’s thyroiditis is likely.

Aetiology

• Thyroiditis is associated with microsomal antibodies in 50%–80% of cases.
• It is considered an autoimmune disorder, with 20%–25% of women having a first-degree relative with autoimmune disease.
• Type 1 diabetics have a three-fold risk.

Recurrence

There is a 10% recurrence risk in future pregnancies.

Further reading

American Endocrine Society. Clinical guidelines: management of thyroid dysfunction during pregnancy and the postpartum. Chevy Chase: American Endocrine Society. 2007.

Hall R., Richards O., Lazarus J.H. The thyroid and pregnancy. British Journal of Obstetrics and Gynaecology. 1993;100:512-515.

Lazarus J.H., Kokandi A. Thyroid disease in relation to pregnancy: a decade of change. Clinical Endocrinology. 2000;53:265-278.

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