Managing Graves' Disease during Pregnancy


© Elaine Moore
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Patients with Graves’ disease have special concerns during pregnancy. For this reason, many doctors in the past have recommended that their patients have radioiodine ablation or surgery before becoming pregnant. With recent knowledge into the autoimmune nature of GD, it appears that this may not necessarily be the best solution for fetal health.

Patients who have become euthyroid or hypothyroid after these treatments are likely to still have high levels of thyroid antibodies, whereas patients who are treated with antithyroid drugs generally experience a significant reduction in their levels of thyroid antibodies.

These antibodies may cross the placental membrane causing transient hyperthyroidism or hypothyroidism in the fetus, depending on the type of antibody present. In patients who are considered “cured” fetal thyroid status is seldom assessed. Endocrinologists familiar with this problem recommend that these patients, especially those who have been treated with radioiodine in the past, have their thyroid antibody titers checked. They also recommend that the fetus be monitored for signs of thyroid dysfunction or goiter.

One type of thyroid antibody, the thyroid peroxidase (TPO) antibody is associated with spontaneous abortion or miscarriage. Stimulating TSH receptor antibodies (also known as thyroid stimulating immunoglobulins or TSI) cause transient hyperthyroidism in the fetus and newborn, and blocking TSH receptor antibodies cause transient hypothyroidism.

Today, physicians are more likely to recommend antithyroid drugs (ATD’s) for their patients who plan to become pregnant in the future. Dr. Gregory Becks from St. Joseph’s Health Center in Ontario writes that it is essential to control the hyperthyroid state before proceeding with pregnancy. While surgery and radioiodine generally work quicker, 40% of patients treated with radioiodine end up having more than one treatment, generally several months after the first. Although ATD’s take longer to achieve remission, most patients on ATD’s become euthyroid within the first 6 weeks of therapy.

In the first trimester of pregnancy, many Graves’ patients experience a slight exacerbation or worsening of symptoms. This is primarily due to estrogen influences and the thyroid stimulating influences of beta-HCG, a hormone that increases in the first trimesters. Even normal pregnant patients experience slight hyperthyroid symptoms, including palpitations, increased metabolic rate, shortness of breath and increased body temperature. The thyroid gland often increases in size during pregnancy in its efforts to trap more iodine. Although the fetus has its own functioning thyroid by about 10-12 weeks gestation, it relies on the maternal circulation for its iodine requirements.

By the last trimester, these symptoms generally resolve and any symptoms of hyperthyroidism resolve. In fact, patients on ATD’s generally need to have their dosages reduced at this time, and hypothyroid patients usually need an increased dose of replacement thyroid hormone.

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