Pregnancy can cause hyperthyroidism, an overactive thyroid condition where the gland produces excessive thyroxine (T4) and triiodothyronine (T3). This excess hormone production results either from a temporary, pregnancy-specific change or from the exacerbation of an underlying chronic disorder. Distinguishing between these two causes is important for proper management and ensuring the health of both the mother and the fetus.
Hormonal Causes: Gestational Transient Thyrotoxicosis
The most direct link between pregnancy and an overactive thyroid is Gestational Transient Thyrotoxicosis (GTT). This temporary condition occurs because the pregnancy hormone human Chorionic Gonadotropin (hCG) shares a structural similarity with Thyroid Stimulating Hormone (TSH). This allows hCG to weakly bind to and activate the thyroid’s TSH receptors.
High circulating levels of hCG, which naturally peak around the tenth week of pregnancy, temporarily stimulate the thyroid gland to produce more T4 and T3. This stimulation causes a mild, transient form of hyperthyroidism characterized by suppressed TSH levels and slightly elevated free T4. GTT is more common in women experiencing severe morning sickness (hyperemesis gravidarum) or those carrying multiples due to higher hCG levels.
GTT typically resolves spontaneously without specific antithyroid medication once hCG levels decline, usually by the end of the first trimester. Monitoring thyroid function tests is the recommended approach, as this is a physiological response to pregnancy hormones rather than a true thyroid disease.
Differentiating True Disease: Symptoms and Diagnosis
Differentiating GTT from a chronic condition, primarily Graves’ disease, is challenging because hyperthyroidism symptoms often overlap with normal physiological changes of pregnancy. Common hyperthyroid symptoms include heat intolerance, rapid heartbeat (tachycardia), anxiety, and fatigue. However, signs like a visibly enlarged thyroid (goiter) or eye changes suggest a chronic underlying cause.
Diagnosis relies on specialized Thyroid Function Tests (TFTs), specifically measuring TSH and free T4 levels. In hyperthyroidism, the pituitary gland reduces its TSH output, resulting in a TSH level below the normal range, accompanied by an elevated free T4. Interpreting these tests requires using trimester-specific reference ranges due to the effects of pregnancy hormones like estrogen.
Graves’ disease accounts for up to 95% of sustained hyperthyroidism in pregnancy. The definitive way to confirm this autoimmune condition is through a blood test for TSH receptor antibodies (TRAb). Since TRAb mimics TSH and continuously stimulates the thyroid, its presence confirms chronic hyperthyroidism requiring medical intervention, while an undetectable level suggests GTT.
Potential Risks for Mother and Fetus
Uncontrolled hyperthyroidism, particularly Graves’ disease, poses serious risks to both the mother and the fetus. For the mother, complications include an increased risk of preeclampsia (high blood pressure and organ damage after 20 weeks of gestation) and maternal heart failure. Untreated hyperthyroidism can also precipitate thyroid storm, a severe medical emergency involving an extreme exaggeration of hyperthyroid symptoms that can be life-threatening.
For the fetus, maternal hyperthyroidism increases the likelihood of adverse outcomes, including preterm birth, low birth weight, and fetal growth restriction. A unique fetal risk is fetal or neonatal hyperthyroidism. This occurs when the mother’s TRAb antibodies cross the placenta and stimulate the baby’s thyroid gland.
Treatment and Management Strategies
The management approach is determined by the cause and severity of the hyperthyroidism. If Gestational Transient Thyrotoxicosis is diagnosed, antithyroid medication is rarely needed since the condition is temporary and mild. Treatment involves careful monitoring of thyroid hormone levels until they normalize, often with symptomatic relief for severe nausea or vomiting.
For true hyperthyroidism caused by Graves’ disease, antithyroid drugs (Thionamides) are necessary to control hormone production and prevent complications. Propylthiouracil (PTU) is the preferred medication during the first trimester due to a lower risk of birth defects compared to Methimazole (MMI).
However, PTU carries a rare risk of liver toxicity, so guidelines recommend switching to MMI starting in the second trimester. The goal of treatment is to maintain the mother’s free T4 level in the upper portion of the pregnancy-specific normal range using the lowest effective dose. This careful dosing is important because both PTU and MMI cross the placenta and can cause fetal hypothyroidism if the dose is too high. Management requires frequent monitoring and close coordination between an endocrinologist and the obstetric care team.