Thyroid disease in pregnancy

Thyroid disease in pregnancy refers to a spectrum of thyroid dysfunctions occurring before or during pregnancy that may affect maternal and fetal outcomes. These include overt hypothyroidism, subclinical hypothyroidism, isolated hypothyroxinaemia, gestational transient thyrotoxicosis and other forms of thyrotoxicosis, overt hyperthyroidism, such as Graves disease and toxic nodular hyperthyroidism, and subclinical hyperthyroidism.

Pregnancy induces complex physiological changes in thyroid function to meet the increased metabolic demands of both mother and fetus. Maternal thyroid hormone production rises by approximately 50%, driven by elevated estrogen and hCG levels. Estrogen increases TBG, raising total T4 and T3 concentrations, while hCG transiently stimulates the thyroid, particularly in the first trimester, leading to temporary increases in free T4 and T3 and suppression of TSH. As pregnancy advances, free thyroid hormone levels gradually decline, and TSH levels rise slightly. These shifts require sufficient iodine intake, as pregnancy increases iodine demand due to greater hormone synthesis, enhanced renal clearance, and fetal use. The fetal thyroid begins concentrating iodine at 10-12 weeks and produces its own hormone from 18-22 weeks; however, fetal neurodevelopment during early gestation depends entirely on the transplacental passage of maternal T4. Maternal thyroid volume increases by 10-30% during the third trimester due to expanded extracellular fluid and blood volume. In hypothyroidism, inadequate hormone production may impair placental and fetal development, especially during the first trimester. In hyperthyroidism, commonly caused by Graves disease, excess hormone increases maternal metabolic activity and can adversely affect placental function and fetal outcomes.

Thyroid dysfunction affects approximately 2 to 3 percent of pregnancies, with hypothyroidism being more common than hyperthyroidism. Gestational transient thyrotoxicosis occurs in 1-5% of pregnancies in Europe and is typically benign and self-limiting. Overt hyperthyroidism is less common and most often due to Graves disease, with a prevalence of 0.5-1.3% for pre-existing Graves disease, 0.05% for new-onset Graves, and 0.1% for toxic nodular disease. Worldwide, iodine deficiency remains the leading cause of preventable neurodevelopmental impairment and is associated with increased risks of goiter, hypothyroidism, miscarriage, and impaired cognitive outcomes. In areas of severe iodine deficiency, thyroid nodules have been reported in up to 30% of pregnant women. In iodine-replete or mildly deficient regions, autoimmune thyroid disease is the most common cause of dysfunction during pregnancy. The prevalence of thyroid autoantibodies in pregnancy ranges from 5-31%, depending on the population studied.

Risk factors include a personal or family history of thyroid disease, autoimmune conditions such as Hashimoto thyroiditis or Graves disease, prior head or neck irradiation, iodine imbalance, and advanced maternal age. Women with T1DM or other autoimmune disorders are at particularly increased risk.

Thyroid disease may be pre-existing or first diagnosed during pregnancy. Hypothyroidism often presents with nonspecific symptoms such as fatigue, weight gain, and cold intolerance, while hyperthyroidism may cause palpitations, heat intolerance, tremors, and weight loss. Uncontrolled hypothyroidism increases the risk of miscarriage, preeclampsia, placental abruption, and impaired fetal neurodevelopment. Uncontrolled hyperthyroidism is associated with fetal loss, low birth weight, and preterm delivery.

With adequate treatment, most individuals with thyroid disease can achieve favorable pregnancy outcomes. However, insufficient control, especially during early gestation, increases the risk of serious maternal and fetal complications. Thyroid function should be closely monitored throughout pregnancy. Ongoing postpartum monitoring is often necessary in individuals with persistent thyroid dysfunction or autoimmune thyroid disease.