Dysfunction to diagnose because its symptoms appear 1 to 8 months postpartum and are often confused with postpartum depression and difficulties adjusting to the demands of the neonate and infant. Postpartum thyroiditis appears to be caused by the combination of a rebounding immune system in the postpartum state and the presence of thyroid autoantibodies. Histologically,
Table 31.15 Guidelines for TSHRAb Testing During Pregnancy with Previously Treated Graves Disease 1. In the woman with antecedent Graves disease in remission after ATD treatment, the risk for fetal–neonatal hyperthyroidism is negligible, and systematic measurement of TSHRAb is not necessary. Thyroid function should be evaluated during pregnancy to detect an unlikely but possible recurrence. In that case, TSHRAb assay is mandatory.
2. In the woman with antecedent Graves disease previously treated with radioiodine or thyroidectomy and regardless of the current thyroid status (euthyroidism with or without thyroxine substitution), TSHRAb should be measured early in pregnancy to evaluate the risk for fetal hyperthyroidism. If the TSHRAb level is high, careful monitoring of the fetus is mandatory for the early detection of signs of thyroid overstimulation (tachycardia, impaired growth rate, oligohydramnios, goiter). Cardiac echography and measurement of circulatory velocity may be confirmatory. Ultrasonographic measurements of the fetal thyroid have been defined from 20 weeks gestational age but require a well-trained operator, and thyroid visibility may be hindered because of fetal head position. Color Doppler ultrasonography is helpful in evaluating thyroid hypervascularization. Because of the potential risks of fetal-neonatal hyperthyroid cardiac insufficiency and the inability to measure the degree of hyperthyroidism in the mother because of previous thyroid ablation, it may be appropriate to consider direct diagnosis in the fetus. Fetal blood sampling through cordocentesis is feasible as early as 25 to 27 weeks gestation with less than 1% adverse effects (fetal bleeding, bradycardia, infection, spontaneous abortion, in utero death) when performed by experienced clinicians. ATD administration to the mother may be considered to treat the fetal hyperthyroidism.
3. In the woman with concurrent hyperthyroid Graves disease, regardless of whether it has preceded the onset of pregnancy, ATD treatment should be monitored and adjusted to keep free T4 in the high-normal range to prevent fetal hypothyroidism and minimize toxicity associated with higher doses of these medications. TSHR-Ab should be measured at the beginning of the last trimester, especially if the required ATD dosage is high. If the TSHRAb assay is negative or the level low, fetal–neonatal hyperthyroidism is rare. If antibody levels are high (TBII ≥40 U/L or TSAb ≥300%), evaluation of the fetus for hyperthyroidism is required. In this condition, there is usually a fair correlation between maternal and fetal thyroid function such that monitoring the ATD dosage according to the mother’s thyroid status is appropriate for the fetus. In some cases in which a high dose of ATD >20 mg/d of methimazole or >300 mg/d of propylthiouracil [PTU]) is necessary, there is a risk of goitrous hypothyroidism in the fetus, which might be indistinguishable from goitrous Graves disease. The correct diagnosis relies on the assay of fetal thyroid hormones and TSH, which allows for optimal treatment.
4. In any woman who has previously given birth to a newborn with hyperthyroidism, a TSHR-Ab assay should be performed early in the course of pregnancy.
TSHRAb, thyroid-stimulating hormone receptor antibodies; ATD, autoimmune thyroid disease; T4, thyroxine; TBII, TSH-binding inhibitory immunoglobulin; TSAb, thyroid-stimulating antibody.