P14.25: Perinatal outcome of prenatally diagnosed congenital cystic adenomatoid malformation

Graves’disease is the most common cause of hyperthyroidism in pregnancy and may cause fetal and neonatal thyroid dysfunction. A case of maternal Graves’disease treated with propylthiouracil (PTU) is presented and prenatal detection and management of fetal goiter are discussed. A 30-year-old-woman, gravida 3, para 2, with Graves’disease was treated with 300 mg/day PTU. Maternal serum concentration of free thyroxine (FT4) was 0.9 ηg/dL (normal 0.6–1.54), thyroidstimulating hormone (TSH) 2.28 mU/L (normal 0.5–4.2) and TSH-receptor autoantibody (TRAb) 14% (normal less than 12%). Fetal thyroid enlargement was noted by sonography at 25 weeks’ gestation. Cordocentesis was performed to assess fetal thyroid function. The fetal serum FT4 was 0.9 ηg/dL (normal 2.3–2.7) and TSH was 98.65 mU/L (normal 8.7–10.5) indicating hypothyroidism. PTU was decreased to 150 mg/day and the fetus was treated with injection of L-thyroxine (250 μg) into amniotic fluid at 32 and 35 weeks’ gestation. The patient remained euthyroid and serial ultrasound scans showed a shrinking of the fetal goiter. Spontaneous onset of labor occurred at 39 weeks’ gestation. The male neonate weighed 2630 g with no discernible thyroid enlargement. The thyroid function tests at birth and on 16th day of life showed euthyroid status. Maternal antithyroid antibodies in patients with Graves’disease, known as THS-receptor autoantibodies (TRAb), can result in stimulation or inhibition of fetal thyroid gland. PTU treatment of Graves’disease in pregnancy may be associated with neonatal goitrous hypothyroidism whereas transplacental passage of stimulating immunoglobulin may cause fetal goiter with hyperthyroidism. Therefore, when fetal goiter is detected, cordocentesis should be offered to assess fetal thyroid function. In cases of fetal hypothyroidism, intra-amniotic injection of thyroxine has shown to be effective in raising serum levels of thyroxine, reducing those of TSH and decreasing the size of goiter.