Fetal Goiter was Resolved with Decreasing Maternal Propylthiouracil Dose Maternal Propiltiyourasil Dozunun Azaltılması ile Kaybolan Fetal Guatr

Fetal goiter is an uncommon, serious problem during pregnancy. Careful routine antenatal ultrasound screening can find out an intrauterine fetal goiter. Fetal goiter has an incidence of 1:40000 live births (1). 80% of cases are caused by dysgenesis of the thyroid gland. The rest 5% and 15% are due to hypothalamohypophyseal abnormalities and dyshormonogenesis, respectively. 8% of cases are due to hyperthyroid pregnant on antithyroid medication (2). The anti-thyroid antibody types and the medication status of the patient may cause hyper, hypo or euthyroid fetuses. Untreated intrauterine hypothyroidism may predispose to motor or cognitive deficits, or impaired intellectual development. A large mass on the anterior neck may lead to extension of fetal head and malpresentation (3). Our study reports a case of fetal goiter successfully treated with incrementally decreasing dose of maternal propylthiouracil (PTU). Maternal thyroid hormone-stimulating antibodies can stimulate a fetal thyroid to result in a goitrous hyperthyroidism. Fetal tachycardia and subsequent fetal hydrops may develop after fetal hyperthyroidism. Elevated maternal anti-thyroid peroxidase (antiTPO) and anti-thyroglobulin titers may give rise to suppression of thyroid hormone synthesis in the fetus. Furthermore, maternal antithyroid therapy may inhibit fetal thyroid peroxidase (2). Fetal hypothyroidism may lead to subsequent neurological impairment. The fetus may be hypothyroid, hyperthyroid or euthyroid when the fetal goiter is detected on the examination. Therefore, the evolution of fetal thyroid hormone levels is essential to decide whether to start early treatment (4). Especially when fetal goiter is diagnosed, serial amniocentesis should be done to check thyroid stimulating hormone (TSH) levels in the amniotic fluid reflecting fetal thyroid metabolism (5). Alternatively, cordocentesis, as the gold standard for the diagnosis, may be done for the assessment of the fetal thyroid hormone status (6). We report a case of fetal goiter diagnosed by detailed ultrasonography. A 33-year-old woman at twenty weeks of gestation was referred to our hospital for detailed ultrasonography. A fetal goiter was identified. She was receiving propylthiouracil (PTU) 100 mg daily for Graves’ disease. Amniocentesis was performed and fetal thyroid function was evaluated as normal. Her recent thyroid function tests were normal, but antithyroid antibodies were positive. The dose of PTU was reduced to 50 mg. However, at twenty six weeks of gestation, maternal thyroid-related autoantibodies became undetectable. A fetal magnetic resonance imaging demonstrated a slight shrinkage of the fetal goiter at 30 weeks. The fetus was delivered vaginally. Thyroid function tests of the neonate were normal, and neonatal goiter was nonpalpable. Fetal goiter is a rare disease. It can be spontaneously resolved by decreasing the maternal dose of PTU.