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Isolation of Leukocytes from the Murine Tissues at the Maternal-Fetal Interface
Published on: May 21, 2015
Fetal hyperthyroidism associated with maternal thyroid autoantibodies: A case report
Paraskevi Kazakou1, Marianna Theodora2, Christina Kanaka-Gantenbein3
1Department of Endocrinology and Diabetes, "Alexandra" Hospital, Athens, Greece.
A 33-year-old Caucasian woman was referred at 24 + 3 weeks of gestation due to fetal tachycardia and hydrops. She had an uncomplicated pregnancy 16 years previously and was on levothyroxine after total thyroidectomy for Graves' disease 6 years previously, when she developed moderate exophthalmos. Laboratory evaluation revealed appropriate thyroid function for this time of gestation: thyroid stimulating hormone (TSH) 1.7 μU/ml (1-3), fT4 18.53 pmol/l (12-22), with positive antibodies: anti-TPO 157 U/ml (<35), TSH receptor antibodies (TRAb) 171.95 U/l (<1.75). The diagnosis was fetal hyperthyroidism due to transplacental passage of stimulating maternal TRAb. Methimazole and digoxin were initiated. The patient remained euthyroid, with fT4 levels in the upper normal range. The fetus showed intrauterine growth retardation, oligohydramnios, aggravating hydrops, goiter with increased central vascularization and improved heart rate without signs of cardiac failure. At 30 + 3 weeks a hydropic hyperthyroid male newborn (birthweight 1560 g) was delivered by cesarean section and admitted to the neonatal intensive care unit. Cord serum showed neonatal hyperthyroidism. Methimazole and propranolol were administered to the newborn. On the 5th postnatal day the infant died because of severe infection inducing respiratory dysfunction, hemodynamic deterioration and cardiac asystole. Graves' disease occurs in about 0.2% of pregnancies. Hyperthyroidism occurs in 1-5% of neonates born to mothers with Graves' disease and the risk correlates with the maternal TRAb titer. Early diagnosis and treatment are crucial not only in pregnant women with active disease, but also in mothers with a history of Graves' disease, even after definitive treatment such as thyroidectomy or ablative therapy.
A 33-year-old Caucasian woman was referred at 24 + 3 weeks of gestation due to fetal tachycardia and hydrops. She had an uncomplicated pregnancy 16 years previously and was on levothyroxine after total thyroidectomy for Graves' disease 6 years previously, when she developed moderate exophthalmos. Laboratory evaluation revealed appropriate thyroid function for this time of gestation: thyroid stimulating hormone (TSH) 1.7 μU/ml (1-3), fT4 18.53 pmol/l (12-22), with positive antibodies: anti-TPO 157 U/ml (<35), TSH receptor antibodies (TRAb) 171.95 U/l (<1.75). The diagnosis was fetal hyperthyroidism due to transplacental passage of stimulating maternal TRAb. Methimazole and digoxin were initiated. The patient remained euthyroid, with fT4 levels in the upper normal range. The fetus showed intrauterine growth retardation, oligohydramnios, aggravating hydrops, goiter with increased central vascularization and improved heart rate without signs of cardiac failure. At 30 + 3 weeks a hydropic hyperthyroid male newborn (birthweight 1560 g) was delivered by cesarean section and admitted to the neonatal intensive care unit. Cord serum showed neonatal hyperthyroidism. Methimazole and propranolol were administered to the newborn. On the 5th postnatal day the infant died because of severe infection inducing respiratory dysfunction, hemodynamic deterioration and cardiac asystole. Graves' disease occurs in about 0.2% of pregnancies. Hyperthyroidism occurs in 1-5% of neonates born to mothers with Graves' disease and the risk correlates with the maternal TRAb titer. Early diagnosis and treatment are crucial not only in pregnant women with active disease, but also in mothers with a history of Graves' disease, even after definitive treatment such as thyroidectomy or ablative therapy.
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