Diagnosis and Successful in utero Treatment of a Fetal Goitrous Hyperthyroidism Caused by Maternal Graves′ Disease

Heckel, S.; Favre, R.; Schlienger, J.-L.; Soskin, P.

doi:10.1159/000264428

Cited by 23 publications

(14 citation statements)

References 20 publications

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“…Ma- fetal therapy, thyroid hormone replacement is needed. Although intrauterine treatment for fetal thyrotoxicosis has been reported in the literature [3][4][5][6][7][8][9][10][11] , it occurs in only a limited number of cases. Therefore, we report this experience to add the number of cases to the existing body of knowledge.…”

Section: Introductionmentioning

confidence: 99%

Fetal Therapy in Fetal Thyrotoxicosis: A Case Report

Srisupundit

Sirichotiyakul²,

Tongprasert³

et al. 2007

Fetal Diagn Ther

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Introduction: Fetal thyrotoxicosis, often caused by maternal Grave’s disease, can have adverse effects on fetal outcomes, such as growth impairment or fetal hydrops. Therefore, intrauterine treatment is recommended. Objective: To describe the experience of intrauterine medical treatment of fetal thyrotoxicosis. Case: A 19-year-old woman with a history of Grave’s disease in a euthyroid clinical status after subtotal thyroidectomy became pregnant 2 months after thyroidectomy. At gestational age 28 weeks, persistent fetal tachycardia was identified and the diagnosis of fetal thyrotoxicosis was established by fetal thyroid function test on umbilical cord blood obtained by cordocentesis. Intrauterine treatment for hyperthyroidism was initiated with antithyroid drugs (150 mg/day of propylthiouracil) via maternal oral administration. Fetal heart rate, size of fetal thyroid gland and umbilical cord blood sampling for thyroid function test were monitored. Fetal heart rate became normal and fetal thyroid function tested on fetal cord blood at 1 month after antithyroid fetal therapy was also normal. Fetal thyrotoxicosis improved but the mother had some degree of hypothyroidism from fetal therapy and needed thyroid hormone replacement. The remaining course of gestation was uneventful. The patient had spontaneous labor and delivery at 38 weeks of gestation resulting in normal female baby, 2,900 g, and had no clinical of neonatal thyrotoxicosis. Maternal thyroid medications were stopped immediately after birth. Conclusion: Intrauterine treatment of fetal thyrotoxicosis with medication via the maternal circulation can possibly improve fetal outcome.

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Section: Introductionmentioning

confidence: 99%

Fetal Therapy in Fetal Thyrotoxicosis: A Case Report

Srisupundit

Sirichotiyakul²,

Tongprasert³

et al. 2007

Fetal Diagn Ther

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“…However, a woman who has been successfully treated for Graves’ disease with thyroid ablation or surgery can still transfer thyroid-stimulating antibodies to the fetus. In the absence of maternal antithyroid medication, these TSIs can cause fetal hyperthyroidism with persistent fetal tachycardia, goiter, growth restriction, or hydrops (Heckel et al ., 1997; Srisupundit et al ., 2008; Ting et al ., 1999). …”

Section: Treatment For Fetal Thyroid Disordersmentioning

confidence: 99%

Prenatal pharmacotherapy for fetal anomalies: a 2011 update

Hui

Bianchi

2011

Prenatal Diagnosis

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Fetal therapy can be defined as any prenatal treatment administered to the mother with the primary indication to improve perinatal or long-term outcomes for the fetus or newborn. This review provides an update of the pharmacological therapies that are solely directed at the fetus with anomalies and outlines a future transcriptomic approach. Fetal anomalies targeted with prenatal pharmacotherapy are a heterogeneous group of structural, endocrine, and metabolic conditions, including congenital cystic adenomatoid malformation (CCAM), congenital adrenal hyperplasia, congenital heart block, fetal tachyarrhythmias, inborn errors of metabolism, fetal thyroid disorders, and polyhydramnios. To date, the majority of pharmacotherapies for fetal anomalies have been evaluated only in retrospective, uncontrolled studies. The way forward will be with an evidence-based approach to prenatal pharmacological interventions.

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“…Fetal goiters can be associated with both fetal hyperthyroidism and hypothyroidism. Our search of the literature found a total of 39 cases of fetal goiter [12][13][14][15][16][17][18][19][20][21][22][23][24][25], which we classified into three patterns regarding the relation to maternal-fetal thyroid function (Table 1). The first pattern is maternal hyperthyroidism and fetal goitrous hypothyroidism influenced by the excessive placental transfer of maternal antithyroid drugs.…”

Section: Case Reportmentioning

confidence: 99%

Fetal Goitrous Hypothyroidism due to Maternal Thyroid Stimulation-Blocking Antibody: A Case Report

Ohira

Miyake²,

Kobara³

et al. 2010

Fetal Diagn Ther

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Most fetal goitrous hypothyroidisms are reportedly caused by the maternal use of an antithyroid drug or fetal dyshormonogenesis. However, fetal goitrous hypothyroidism due to the transplacental passage of maternal thyroid stimulation-blocking antibody (TSBAb) is extremely rare. A woman at 28 weeks of gestation was found to have a fetal goiter by ultrasonography. Because the maternal serum showed hypothyroidism with an elevated titer of TSBAb, levothyroxine sodium was administered. The patient delivered a male infant, 3,412 g, with a goiter at term. Umbilical blood revealed primary hypothyroidism with increased TSBAb, and the infant was given levothyroxine sodium. After a month, neonatal thyroid function and TSBAb levels became normal. Attention should be paid to possible fetal hypothyroidism when a fetal goiter is observed to avoid impaired mental development of the neonate.

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Diagnosis and Successful in utero Treatment of a Fetal Goitrous Hyperthyroidism Caused by Maternal Graves′ Disease

Cited by 23 publications

References 20 publications

Fetal Therapy in Fetal Thyrotoxicosis: A Case Report

Fetal Therapy in Fetal Thyrotoxicosis: A Case Report

Prenatal pharmacotherapy for fetal anomalies: a 2011 update

Fetal Goitrous Hypothyroidism due to Maternal Thyroid Stimulation-Blocking Antibody: A Case Report

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