Fetal therapy in fetal thyrotoxicosis: A case report

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 feta...

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Main Authors: Srisupundit K., Sirichotiyakul S., Tongprasert F., Luewan S., Tongsong T.
Format: Article
Language:English
Published: 2014
Online Access:http://www.scopus.com/inward/record.url?eid=2-s2.0-40049093261&partnerID=40&md5=32afce2568ffb3ceee9876bc08c72151
http://www.ncbi.nlm.nih.gov/pubmed/18033967
http://cmuir.cmu.ac.th/handle/6653943832/2483
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Institution: Chiang Mai University
Language: English
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spelling th-cmuir.6653943832-24832014-08-30T02:00:54Z Fetal therapy in fetal thyrotoxicosis: A case report Srisupundit K. Sirichotiyakul S. Tongprasert F. Luewan S. Tongsong T. 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. Copyright © 2007 S. Karger AG. 2014-08-30T02:00:54Z 2014-08-30T02:00:54Z 2008 Article 10153837 10.1159/000111589 18033967 FDTHE http://www.scopus.com/inward/record.url?eid=2-s2.0-40049093261&partnerID=40&md5=32afce2568ffb3ceee9876bc08c72151 http://www.ncbi.nlm.nih.gov/pubmed/18033967 http://cmuir.cmu.ac.th/handle/6653943832/2483 English
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
language English
description 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. Copyright © 2007 S. Karger AG.
format Article
author Srisupundit K.
Sirichotiyakul S.
Tongprasert F.
Luewan S.
Tongsong T.
spellingShingle Srisupundit K.
Sirichotiyakul S.
Tongprasert F.
Luewan S.
Tongsong T.
Fetal therapy in fetal thyrotoxicosis: A case report
author_facet Srisupundit K.
Sirichotiyakul S.
Tongprasert F.
Luewan S.
Tongsong T.
author_sort Srisupundit K.
title Fetal therapy in fetal thyrotoxicosis: A case report
title_short Fetal therapy in fetal thyrotoxicosis: A case report
title_full Fetal therapy in fetal thyrotoxicosis: A case report
title_fullStr Fetal therapy in fetal thyrotoxicosis: A case report
title_full_unstemmed Fetal therapy in fetal thyrotoxicosis: A case report
title_sort fetal therapy in fetal thyrotoxicosis: a case report
publishDate 2014
url http://www.scopus.com/inward/record.url?eid=2-s2.0-40049093261&partnerID=40&md5=32afce2568ffb3ceee9876bc08c72151
http://www.ncbi.nlm.nih.gov/pubmed/18033967
http://cmuir.cmu.ac.th/handle/6653943832/2483
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