Fetal Goitrous Hypothyroidism Research Articles

Conservative Treatment of Fetal Goitrous Hypothyroidism Due to Thyroglobulin Mutations: A Case Report and Literature Review

Abstract With the advances in fetal medicine, there will be more cases of congenital hypothyroidism (CH) diagnosed in the fetal period. However, there is no consensus on the management protocol. We present a successful case of conservatively managed fetal goitrous hypothyroidism due to compound heterozygous TG mutations. Goiter was observed in a fetus at 23 weeks of gestation. Because there was no evidence of transplacental passage of antithyroid antibody and drugs, iodine overload, and iodine deficiency, the fetus was highly suspected to have CH. Considering the potential risks of amniocentesis/cordocentesis, and lack of available parenteral levothyroxine in China, the fetus was closely monitored thereafter. A male neonate was delivered vaginally without complications at 39 weeks of gestation. We verified severe hypothyroidism in the infant and immediately initiated levothyroxine therapy. His growth and mental development were normal at the age of 8 month. Whole-exome sequencing showed that the neonate had two compound heterozygous mutations in the TG gene. We also performed a literature review of the prognosis of postnatal treatment of CH due to TG mutations and the result showed that postnatal treatment of CH due to TG mutations has a favorable prognosis. However, further prospective studies are warranted to verify this conclusion.

Successful intra‐amniotic levothyroxine treatment for fetal goitrous hypothyroidism in a triplet pregnancy

We report an extremely challenging case of fetal goitrous hypothyroidism involving all three fetuses of a triplet pregnancy in which successful fetal treatment led to a favorable pregnancy outcome. The patient had a trichorionic, triamniotic triplet pregnancy and was referred to us at 24 weeks gestation after goiters affecting all three fetuses and polyhydramnios involving two fetuses were noted. Immediately before the conception, she underwent hysterosalpingography with an oil-soluble iodinated contrast medium. After the diagnosis of fetal hypothyroidism was made, intra-amniotic injection of levothyroxine was performed for two fetuses with polyhydramnios 3 times between 28 and 31 weeks gestation. The goiters shrunk and the polyhydramnios improved in response to the in utero treatment. No complications occurred. Cesarean section was performed at 33 weeks gestation. None of the three neonates developed respiratory insufficiency. Our experience suggested that successful intrauterine treatment is possible for fetal goitrous hypothyroidism, even in a triplet pregnancy. The indication, treatment timing, and diagnostic and assessment strategies should be carefully discussed to minimize puncture-related complications.

Antenatal diagnosis and treatment of fetal goitrous hypothyroidism

Fetal goitre secondary to hypothyroidism is the leading cause of intellectual disability. Despite its rarity, many cases of fetal goitre are diagnosed and require prenatal management. We present a comprehensive review about the pre­na­tal diagnosis and treatment of fetal hypo­thy­roid goitre. Fetal thyroid size can be measured by transvaginal ultra­so­no­gra­phy from 14 weeks, and by trans­ab­do­mi­nal ultrasonography from 18 weeks of ges­ta­tion. The size of the fetal thyroid de­pends on ges­ta­tio­nal age. Because fetal goitre can lead to intra­ute­rine, perinatal and obstetrical complications, the op­ti­mal treat­ment is required. Fetal com­pli­cations are: fetal growth res­tric­tion, polyhydramnios, pleural effusion, preterm de­li­ve­ry, craniosynostosis, neuro­developmental disorders and neo­na­tal asphyxia or fetal death. The optimal intraamniotic L-thiroxine treatment did not normalize the thyroid hormonal le­vels, but these infants have normal neuromotor and psy­cho­­emo­­tio­nal development.

Conservative in utero treatment of fetal dyshormonogenetic goiter with levothyroxine, a systematic literature review.

Fetal goitrous hypothyroidism is a rare condition associated with important obstetrical, neonatal complications, and neurodevelopmental impairments. Prenatal treatment remains controversial, and the risk to benefit ratio must be accurately assessed and considered for individualized management. The objective of this review was to evaluate the feasibility, safety, and effectiveness of the conservative in utero treatment of fetal goitrous hypothyroidism. In total, 25 reports that met our inclusion criteria were selected and the management of 38 cases was analyzed. Prenatal diagnosis consisted mainly of ultrasonographic findings. Fetal thyroid status was assessed by cordocentesis. Prenatal treatment varied widely in terms of levothyroxine (LT4) route of administration, dosage, number of injections, and frequency. Although different regimens and routes of administration were proposed, they seem to have similar results regarding fetal goiter reduction and thyroid status at birth. At birth, most babies had hypothyroidism, but the long-term follow-up indicated a normal psycho-neuromotor development. Our data confirm the feasibility of conservative treatment with LT4 for fetal goitrous hypothyroidism. Further studies are needed to determine the optimal management of this disorder.

Prenatal Diagnosis and Management of Fetal Goiter: A Case Series from Tertiary Perinatal Center in South India

ABSTRACTAims and objectivesThe reported incidence of fetal goiter is 1 in 40,000 live births. The effects of fetal goiter and thyroid dysfunction are significant. The objective of our study is to assess the safety, feasibility, and efficacy of intra-amniotic instillation of levothyroxine (LT4) in fetal goitrous hypothyroidism.Materials and methodsA retrospective observational study of prenatally diagnosed cases of fetal goiter on routine antenatal ultrasound between January 2010 and January 2018 at Fernandez Hospital Foundation, Hyderabad, tertiary perinatal referral center. Data retrieved from electronic database.ResultsDuring this period, 9 cases of fetal goiter were diagnosed on routine ultrasonography with the incidence of 1 in 7,000 live births. The gestation age at diagnosis ranged between 21 weeks and 29 weeks (mean 26 weeks). Of the nine fetuses with goiter, two were excluded as one ended in a miscarriage at 22 weeks and the other was terminated elsewhere at 26 weeks. Data were analyzed in the remaining seven fetuses. Cordocentesis was performed in five fetuses and amniocentesis was performed in one woman with dichorionic diamniotic (DCDA) twin gestation which revealed hypothyroid status. Fetal therapy was offered to all the remaining seven fetuses with intra-amniotic instillation of LT4 100 to 200 μg at 2–3 weeks’ interval. First dose of LT4 was given at mean gestation of 27 weeks (range 23–30 weeks), and the mean time between the identification of fetal goiter and the first dose of LT4 was 6 days (range 2–15 days). Number of injections given ranged between 1 and 7. No adverse events were recorded. Follow-up sonogram showed subjective reduction in the goiter size. All the babies had hypothyroidism at birth.ConclusionOur case series confirms the safety and feasibility of intra-amniotic instillation of LT4 for fetal goitrous hypothyroidism. Although fetal therapy has resulted in reduction in the size of the goiter, the thyroid hormone levels at birth were low. Further research is required to establish the proper management guidelines for this disorder.How to cite this articleBudidapadu M, Vavilala S, Kolar G. Prenatal Diagnosis and Management of Fetal Goiter: A Case Series from Tertiary Perinatal Center in South India. Int J Infertil Fetal Med 2019;10(3):37–41.

Intrauterine death following intraamniotic triiodothyronine and thyroxine therapy for fetal goitrous hypothyroidism associated with polyhydramnios and caused by a thyroglobulin mutation.

In the absence of maternal thyroid disease or iodine deficiency, fetal goitre is rare and usually attributable to dyshormonogenesis, for which genetic ascertainment is not always undertaken in the UK. Mechanical complications include tracheal and oesophageal compression with resultant polyhydramnios, malpresentation at delivery and neonatal respiratory distress. We report an Indian kindred in which the proband (first-born son) had congenital hypothyroidism (CH) without obvious neonatal goitre. His mother’s second pregnancy was complicated by fetal hypothyroid goitre and polyhydramnios, prompting amniotic fluid drainage and intraamniotic therapy (with liothyronine, T3 and levothyroxine, T4). Sadly, intrauterine death occurred at 31 weeks. Genetic studies in the proband demonstrated compound heterozygous novel (c.5178delT, p.A1727Hfs*26) and previously described (c.7123G > A, p.G2375R) thyroglobulin (TG) mutations which are the likely cause of fetal goitre in the deceased sibling. TG mutations rarely cause fetal goitre, and management remains controversial due to the potential complications of intrauterine therapy however an amelioration in goitre size may be achieved with intraamniotic T4, and intraamniotic T3/T4 combination has achieved a favourable outcome in one case. A conservative approach, with surveillance, elective delivery and commencement of levothyroxine neonatally may also be justified, although intubation may be required post delivery for respiratory obstruction. Our observations highlight the lethality which may be associated with fetal goitre. Additionally, although this complication may recur in successive pregnancies, our case highlights the possibility of discordance for fetal goitre in siblings harbouring the same dyshormonogenesis-associated genetic mutations. Genetic ascertainment may facilitate prenatal diagnosis and assist management in familial cases.Learning points:CH due to biallelic, loss-of-function TG mutations is well-described and readily treatable in childhood however mechanical complications from associated fetal goitre may include polyhydramnios, neonatal respiratory compromise and neck hyperextension with dystocia complicating delivery.CH due to TG mutations may manifest with variable phenotypes, even within the same kindred.Treatment options for hypothyroid dyshormogenic fetal goitre in a euthyroid mother include intraamniotic thyroid hormone replacement in cases with polyhydramnios or significant tracheal obstruction. Alternatively, cases may be managed conservatively with radiological surveillance, elective delivery and neonatal levothyroxine treatment, although intubation and ventilation may be required to support neonatal respiratory compromise.Genetic ascertainment in such kindreds may enable prenatal diagnosis and anticipatory planning for antenatal management of further affected offspring.

Intrauterine diagnosis and treatment of fetal goitrous hypothyroidism

We present two cases of fetal hypothyroidism with goiter which were successfully diagnosed and treated in utero. In both cases, ultrasonographic examination demonstrated a bilobed solid anterior neck mass with increased vascularity compatible with enlarged thyroid gland. Fetal blood sampling revealed hypothyroidism. Intra-amniotic injection of L-thyroxin caused a reduction in thyroid gland size and enabled vaginal delivery without complication. In the first case, maternal thyroid hormone levels and autoantibodies were normal and the neonate had hypothyroidism suggesting the diagnosis of dyshormonogenesis. In the second case, the fetus had transient hypothyroidism, which resolved spontaneously after delivery. Maternal thyroid function tests and autoantibodies were normal and both the mother and neonate had normal urinary iodine, excluding the diagnosis of iodine deficiency or excess. Thus, we believe that transplacental transfer of undetermined factors might be a cause of transient congenital hypothyroidism. Also, we reviewed the literature and described controversial issues regarding the management of fetal goiter.

In utero treatment of fetal goitrous hypothyroidism in a euthyroid mother: A case report

Fetal goitrous hypothyroidism is a rare condition in euthyroid pregnant women. Complications such as tracheal and esophageal compression with resultant polyhydramnios, as well as the possibility of neurodevelopmental effects of hypothyroidism, have prompted prenatal treatment with intra-amniotic L-thyroxine. We report a case of this condition and its in utero management.

Response: The Benefits of Invasive Treatment of Fetal Goitrous Hypothyroidism in Maternal Graves' Disease

ThyroidVol. 21, No. 8 Letters to the EditorResponse: The Benefits of Invasive Treatment of Fetal Goitrous Hypothyroidism in Maternal Graves' DiseaseSofie Bliddal, Ase K. Rasmussen, Karin Sundberg, Vibeke Brocks, Peter Skovbo, and Ulla Feldt-RasmussenSofie BliddalDepartment of Medical Endocrinology, Copenhagen University Hospital, Copenhagen, Denmark.Search for more papers by this author, Ase K. RasmussenDepartment of Medical Endocrinology, Copenhagen University Hospital, Copenhagen, Denmark.Search for more papers by this author, Karin SundbergDepartment of Fetal Medicine and Ultrasound, Copenhagen University Hospital, Copenhagen, Denmark.Search for more papers by this author, Vibeke BrocksDepartment of Fetal Medicine and Ultrasound, Copenhagen University Hospital, Copenhagen, Denmark.Search for more papers by this author, Peter SkovboDepartment of Gynecology and Obstetrics, Aalborg Hospital, Aalborg, Denmark.Search for more papers by this author, and Ulla Feldt-RasmussenDepartment of Medical Endocrinology, Copenhagen University Hospital, Copenhagen, Denmark.Search for more papers by this authorPublished Online:2 Aug 2011https://doi.org/10.1089/thy.2011.0066.rsAboutSectionsView articleView Full TextPDF/EPUB ToolsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View articleFiguresReferencesRelatedDetails Volume 21Issue 8Aug 2011 InformationCopyright 2011, Mary Ann Liebert, Inc.To cite this article:Sofie Bliddal, Ase K. Rasmussen, Karin Sundberg, Vibeke Brocks, Peter Skovbo, and Ulla Feldt-Rasmussen.Response: The Benefits of Invasive Treatment of Fetal Goitrous Hypothyroidism in Maternal Graves' Disease.Thyroid.Aug 2011.932-933.http://doi.org/10.1089/thy.2011.0066.rsPublished in Volume: 21 Issue 8: August 2, 2011Online Ahead of Print:July 11, 2011PDF download

Antithyroid drug-induced fetal goitrous hypothyroidism

Maternal overtreatment with antithyroid drugs can induce fetal goitrous hypothyroidism. This condition can have a critical effect on pregnancy outcome, as well as on fetal growth and neurological development. The purpose of this Review is to clarify if and how fetal goitrous hypothyroidism can be prevented, and how to react when prevention has failed. Understanding the importance of pregnancy-related changes in maternal thyroid status when treating a pregnant woman is crucial to preventing fetal goitrous hypothyroidism. Maternal levels of free T(4) are the most consistent indication of maternal and fetal thyroid status. In patients with fetal goitrous hypothyroidism, intra-amniotic levothyroxine injections improve fetal outcome. The best way to avoid maternal overtreatment with antithyroid drugs is to monitor closely the maternal thyroid status, especially estimates of free T(4) levels.

Antenatal diagnosis and treatment of a case of fetal goitrous hypothyroidism

Antenatal diagnosis and treatment of a case of fetal goitrous hypothyroidism

Graves' Disease in Two Pregnancies Complicated by Fetal Goitrous Hypothyroidism: Successful In Utero Treatment with Levothyroxine

Treatment of Graves' disease during pregnancy with antithyroid drugs (ATDs) poses a risk of inducing hypothyroidism and, thus, development of a goiter to the fetus. We report two patients referred to our department after discovery of a fetal goiter by ultrasound examination in the second trimester of pregnancy. The women receiving 400 mg/day propylthiouracil and 10 mg/day thiamizole, respectively, had thyrotropin and total thyroxine values within the normal reference range but a lowered free thyroxine level. Fetal blood sampling by cordocentesis revealed severe fetal hypothyroidism as the cause of goiter development. Reduction of maternal ATD dose and injection of levothyroxine intra-amniotically quickly reduced the goiter size, and both babies were born euthyroid and without goiters. Two pregnant women with Graves' disease were overtreated with ATDs inducing iatrogenic goiter in the fetuses. Successful treatment with intra-amniotic levothyroxine injections rendered the babies euthyroid and nongoitrous at birth. Correct interpretation of thyroid function tests during pregnancy in general--and during ATD therapy of Graves' disease in particular--is difficult. Awareness of pregnancy-related changes in maternal thyroid status, and a close teamwork among endocrinologists, obstetricians, and experts in fetal medicine, is pivotal in ensuring normal growth and development of the unborn child of these patients.

Use of 3-Dimensional Sonography for Prenatal Evaluation and Follow-up of Fetal Goitrous Hypothyroidism

Fetal goitrous hypothyroidism is a rare and potentially lethal condition. Consequently, its early diagnosis and treatment improve prognosis. Thyroid hormone measurement in either fetal serum or amniotic fluid implies important risks. Here we present a fetal goiter and the follow-up procedure, both done by the traditional method and by using 3-dimensional power Doppler (3DPD) imaging and virtual organ computer-aided analysis (VOCAL). A single well-documented case of fetal goiter was followed weekly from 22 weeks until delivery. Amniocentesis for thyrotropin (TSH) and free thyroxine (T(4)) measurement as well as levothyroxine injections were performed at every control. In addition to amniocentesis, every control involved a sonographic evaluation, which included standard measurements of the gland and the capture of volume image sets in gray scale and 3DPD. Volume calculation of the gland was done using VOCAL software. Vascularization of the gland was evaluated by the vascularization index (VI) included in the software. With treatment, TSH levels decreased progressively until normalization. Free T(4) levels increased toward the end of gestation. Sonographic measurements of the gland volume to estimated fetal weight ratio decreased across treatment as levels of TSH did. The VI clearly depicted the vascular regression of the goiter, decreasing throughout treatment in a consistent way until 24 hours before delivery. Gray scale and 3DPD evaluations of the thyroid gland have been validated under similar circumstances and might be reliable complements to the invasive methods used in the management of this fetal condition.

Intrauterine diagnosis and management of fetal goiter: A case report

Fetal goiter can be the result of maternal hyperthyroidism treated with antithyroid drugs. Polyhydramnios may be the presenting symptom and can be diagnosed prenatally by sonography. We report a case of fetal goiter diagnosed at 30 weeks of gestation and fetal hypothyroidism confirmed by cordocentesis. Intra-amniotic levothyroxine was administered. Onset of preterm labor could not be prevented. The risks and benefits of intrauterine treatment of fetal goitrous hypothyroidism are discussed.

Treatment of fetal goitrous hypothyroidism: value of direct intramuscular L‐thyroxine therapy

Treatment of fetal goitrous hypothyroidism: value of direct intramuscular L‐thyroxine therapy

Experience with Intraamniotic Thyroxine Treatment in Nonimmune Fetal Goitrous Hypothyroidism in 12 Cases

Experience with Intraamniotic Thyroxine Treatment in Nonimmune Fetal Goitrous Hypothyroidism in 12 Cases

Experience with Intraamniotic Thyroxine Treatment in Nonimmune Fetal Goitrous Hypothyroidism in 12 Cases

Nonimmune fetal goitrous hypothyroidism is a rare condition that can induce obstetrical and/or neonatal complications and neurodevelopmental impairments such as those still seen in some patients with congenital hypothyroidism. Prenatal treatment to prevent these adverse outcomes is appealing, but experience is limited and the risk to benefit ratio controversial. The objective of the study was to evaluate the feasibility, safety, and effectiveness of intrauterine l-thyroxine treatment in a large cohort with nonimmune fetal goitrous hypothyroidism. This was a retrospective study of 12 prenatally treated fetuses diagnosed between 1991 and 2005 in France. During pregnancy, goiter size and thyroid hormone levels were compared before and after prenatal treatment. At birth, clinical, laboratory, and ultrasound data were evaluated. Prenatal treatment varied widely in terms of l-thyroxine dosage (200-800 microg/injection), number of injections (one to six), and frequency (every 1-4 wk). No adverse events were recorded. During pregnancy, thyroid size decreased in eight of nine cases and amniotic-fluid TSH levels decreased in the six investigated cases, returning to normal in four. However, at birth, all babies had hypothyroidism, indicating that intraamniotic TSH levels did not reliably reflect fetal thyroid function. Our data confirm the feasibility and safety of intraamniotic l-thyroxine treatment for nonimmune fetal goitrous hypothyroidism. Although goiter size reduction is usually obtained, thyroid hormone status remains deficient at birth. Amniocentesis seems inadequate for monitoring fetal thyroid function. Further studies are needed to determine the optimal management of this disorder.

Controversies Surrounding Pregnancy, Maternal Thyroid Status, and Fetal Outcome

ThyroidVol. 19, No. 4 EditorialFree AccessControversies Surrounding Pregnancy, Maternal Thyroid Status, and Fetal OutcomeKenneth D. BurmanKenneth D. BurmanSearch for more papers by this authorPublished Online:8 Apr 2009https://doi.org/10.1089/thy.2009.1570AboutSectionsPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail FiguresReferencesRelatedDetailsCited byInconsistencies in the management of neonates born to mothers with “thyroid diseases”5 September 2018 | European Journal of Pediatrics, Vol. 177, No. 11Thyroid glard disorders in pregnancyMedicína pro praxi, Vol. 14, No. 4Randomized Trial Comparing Two Algorithms for Levothyroxine Dose Adjustment in Pregnant Women With Primary Hypothyroidism3 July 2017 | The Journal of Clinical Endocrinology & Metabolism, Vol. 102, No. 9Knowledge of Thyroid Disorders during Pregnancy among General Practitioners in Iran21 June 2017 | International Journal of Endocrinology and Metabolism, Vol. In Press, No. In PressThyroid and Parathyroid Diseases in PregnancyPersistent Organic Pollutants and the Association with Maternal and Infant Thyroid Homeostasis: A Multipollutant AssessmentEnvironmental Health Perspectives, Vol. 125, No. 1Prevalent Practices of Thyroid Diseases During Pregnancy Among Endocrinologists, Internists and General Practitioners7 November 2015 | International Journal of Endocrinology and Metabolism, Vol. 14, No. 1Preconceptional thyroid-stimulating hormone levels and outcomes of intrauterine insemination among euthyroid infertile womenFertility and Sterility, Vol. 103, No. 1Screening and management of hypothyroidism in pregnancy: Results of an Asian surveyEndocrine Journal, Vol. 61, No. 7Maternal Screening for Hypothyroidism and Thyroiditis Using Filter Paper Specimens T.P. Foley, J.J. Henry, L.F. Hofman, R.D. Thomas, J.S. Sanfilippo, and E.W. Naylor5 November 2013 | Journal of Women's Health, Vol. 22, No. 11Clinical Diagnostic Laboratory Play a Crucial Role in the Management of Thyroid Disorders: A Literature ReviewJournal of Biological Sciences, Vol. 13, No. 8Thyroid function during controlled ovarian hyperstimulation as part of in vitro fertilizationFertility and Sterility, Vol. 97, No. 3Thyroid and Parathyroid Diseases in PregnancyTreatment and screening of hypothyroidism in pregnancy: results of a European surveyEuropean Journal of Endocrinology, Vol. 166, No. 1Thyroid dysfunction in pregnancy: definition of TSH cut-off should precede the decision of screening in low-risk pregnant women26 May 2010 | Gynecological Endocrinology, Vol. 27, No. 3Graves' Disease in Two Pregnancies Complicated by Fetal Goitrous Hypothyroidism: Successful In Utero Treatment with Levothyroxine Sofie Bliddal, Åse Krogh Rasmussen, Karin Sundberg, Vibeke Brocks, Peter Skovbo, and Ulla Feldt-Rasmussen10 January 2011 | Thyroid, Vol. 21, No. 1Levothyroxine Treatment in Pregnancy: Indications, Efficacy, and Therapeutic RegimenJournal of Thyroid Research, Vol. 2011Thyroid Function and Human Reproductive HealthEndocrine Reviews, Vol. 31, No. 5Serum TSH determinations in pregnancy: how, when and why?8 June 2010 | Nature Reviews Endocrinology, Vol. 6, No. 9Diagnosis and Management of Thyroid Disease in PregnancyObstetrics and Gynecology Clinics of North America, Vol. 37, No. 2Newborn Thyroid Screening1 June 2010 | Proceedings of Singapore Healthcare, Vol. 19, No. 2The Role of Clinical Guidelines in Patient Care: Thyroid Hormone Replacement in Women of Reproductive Age Megan Rist Haymart28 February 2010 | Thyroid, Vol. 20, No. 3 Volume 19Issue 4Apr 2009 InformationCopyright 2009, Mary Ann Liebert, Inc.To cite this article:Kenneth D. Burman.Controversies Surrounding Pregnancy, Maternal Thyroid Status, and Fetal Outcome.Thyroid.Apr 2009.323-326.http://doi.org/10.1089/thy.2009.1570Published in Volume: 19 Issue 4: April 8, 2009PDF download

Antenatal Diagnosis and Treatment of a Dyshormonogenetic Fetal Goiter

Journal of Ultrasound in MedicineVolume 28, Issue 1 p. 67-71 Case Report Antenatal Diagnosis and Treatment of a Dyshormonogenetic Fetal Goiter Kathleen A. Mayor-Lynn MD, Corresponding Author Kathleen A. Mayor-Lynn MD mayorlyn@obgyn.ufl.edu Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USAAddress correspondence to Kathleen A. Mayor-Lynn, MD, Department of Obstetrics and Gynecology, University of Florida College of Medicine, 1600 SW Archer Rd, Box 100294, Gainesville, FL 32610-0294 USA.Search for more papers by this authorHenry J. Rohrs III MD, Henry J. Rohrs III MD Department of Pediatric Endocrinology, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorAmelia C. Cruz MD, Amelia C. Cruz MD Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorJanet H. Silverstein MD, Janet H. Silverstein MD Department of Pediatric Endocrinology, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorDouglas Richards MD, Douglas Richards MD Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this author Kathleen A. Mayor-Lynn MD, Corresponding Author Kathleen A. Mayor-Lynn MD mayorlyn@obgyn.ufl.edu Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USAAddress correspondence to Kathleen A. Mayor-Lynn, MD, Department of Obstetrics and Gynecology, University of Florida College of Medicine, 1600 SW Archer Rd, Box 100294, Gainesville, FL 32610-0294 USA.Search for more papers by this authorHenry J. Rohrs III MD, Henry J. Rohrs III MD Department of Pediatric Endocrinology, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorAmelia C. Cruz MD, Amelia C. Cruz MD Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorJanet H. Silverstein MD, Janet H. Silverstein MD Department of Pediatric Endocrinology, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this authorDouglas Richards MD, Douglas Richards MD Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, University of Florida College of Medicine, Gainesville, Florida USASearch for more papers by this author First published: 01 January 2009 https://doi.org/10.7863/jum.2009.28.1.67Citations: 12Read the full textAboutRelatedInformationPDFPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessClose modalShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume28, Issue1January 2009Pages 67-71 RelatedInformation RecommendedPrenatal diagnosis and successful intrauterine treatment of severe congenital hypothyroidism associated with fetal goiterVladimír Ferianec, Peter Papcun, František Grochal, Katarína Schenková, Michaela Bártová, Journal of Obstetrics and Gynaecology ResearchIntrauterine diagnosis and management of fetal goiter: A case reportFaik Mumtaz Koyuncu, Aslı Goker Tamay, Sultan Bugday, Journal of Clinical UltrasoundAntenatal diagnosis and treatment of fetal goitrous hypothyroidism: case report and review of the literatureA. Z. Abuhamad, D. A. Fisher, S. L. Warsoff, R. N. Slotnick, P. G. Pyle, S.-Y. Wu, A. T. Evans, Ultrasound in Obstetrics & GynecologyIntrauterine diagnosis and treatment of fetal goitrous hypothyroidismAytul Corbacioglu Esmer, Ahmet Gul, Hediye Dagdeviren, Isil Turan Bakirci, Orhan Sahin, Journal of Obstetrics and Gynaecology Research

Successful Intrauterine Therapy for Fetal Goitrous Hypothyroidism during Late Gestation

We experienced a case of fetal goitrous hypothyroidism in an infant delivered by a 33-year-old woman receiving 300 mg/day of propylthiouracil (PTU) for hyperthyroidism due to Graves' disease. A large fetal goiter (maximum diameter, 60 mm) was detected by magnetic resonance imaging (MRI) at 36 weeks of gestation. Initial fetal blood sampling revealed hypothyroidism with a serum thyroid-stimulating hormone (TSH) of 99 microIU/mL, free triiodothyronine (T(3)) of 1.97 pg/mL, and free thyroxine (T(4)) of 0.29 ng/dL. Consequently, a diagnosis of fetal goitrous hypothyroidism due to transplacental passage of maternal PTU was made. To reduce the risk of perinatal complications, 300 microg of levothyroxine sodium (L-T(4)) was administered into the maternal amniotic fluid twice between 37 and 38 weeks of gestation. Subsequent fetal MRI showed that the size of goiter had decreased. At 38 weeks and 5 days of gestation, a 3042-g male infant was born by cesarean section. There were no severe complications at delivery, although mild tachypnea was observed and the infant's thyroid gland was slightly enlarged. He was treated with L-T(4) for two weeks. At present, his growth and neurological development are normal. This case indicates that intrauterine therapy by the intraamniotic administration of L-T(4) can be effective in treating fetal goitrous hypothyroidism even during late gestation.