scholarly journals VP13.18: Fetal goiter caused by dyshormonogenesis

2021 ◽  
Vol 58 (S1) ◽  
pp. 153-153
Author(s):  
M. Isayeva ◽  
A.T. Farajov ◽  
U. Jafarova ◽  
E. Bagirova ◽  
H. Mammadzade ◽  
...  
Keyword(s):  
Fetal Goiter

scholarly journals MR Imaging of Fetal Goiter: Fig 1.

2011 ◽  
Vol 32 (8) ◽  
pp. E160-E160 ◽  
Author(s):  
J. H. Harreld ◽  
R.K. Kilani ◽  
C.D. Lascola ◽  
S.K. Bartz
Keyword(s):  
Mr Imaging ◽  
Fetal Goiter

Iatrogenic fetal goiter. Conservative management and spontaneous resolution

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Margarita Alvarez de la Rosa ◽  
Olga Rosales Aedo ◽  
Ricardo Darias Garzón ◽  
Ana Isabel Padilla Pérez ◽  
Juan Mario Troyano Luque
Keyword(s):  
Conservative Treatment ◽  
Perinatal Asphyxia ◽  
Mass Effect ◽  
Neck Mass ◽  
Spontaneous Resolution ◽  
Anterior Neck ◽  
Case Presentation ◽  
Fetal Goiter ◽  
Fetal Thyroid ◽  
Intrauterine Treatment

AbstractObjectivesWe aim to report a case of a fetal goiter with postpartum spontaneous resolution. Fetal goiter can be secondary to maternal treatment and range from clinically asymptomatic or cause alterations in the fetus, from impaired swallowing to difficulty in vaginal delivery and even perinatal asphyxia due to the mass effect. The need for intrauterine treatment remains controversial.Case presentationWe present a case of fetal goiter with postpartum resolution. A 34-year-old multigravida presented to the emergency department with hiperemesis gravidarum at 10 weeks’ gestation. During evaluation for severe vomiting, Graves disease was diagnosed and treated with propylthiouracil. A routine ultrasound scan at 28 weeks gestation revealed a fetal anterior neck mass suggesting a fetal goiter. Cordocentesis showed fetal iatrogenic hypothyroidism. Conservative treatment was decided. Pregnancy concluded uneventful and the mass resolved spontaneously in the newborn.ConclusionsThe fetal thyroid gland is a structure that usually goes unnoticed during the process of prenatal diagnosis. In cases of maternal Graves diseases, fetal thyroid needs monitoring during pregnancy and conservative treatment is an option. Fetal goiter should be searched for secondary to thyroid alterations of the gravida, and in selected cases it can be managed without intrauterine treatment.

scholarly journals Fetal goiter conservatively monitored during the prenatal period associated with maternal and neonatal euthyroid status

2016 ◽  
Vol 59 (1) ◽  
pp. 54 ◽  
Author(s):  
José Ferreira Gomes Neto ◽  
Edward Araujo Júnior ◽  
Jesus Irajacy Fernandes Costa ◽  
Daniel Aguiar Dias ◽  
Lindemberg Barbosa Aguiar ◽  
...  
Keyword(s):  
Prenatal Period ◽  
Fetal Goiter ◽  
Euthyroid Status

Intrauterine Diagnosis and Management of Fetal Goitrous Hypothyroidism: A Report of an Iranian Family with Three Consecutive Pregnancies Complicated by Fetal Goiter

Thyroid ◽  
2005 ◽  
Vol 15 (12) ◽  
pp. 1341-1347 ◽  
Author(s):  
Ali-Asghar Mirsaeid Ghazi ◽  
Arash Ordookhani ◽  
Marina Pourafkari ◽  
Masoumeh Fallahian ◽  
Adeleh Bahar ◽  
...  
Keyword(s):  
Diagnosis And Management ◽  
Intrauterine Diagnosis ◽  
Iranian Family ◽  
Fetal Goiter

Antenatal Diagnosis and Treatment of a Dyshormonogenetic Fetal Goiter

2009 ◽  
Vol 28 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Kathleen A. Mayor-Lynn ◽  
Henry J. Rohrs ◽  
Amelia C. Cruz ◽  
Janet H. Silverstein ◽  
Douglas Richards
Keyword(s):  
Antenatal Diagnosis ◽  
Diagnosis And Treatment ◽  
Fetal Goiter

Fetal Goiter and Bilateral Ovarian Cysts

2007 ◽  
Vol 23 (2) ◽  
pp. 132-135 ◽  
Author(s):  
Pernille D. Lassen ◽  
Karin Sundberg ◽  
Anders Juul ◽  
Lillian Skibsted
Keyword(s):  
Ovarian Cysts ◽  
Fetal Goiter

scholarly journals Prenatal Diagnosis of Thyroid Hormone Resistance

1999 ◽  
Vol 84 (2) ◽  
pp. 405-410 ◽  
Author(s):  
C. Asteria ◽  
O. Rajanayagam ◽  
T. N. Collingwood ◽  
L. Persani ◽  
R. Romoli ◽  
...  
Keyword(s):  
Prenatal Diagnosis ◽  
Thyroid Hormone ◽  
Fetal Development ◽  
Normal Values ◽  
Assay Method ◽  
Common Finding ◽  
Adequate Treatment ◽  
Fetal Goiter ◽  
Tsh Levels ◽  
Biochemical Features

A 29-yr-old woman with pituitary resistance to thyroid hormones (PRTH) was found to harbor a novel point mutation (T337A) on exon 9 of the thyroid hormone receptor β (TRβ) gene. She presented with symptoms and signs of hyperthyroidism and was successfully treated with 3,5,3′-triiodothyroacetic acid (TRIAC) until the onset of pregnancy. This therapy was then discontinued in order to prevent TRIAC, a compound that crosses the placental barrier, from exerting adverse effects on normal fetal development. However, as the patient showed a recurrence of thyrotoxic features after TRIAC withdrawal, we sought to verify, by means of genetic analysis and hormone measurements, whether the fetus was also affected by RTH, in order to rapidly reinstitute TRIAC therapy, which could potentially be beneficial to both the mother and fetus. At 17 weeks gestation, fetal DNA was extracted from chorionic villi and was used as a template for PCR and restriction analysis together with direct sequencing of the TRβ gene. The results indicated that the fetus was also heterozygous for the T337A mutation. Accordingly, TRIAC treatment at a dose of 2.1 mg/day was restarted at 20 weeks gestation. The mother rapidly became euthyroid, and the fetus grew normally up to 24 weeks gestation. At 29 weeks gestation mild growth retardation and fetal goiter were observed, prompting cordocentesis. Circulating fetal TSH was very high (287 mU/L) with a markedly reduced TSH bioactivity (B/I: 1.1 ± 0.4 vs 12.7 ± 1.2), while fetal FT4 concentrations were normal (8.7 pmol/L; normal values in age-matched fetuses: 5–22 pmol/L). Fetal FT3 levels were raised (7.1 pmo/L; normal values in age-matched fetuses: <4 pmol/L), as a consequence of 100% cross-reactivity of TRIAC in the FT3 assay method. To reduce the extremely high circulating TSH levels and fetal goiter, the dose of TRIAC was increased to 3.5 mg/day. To monitor the possible intrauterine hypothyroidism, another cordocentesis was performed at 33 weeks gestation, showing that TSH levels were reduced by 50% (from 287 to 144 mU/L). Furthermore, a simultaneous ultrasound examination revealed a clear reduction in fetal goiter. After this latter cordocentesis, acute complications occured, prompting delivery by cesarean section. The female neonate was critically ill, with multiple-organ failure and respiratory distress syndrome. In addition, a small goiter and biochemical features of hypothyroidism were noted transiently and probably related to the prematurity of the infant. At present, the baby is clinically euthyroid, without goiter, and only exhibits biochemical features of RTH. In summary, although further fetal studies in cases of RTH are necessary to determine whether elevated TSH levels with a markedly reduced bioactivity are a common finding, our data suggest transient biochemical hypothyroidism in RTH during fetal development. Furthermore, we advocate prenatal diagnosis of RTH and adequate treatment of the disease in case of maternal hyperthyroidism, to avoid fetal thyrotrope hyperplasia, reduce fetal goiter, and maintain maternal euthyroidism during pregnancy.

Fetal Goiter Mimicking Anomalous Pulmonary Venous Connection

2010 ◽  
Vol 5 (5) ◽  
pp. 482-485
Author(s):  
Jeffrey M. Vinocur ◽  
Shanthi Sivanandam
Keyword(s):  
Fetal Goiter ◽  
Anomalous Pulmonary Venous Connection

Erratum: Prenatal Diagnosis of Fetal Goiter in a Euthyroid Mother

2016 ◽  
Vol 27 (1) ◽  
pp. 70
Author(s):  
Jin Young Bae ◽  
Lee Hyun Joo ◽  
Ji Eun Jeong ◽  
Seong Yeon Hong
Keyword(s):  
Prenatal Diagnosis ◽  
Fetal Goiter
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