scholarly journals Erratum: Treating fetal thyroid and adrenal disorders through the mother

2009 ◽  
Vol 5 (2) ◽  
pp. 122-122 ◽  
Author(s):  
Guy Van Vliet ◽  
Michel Polak ◽  
E Martin Ritzén
Keyword(s):  
Fetal Thyroid

scholarly journals Involvement of Thyroid Hormones in Brain Development and Cancer

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2693
Author(s):  
Gabriella Schiera ◽  
Carlo Maria Di Liegro ◽  
Italia Di Liegro
Keyword(s):  
Nervous System ◽  
Thyroid Hormones ◽  
Brain Development ◽  
Placental Transfer ◽  
Regulation Of Gene Expression ◽  
Mammalian Brain ◽  
Cancer Proliferation ◽  
Fetal Thyroid ◽  
Genomic Effects ◽  
And Function

The development and maturation of the mammalian brain are regulated by thyroid hormones (THs). Both hypothyroidism and hyperthyroidism cause serious anomalies in the organization and function of the nervous system. Most importantly, brain development is sensitive to TH supply well before the onset of the fetal thyroid function, and thus depends on the trans-placental transfer of maternal THs during pregnancy. Although the mechanism of action of THs mainly involves direct regulation of gene expression (genomic effects), mediated by nuclear receptors (THRs), it is now clear that THs can elicit cell responses also by binding to plasma membrane sites (non-genomic effects). Genomic and non-genomic effects of THs cooperate in modeling chromatin organization and function, thus controlling proliferation, maturation, and metabolism of the nervous system. However, the complex interplay of THs with their targets has also been suggested to impact cancer proliferation as well as metastatic processes. Herein, after discussing the general mechanisms of action of THs and their physiological effects on the nervous system, we will summarize a collection of data showing that thyroid hormone levels might influence cancer proliferation and invasion.

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.

THE COLLECTION OF RADIOACTIVE IODINE BY THE HUMAN FETAL THYROID*

1948 ◽  
Vol 8 (9) ◽  
pp. 717-720 ◽  
Author(s):  
EARLE M. CHAPMAN ◽  
G. W. CORNER ◽  
DAVID ROBINSON ◽  
R. D. EVANS
Keyword(s):  
Radioactive Iodine ◽  
Fetal Thyroid

scholarly journals Placental 5-Deiodinase Activity and Fetal Thyroid Hormone Economy Are Unaffected by Selenium Deficiency in the Rat

1993 ◽  
Vol 34 (3) ◽  
pp. 288-292 ◽  
Author(s):  
Jean-Pierre Chanoine ◽  
Sharon Alex ◽  
Scott Stone ◽  
Shih Lieh Fang ◽  
Irini Veronikis ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Selenium Deficiency ◽  
Deiodinase Activity ◽  
Fetal Thyroid

scholarly journals Fetal Thyroid Function, Birth Weight, andin UteroExposure to Fine Particle Air Pollution: A Birth Cohort Study

2017 ◽  
Vol 125 (4) ◽  
pp. 699-705 ◽  
Author(s):  
Bram G. Janssen ◽  
Nelly D. Saenen ◽  
Harry A. Roels ◽  
Narjes Madhloum ◽  
Wilfried Gyselaers ◽  
...  
Keyword(s):  
Air Pollution ◽  
Cohort Study ◽  
Birth Weight ◽  
Birth Cohort ◽  
Thyroid Function ◽  
Fine Particle ◽  
Birth Cohort Study ◽  
Fetal Thyroid

scholarly journals Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

2000 ◽  
Vol 83 (5) ◽  
pp. 3101-3112 ◽  
Author(s):  
Marlies Knipper ◽  
Christoph Zinn ◽  
Hannes Maier ◽  
Mark Praetorius ◽  
Karin Rohbock ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Auditory System ◽  
Critical Time ◽  
Organ Of Corti ◽  
Thyroid Gland Function ◽  
Distortion Product ◽  
Fetal Thyroid ◽  
Gland Function ◽  
Dependent Processes

Both a genetic or acquired neonatal thyroid hormone (TH) deficiency may result in a profound mental disability that is often accompanied by deafness. The existence of various TH-sensitive periods during inner ear development and general success of delayed, corrective TH treatment was investigated by treating pregnant and lactating rats with the goitrogen methimazole (MMI). We observed that for the establishment of normal hearing ability, maternal TH, before fetal thyroid gland function on estrus days 17–18, is obviously not required. Within a crucial time between the onset of fetal thyroid gland function and the onset of hearing at postnatal day 12 ( P12), any postponement in the rise of TH-plasma levels, as can be brought about by treating lactating mothers with MMI, leads to permanent hearing defects of the adult offspring. The severity of hearing defects that were measured in 3- to 9-mo-old offspring could be increased with each additional day of TH deficiency during this critical period. Unexpectedly, the active cochlear process, assayed by distortion product otoacoustic emissions (DPOAE) measurements, and speed of auditory brain stem responses, which both until now were not thought to be controlled by TH, proved to be TH-dependent processes that were damaged by a delay of TH supply within this critical time. In contrast, no significant differences in the gross morphology and innervation of the organ of Corti or myelin gene expression in the auditory system, detected as myelin basic protein (MBP) and proteolipid protein (PLP) mRNA using Northern blot approach, were observed when TH supply was delayed for few days. These classical TH-dependent processes, however, were damaged when TH supply was delayed for several weeks. These surprising results may suggest the existence of different TH-dependent processes in the auditory system: those that respond to corrective TH supply (e.g., innervation and morphogenesis of the organ of Corti) and those that do not, but require T3 activity during a very tight time window (e.g., active cochlear process, central processes).

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