Review shows that thyroid hormone substitution could benefit transient hypothyroxinaemia of prematurity but treatment strategies need to be clarified

Eerdekens, An; Langouche, Lies; Berghe, Greet Van den; Verhaeghe, Johan; Naulaers, Gunnar; Vanhole, Christine

doi:10.1111/apa.14685

Cited by 15 publications

(17 citation statements)

References 64 publications

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“…Premature infants with low birth weight represent a particular and separate subgroup of patients treated in the neonatal intensive care environment. Preterm infants often present with transient hypothyroxinemia of prematurity (THOP), which is characterized by low circulating T4 and T3 without a concomitant rise in TSH [66, 67]. Although the changes in T4, T3, and TSH are quite similar to what is observed in NTIS in adults, children, and term infants, the underlying mechanisms are even more complex, given that the hypothalamus–pituitary–thyroid axis matures until the end of full-term pregnancy.…”

Section: Ntis In Premature Newborns Treated In the Neonatal Icumentioning

confidence: 99%

“…Although the changes in T4, T3, and TSH are quite similar to what is observed in NTIS in adults, children, and term infants, the underlying mechanisms are even more complex, given that the hypothalamus–pituitary–thyroid axis matures until the end of full-term pregnancy. Hence, thyroid axis immaturity likely contributes to the thyroid hormone alterations observed in preterm newborns [66, 67]. The most immature newborns, who suffer from the highest morbidity rates, also have the most pronounced THOP [68].…”

Section: Ntis In Premature Newborns Treated In the Neonatal Icumentioning

confidence: 99%

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Nonthyroidal Illness Syndrome Across the Ages

Langouche

Jacobs

Berghe

2019

Journal of the Endocrine Society

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In conditions of acute illness, patients present with reduced plasma T3 concentrations without a concomitant rise in TSH. In contrast, plasma concentrations of the inactive hormone rT3 increase, whereas plasma concentrations of T4 remain low-normal. This constellation of changes, referred to as nonthyroidal illness syndrome (NTIS), is present across all ages, from preterm neonates and over-term critically ill infants and children to critically ill adults. Although the severity of illness strongly correlates with the severity of the NTIS phenotype, the causality of this association remains debated, and pathophysiological mechanisms remain incompletely understood. In the acute phase of illness, NTIS appears to be caused predominantly by an increased peripheral inactivation of thyroid hormones, in which reduced nutritional intake plays a role. Current evidence suggests that these acute peripheral changes are part of a beneficial adaptation of the body to reduce expenditure of energy and to activate the innate immune response, which is important for survival. In contrast, in more severely ill and prolonged critically ill patients, an additional central suppression of the thyroid hormone axis alters and further aggravates the NTIS phenotype. Recent studies suggest that this central suppression may not be adaptive. Whether treatment of this central component of NTIS in prolonged critically ill patients, with the use of hypothalamic releasing factors, improves outcome remains to be investigated in large randomized control trials.

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Section: Ntis In Premature Newborns Treated In the Neonatal Icumentioning

confidence: 99%

Section: Ntis In Premature Newborns Treated In the Neonatal Icumentioning

confidence: 99%

Nonthyroidal Illness Syndrome Across the Ages

Langouche

Jacobs

Berghe

2019

Journal of the Endocrine Society

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“…Two forms of thyroid function anomaly may occur in VPIs. One is delayed elevated TSH [7,8], and the other is transient hypothyroxinemia of prematurity (THOP) [9,10]. Therefore, certain very preterm infants may experience normal TSH with low serum thyroxin for weeks.…”

Section: Introductionmentioning

confidence: 99%

“…Williams et al voiced concerns regarding the current clinical screening protocols [17]; however, relatively little is known about the optimal timing of extra postnatal screening beyond national newborn screening policies. Furthermore, the effect of any renewal protocol on long-term neurodevelopmental outcomes should be further investigated along with the neonatal morbidities of prematurity [7,9].…”

Section: Introductionmentioning

confidence: 99%

Postnatal Serum Total Thyroxine of Very Preterm Infants and Long-Term Neurodevelopmental Outcome

et al. 2021

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Primary congenital hypothyroidism is a disease associated with low serum thyroxine and elevated thyroid-stimulating hormone (TSH) levels. The processes of screening and treating congenital hypothyroidism, in order to prevent neurodevelopmental impairment (NDI) in newborns, have been well investigated. Unlike term infants, very preterm infants (VPIs) may experience low thyroxine with normal TSH levels (<10.0 μIU/mL) during long-stay hospitalization. In the current literature, thyroxine treatment has been evaluated only for TSH-elevated VPIs. However, the long-term impact of low thyroxine levels in certain VPIs with normal TSH levels deserves more research. Since July 2007, VPIs of this study unit received screenings at 1 month postnatal age (PNA) for serum TSH levels and total thyroxine (TT4), in addition to two national TSH screenings scheduled at 3–5 days PNA and at term equivalent age. This study aimed to establish the correlation between postnatal 1-month-old TT4 concentration and long-term NDI at 24 months corrected age among VPIs with serial normal TSH levels. VPIs born in August 2007–July 2016 were enrolled. Perinatal demography, hospitalization morbidities, and thyroid function profiles were analyzed, and we excluded those with congenital anomalies, brain injuries, elevated TSH levels, or a history of thyroxine treatments. In total, 334 VPIs were analyzed and 302 (90.4%) VPIs were followed-up. The postnatal TT4 concentration was not associated with NDI after multivariate adjustment (odd ratios 1.131, 95% confidence interval 0.969–1.32). To attribute the NDI of TSH-normal VPIs to a single postnatal TT4 concentration measurement may require more research.

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“…During gestation, the fetus is largely dependent on the maternal TH supply until the fetal hypothyroid-pituitary-thyroid (HPT) axis starts developing in the third trimester. 12 Thus hypothyroidism is a common occurrence in preterm infants, and more than 50% of the low-birth weight preterm infants have some type of thyroid dysfunction. 13 Many preterm infants can also develop retinopathy of prematurity (ROP).…”

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confidence: 99%

Thyroid Activating Enzyme, Deiodinase II Is Required for Photoreceptor Function in the Mouse Model of Retinopathy of Prematurity

Sawant

Jidigam

Wilcots

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Retinopathy of prematurity (ROP) is a severe complication of premature infants, leading to vision loss when untreated. Presently, the molecular mechanisms underlying ROP are still far from being clearly understood. This study sought to investigate whether thyroid hormone (TH) signaling contributes to the neuropathology of ROP using the mouse model of ROP to evaluate longitudinal photoreceptor function. METHODS. Animals were exposed to hyperoxia from P7 to P12 to induce retinopathy, thereafter the animals were returned to room air (normoxia). The thyroid-activating enzyme type 2 deiodinases (Dio2) knockout (KO) mice and the littermate controls that were exposed to hyperoxia or maintained in room air and were then analyzed. The retinal function was evaluated using electroretinograms (ERGs) at three and seven weeks followed by histologic assessments with neuronal markers to detect cellular changes in the retina. Rhodopsin protein levels were measured to validate the results obtained from the immunofluorescence analyses. RESULTS. In the ROP group, the photoreceptor ERG responses are considerably lower both in the control and the Dio2 KO animals at P23 compared to the non-ROP group. In agreement with the ERG responses, loss of Dio2 results in mislocalized cone nuclei, and abnormal rod bipolar cell dendrites extending into the outer nuclear layer. The retinal function is compromised in the adult Dio2 KO animals, although the cellular changes are less severe. Despite the reduction in scotopic a-wave amplitudes, rhodopsin levels are similar in the adult mice, across all genotypes irrespective of exposure to hyperoxia. CONCLUSIONS. Using the mouse model of ROP, we show that loss of Dio2 exacerbates the effects of hyperoxia-induced retinal deficits that persist in the adults. Our data suggest that aberrant Dio2/TH signaling is an important factor in the pathophysiology of the visual dysfunction observed in the oxygen-induced retinopathy model of ROP.

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Review shows that thyroid hormone substitution could benefit transient hypothyroxinaemia of prematurity but treatment strategies need to be clarified

Cited by 15 publications

References 64 publications

Nonthyroidal Illness Syndrome Across the Ages

Nonthyroidal Illness Syndrome Across the Ages

Postnatal Serum Total Thyroxine of Very Preterm Infants and Long-Term Neurodevelopmental Outcome

Thyroid Activating Enzyme, Deiodinase II Is Required for Photoreceptor Function in the Mouse Model of Retinopathy of Prematurity

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