Maturation of the Secretion of Thyroid Hormone and Thyroid-Stimulating Hormone in the Fetus

Thorpe-Beeston, J. G.; Nicolaides, Kypros H.; Felton, Carl V.; Butler, Jane; McGregor, A. M.

doi:10.1056/nejm199102213240805

Cited by 361 publications

(201 citation statements)

References 17 publications

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“…Previous studies have also observed that premature children have lower levels of TSH and free t3 and t4 that progressively increase as levels of prematurity decrease (20,21). The levels of three enzymes we examined did not follow a clear pattern of effect with increasing prematurity.…”

Section: Metabolomics Of Prematuritymentioning

confidence: 68%

Metabolomics of prematurity: analysis of patterns of amino acids, enzymes, and endocrine markers by categories of gestational age

et al. 2013

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Background: Prematurity may influence the levels of amino acids, enzymes, and endocrine markers obtained through newborn screening. Identifying which analytes are the most affected by degree of prematurity could provide insight into how prematurity impacts metabolism. Methods: Analytes from blood spots assayed by Newborn Screening Ontario between March 2006 and April 2009 were used in this analysis. We examined the associations between the degree of prematurity and the levels of amino acids, enzymes, and endocrine markers in all newborns with and without adjustment for birth weight, feeding status, sample timing, transfusion, and sex. results: Our analysis included the following cohorts: 373,819 children born at term (>36 wk gestation), 26,483 near-term children (33-36 wk gestation), 4,354 very premature children (28-32 wk gestation), and 1,146 extremely premature children (<28 wk gestation). Of the amino acids showing consistent trends across categories of prematurity, the levels of three amino acids (arginine, leucine, and valine) were at least 50% different between the cohorts of extremely premature and term children. The levels of 17-hydroxyprogesterone increased with increasing prematurity, while thyrotropin-stimulating hormone values consistently decreased with increasing prematurity. None of the three enzyme markers we examined showed a trend in levels across categories of prematurity. conclusion: This study demonstrates that children at different stages of prematurity are metabolically distinct. Future research should focus on the mechanism by which specific analytes are influenced by prematurity.i n population-wide newborn screening, dried blood spot samples are obtained usually within 24-72 h of birth from which levels of various analytes are measured (1,2). In Ontario and several other jurisdictions, these analytes include markers of amino acid metabolism, fatty acid oxidation, and endocrine function (3-7). Analyte results are used to calculate risk for rare inborn errors of metabolism and endocrine disorders.Children having positive screening results are sent for confirmatory testing.It is generally recognized that, aside from the presence of a rare metabolic or endocrine disease, several other factors can affect the analytes measured for newborn screening. One of these is gestational age (GA) at birth (8-11). Prematurity may influence analyte levels through a variety of mechanisms, including increased catabolic stress, lessened maturation of metabolic pathways and/ or organ systems, and differential distribution of other confounding variables such as feeding status (9,12). Identifying which analytes are the most affected by extent of prematurity could provide insight into how prematurity influences metabolism.In Ontario, Canada, virtually every child undergoes newborn screening (13). Results for all analytes measured are stored along with key demographic variables. We examined the associations between different degrees of prematurity and subclinical levels of specific analytes, after removing screen...

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Section: Metabolomics Of Prematuritymentioning

confidence: 68%

Metabolomics of prematurity: analysis of patterns of amino acids, enzymes, and endocrine markers by categories of gestational age

et al. 2013

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“…Normal maternal thyroid hormone concentrations thus appear critical, particularly in the first trimester, to attain normal neurodevelopment. Appreciable amounts of thyroid hormones are only detectable in the human fetal circulation from 14-16 weeks of gestation, which is believed to represent the time of onset of endogenous thyroid hormone release (Thorpe-Beeston et al 1991, Fisher 1997 even though the fetal thyroid gland begins accumulating iodide from 10-12 weeks of gestation (Shepard 1967, Fisher et al 1976). The fetus is, therefore, entirely reliant on the maternal supply of thyroid hormones for normal development in the first and early part of the second trimester.…”

Section: Thyroid Hormones and The Neurological Systemmentioning

confidence: 99%

Thyroid hormone in health and disease

Boelaert

Franklyn²

2005

Journal of Endocrinology

225

127

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Thyroid disease is common, affecting around 2% of women and 0·2% of men in the UK. Our understanding of the effects of thyroid hormones under physiological circumstances, as well as in pathological conditions, has increased dramatically during the last two centuries and it has become clear that overt thyroid dysfunction is associated with significant morbidity and mortality. Both hypoand hyperthyroidism and their treatments have been linked with increased risk from cardiovascular disease and the adverse effects of thyrotoxicosis in terms of osteoporosis risk are well established. Although the evidence suggests that successful treatment of overt thyroid dysfunction significantly improves overall survival, the issue of treating mild or subclinical hyper-and hypothyroidism remains controversial. Furthermore, the now wellestablished effects of thyroid hormones on neurodevelopment have sparked a whole new debate regarding the need to screen pregnant women for thyroid function abnormalities. This review describes the current evidence of the effects of thyroid hormone on the cardiovascular, skeletal and neurological systems, as well as the influence of thyroid diseases and their treatments on the development of malignancy. Furthermore we will describe some recent developments in our understanding of the relationship between thyroid status and health.

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“…ThorpeBeeston et al showed that the foetal serum TSH concentration throughout pregnancy was well above the maternal TSH concentration, with foetal concentrations up to 12 mIU l 21 near full term 27 . Foetal TSH was positively correlated with foetal fT 4 (r ¼ 0.896, P , 0.001) 27 . Foetal TSH has a higher bioactivity than maternal TSH, and its synthesis is not under hypothalamic control, as shown by the high cord serum TSH concentration found in anencephalic foetuses 28,29 .…”

Section: Introductionmentioning

confidence: 99%

Iodine deficiency and brain development in the first half of pregnancy

Escobar

Obregón

Rey

2007

Public Health Nutr.

277

213

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An inadequate supply of iodine during gestation results in damage to the foetal brain that is irreversible by mid-gestation unless timely interventions can correct the accompanying maternal hypothyroxinemia. Even mild to moderate maternal hypothyroxinemia may result in suboptimal neurodevelopment. This review mainly focuses on iodine and thyroid hormone economy up to mid-gestation, a period during which the mother is the only source for the developing brain of the foetus. The cerebral cortex of the foetus depends on maternal thyroxine (T 4 ) for the production of the 3 0 ,3,5-tri-iodothyronine (T 3 ) for nuclear receptor-binding and biological effectiveness. Maternal hypothyroxinemia early in pregnancy is potentially damaging for foetal brain development. Direct evidence has been obtained from experiments on animals: even a relatively mild and transient hypothyroxinemia during corticogenesis, which takes place mostly before mid-gestation in humans, affects the migration of radial neurons, which settle permanently in heterotopic locations within the cortex and hippocampus. Behavioural defects have also been detected. The conceptus imposes important early changes on maternal thyroid hormone economy that practically doubles the amount of T 4 secreted something that requires a concordant increase in the availability of iodine, from 150 to 250-300 mg I day 21 . Women who are unable to increase their production of T 4 early in pregnancy constitute a population at risk for having children with neurological disabilities. As a mild to moderate iodine deficiency is still the most widespread cause of maternal hypothyroxinemia, the birth of many children with learning disabilities may be prevented by advising women to take iodine supplements as soon as pregnancy starts, or earlier if possible, in order to ensure that their requirements for iodine are met.

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Maturation of the Secretion of Thyroid Hormone and Thyroid-Stimulating Hormone in the Fetus

Cited by 361 publications

References 17 publications

Metabolomics of prematurity: analysis of patterns of amino acids, enzymes, and endocrine markers by categories of gestational age

Metabolomics of prematurity: analysis of patterns of amino acids, enzymes, and endocrine markers by categories of gestational age

Thyroid hormone in health and disease

Iodine deficiency and brain development in the first half of pregnancy

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