scholarly journals The Hypothalamic-Pituitary-Thyroid Axis in Preterm Infants; Changes in the First 24 Hours of Postnatal Life

2004 ◽  
Vol 89 (6) ◽  
pp. 2824-2831 ◽  
Author(s):  
Nuala Murphy ◽  
Robert Hume ◽  
Hans van Toor ◽  
Tom G. Matthews ◽  
Simon A. Ogston ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Age Groups ◽  
Postnatal Life ◽  
Free T4 ◽  
Thyroxine Binding Globulin ◽  
Time Points ◽  
Pituitary Thyroid Axis ◽  
Serum T4 ◽  
Thyroid Axis ◽  
Immature Group

Abstract The purpose of this study was to measure serum T4, free T4, TSH, T3, rT3, T4 sulfate, and thyroxine binding globulin at four time points within the first 24 h of life (cord and 1, 7, and 24 h) in infants between 24 and 34 wk gestation. The infants were subdivided into gestational age groups: 24–27 wk (n = 22); 28–30 wk (n = 26); and 31–34 wk (n = 24). The TSH surge in the first hour of postnatal life was markedly attenuated in infants of 24–27 wk gestation [8 compared with 20 (28–30 wk) and 23 mU/liter (31–34 wk)]. T4 levels in the most immature group declined over the first 24 h, whereas levels increased in the more mature groups [mean cord and 24-h levels: 65 and 59 (NS) vs. 70 and 84 (P < 0.002) vs. 98 and 125 (NS) nmol/liter]. Free T4 and T3 showed only small, transient increases in the most immature group and progressively larger and sustained increases in the other gestational groups. rT3 and T4 sulfate levels in cord serum were higher in the most immature infants, and in all groups levels decreased initially and then variably increased. The features of a severely attenuated or failed hypothalamic-pituitary-thyroid response to delivery critically define this 24- to 27-wk group as distinct from more mature preterm infants.

scholarly journals Distinct Roles of Deiodinases on the Phenotype of Mct8 Defect: A Comparison of Eight Different Mouse Genotypes

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1180-1191 ◽  
Author(s):  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Alexandra M. Dumitrescu ◽  
Arturo Hernandez ◽  
Jacqueline Van Sande ◽  
...  
Keyword(s):  
Growth Response ◽  
Pituitary Thyroid Axis ◽  
Severe Impairment ◽  
Serum T3 ◽  
Serum T4 ◽  
Thyroid Axis ◽  
Mct8 Deficiency ◽  
The Brain ◽  
Insight Into ◽  
Serum Tsh

Mice deficient in the thyroid hormone (TH) transporter Mct8 (Mct8KO) have increased 5′-deiodination and impaired TH secretion and excretion. These and other unknown mechanisms result in the low-serum T4, high T3, and low rT3 levels characteristic of Mct8 defects. We investigated to what extent each of the 5′-deiodinases (D1, D2) contributes to the serum TH abnormalities of the Mct8KO by generating mice with all combinations of Mct8 and D1 and/or D2 deficiencies and comparing the resulting eight genotypes. Adding D1 deficiency to that of Mct8 corrected the serum TH abnormalities of Mct8KO mice, normalized brain T3 content, and reduced the impaired expression of TH-responsive genes. In contrast, Mct8D2KO mice maintained the serum TH abnormalities of Mct8KO mice. However, the serum TSH level increased 27-fold, suggesting a severely impaired hypothalamo-pituitary-thyroid axis. The brain of Mct8D2KO manifested a pattern of more severe impairment of TH action than Mct8KO alone. In triple Mct8D1D2KO mice, the markedly increased serum TH levels produced milder brain defect than that of Mct8D2KO at the expense of more severe liver thyrotoxicosis. Additionally, we observed that mice deficient in D2 had an unexplained marked reduction in the thyroid growth response to TSH. Our studies on these eight genotypes provide a unique insight into the complex interplay of the deiodinases in the Mct8 defect and suggest that D1 contributes to the increased serum T3 in Mct8 deficiency, whereas D2 mainly functions locally, converting T4 to T3 to compensate for distinct cellular TH depletion in Mct8KO mice.

Effect of winter sleep on pituitary-thyroid axis in American black bear.

1979 ◽  
Vol 237 (3) ◽  
pp. E227 ◽  
Author(s):  
F Azizi ◽  
J E Mannix ◽  
D Howard ◽  
R A Nelson
Keyword(s):  
Black Bear ◽  
Delayed Response ◽  
American Black Bear ◽  
Pituitary Thyroid Axis ◽  
Serum T3 ◽  
Serum T4 ◽  
Thyroid Axis ◽  
American Black ◽  
Maximum Increment ◽  
Winter Sleep

During winter sleep the black bear has decreased levels of serum total and free thyroxine (T4) and triiodothyronine (T3) and a prolonged, delayed response of serum thyrotropin (TSH) (bioassay) to thyrotropin-releasing hormone (TRH). Four weeks after the end of winter sleep, levels of serum thyroid hormones increase, and TSH response to TRH is short and brisk. Serum T4 and T3 rise after TRH administration both during and after winter sleep; however, the maximum increment in serum T3 is greater during winter sleep when the TSH rise is also prolonged and exaggerated. These observations suggest that transient hypothyroidism of possible hypothalamic origin occurs in bears during winter sleep.

Serum concentrations of thyrotropin, thyroxine, triiodothyronine and thyroxine binding globulin in female endurance runners and joggers

1987 ◽  
Vol 114 (1) ◽  
pp. 41-46 ◽  
Author(s):  
H. Hohtari ◽  
A. Pakarinen ◽  
A. Kauppila
Keyword(s):  
Endurance Training ◽  
Anterior Pituitary ◽  
Luteal Phase ◽  
Serum Concentrations ◽  
Endurance Running ◽  
Thyroxine Binding Globulin ◽  
Trh Stimulation ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Serum Tsh

Abstract. The effects of endurance training and season on the function of the anterior pituitary-thyroid axis were studied in 18 female runners and their 12 controls, and in 13 joggers and their 11 controls in Northern Finland, with a large seasonal difference in environmental factors. The serum concentrations of thyrotropin (TSH), thyroxine (T4), free thyroxine (fT4), triiodothyronine (T3), thyroxine binding globulin (TBG) and oestradiol (E2) were measured during one menstrual cycle in the light training season (autumn) and in the hard training season (spring). The responses of TSH to intravenous TRH stimulation were also measured in the luteal phase of the cycle during the hard training season. Endurance running did not affect the basal or TRH-stimulated serum TSH concentrations, while those of T4 and fT4 in runners were lowered in both seasons and that of T3 in the light training season in relation to control subjects. The serum concentrations of TBG were also significantly lower in runners than their controls in the luteal phase in both seasons. The effect of jogging on thyroid hormones was less pronounced. Serum concentrations of TSH, T4, fT4, T3 and TBG were generally slightly higher in spring than in autumn. Strenuous endurance training seems to have minor changes on the function of the thyroid gland. Depressed T4 levels in runners may rather be due to lowered TBG levels than due to direct effect of training. In spring the function of anterior pituitary-thyroid axis is more active than in autumn.

scholarly journals Thyroid dysfunction in preterm infants born before 32 gestational weeks

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Hye-Rim Kim ◽  
Young Hwa Jung ◽  
Chang Won Choi ◽  
Hye Rim Chung ◽  
Min-Jae Kang ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Thyroid Dysfunction ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Function Tests ◽  
Academic Center ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis ◽  
Delayed Maturation ◽  
Levothyroxine Treatment ◽  
Serum Tsh

Abstract Background Thyroid hormones are critical for growth and brain development during the newborn period and infancy. Because of delayed maturation of the hypothalamic-pituitary-thyroid axis in preterm infants, thyroid dysfunction is common, and thyroid stimulating hormone (TSH) elevation is often delayed in preterm infants. The objective of this study was to determine the incidence of thyroid dysfunction requiring levothyroxine treatment and to identify its risk factors in preterm infants. Methods A retrospective cohort study was performed on preterm infants who were born before 32 gestational weeks and admitted to a single tertiary academic center for more than 8 weeks between January 2008 and December 2014. In these infants, serial thyroid function tests (TFTs) measuring serum TSH and free thyroxine (fT4) were routinely performed at 1, 3, and 6 weeks of postnatal age. Results Of the 220 preterm infants enrolled, 180 infants underwent TFTs at 1, 3, and 6 weeks of postnatal age and were included in the study. Of the 180 infants, 35 infants (19.4%) were started on levothyroxine treatment based on the results of serial TFTs. Among the 35 infants who were treated with levothyroxine, 16 infants (45.7%) had normal results on the initial TFT. Three of these 16 infants continued to have normal results on the second TFT. Thyroid dysfunction requiring levothyroxine treatment was significantly associated with maternal pregnancy-induced hypertension (adjusted odds ratio 2.64, 95% confidence interval 1.02–6.81). Conclusions Thyroid dysfunction requiring levothyroxine treatment occurred in nearly one-fifth of preterm infants born before 32 gestational weeks. Nearly half of the preterm infants who were treated with levothyroxine had normal TSH and fT4 levels at 1 week of postnatal age. The findings of the present study suggest that serial TFTs is important to find preterm infants who require levothyroxine treatment.

Longitudinal Assessment of Pituitary-Thyroid Axis and Adrenal Function in Preterm Infants Raised by ‘Kangaroo Mother Care’

2002 ◽  
Vol 57 (1-2) ◽  
pp. 22-26 ◽  
Author(s):  
Aron Weller ◽  
Aviram Rozin ◽  
Abraham Goldstein ◽  
Nathalie Charpak ◽  
Juan G. Ruiz-Pelaez ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Kangaroo Mother Care ◽  
Adrenal Function ◽  
Longitudinal Assessment ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Significance of Transient Postnatal Hypothyroxinemia in Premature Infants With and Without Respiratory Distress Syndrome

PEDIATRICS ◽  
1981 ◽  
Vol 68 (4) ◽  
pp. 494-498
Author(s):  
Anthony J. Hadeed ◽  
Lyal D. Asay ◽  
Alan H. Klein ◽  
Delbert A. Fisher
Keyword(s):  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Preterm Infants ◽  
Premature Infants ◽  
Intellectual Development ◽  
Distress Syndrome ◽  
Free T4 ◽  
Term Infants ◽  
Serum T4 ◽  
Relative Delay

The significance of relatively low thyroxine (T4) levels in preterm infants with and without respiratory distress syndrome (RDS) was assessed by evaluating the free T4 level, the thyrotropin (TSH) response to thyrotropin releasing hormone (TRH), and intellectual development in infants ≤35 weeks with cord blood T4 concentrations sjlt 6.5 µg/100 ml. Fifty-four (19 well, 28 with RDS, and seven without RDS and sick) of 215 premature infants (25%) and 27 of 8,831 term infants (0.3%) had cord T4 levels sjlt 6.5 µg/100 ml. Serum T4 levels were measured in 39 surviving preterm infants (20 RDS and 19 well) during the first 5 days of life and at 2, 4, 24, and 52 weeks postnatally. Serum total T4 level during the first week was 4.5 ± 0.3 µg/100 ml (mean ± SEM). Free T4 levels ranged from 1.1 to 2.2 ng/100 ml (normal adult range 0.8 to 2.3 ng/100 ml). Administration of TRH resulted in a clear increase in both TSH and T4 levels in all infants. T4 levels increased significantly (r = .70, P sjlt .01) with increasing postnatal age, reaching stable levels by 6 to 7 weeks. Developmental quotients obtained in the infants with low T4 levels were no different from those found in a matched control population at 12 months of age. The low T4, free T4, and TSH concentrations and normal TSH responses to TRH found in these infants are characteristic of hypothalamic (tertiary) hypothyroidism, but differ from classic tertiary hypothyroidism in that the disorder was transient. The normal intellectual development at 12 months of age and the spontaneous increase in T4 levels that occurs over the first six weeks of life suggest that the low T4 levels in these infants reflect a benign relative delay in maturation of hypothalamic-pituitary-thyroid control.

scholarly journals In Vivo Interaction of Steroid Receptor Coactivator (SRC)-1 and the Activation Function-2 Domain of the Thyroid Hormone Receptor (TR) β in TRβ E457A Knock-In and SRC-1 Knockout mice

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3927-3934 ◽  
Author(s):  
Manuela Alonso ◽  
Charles Goodwin ◽  
XiaoHui Liao ◽  
Tania Ortiga-Carvalho ◽  
Danielle S. Machado ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormone Receptor ◽  
Steroid Receptor ◽  
Activation Function ◽  
Steroid Receptor Coactivator ◽  
Pituitary Thyroid Axis ◽  
Serum T4 ◽  
Thyroid Axis

The activation function-2 (AF-2) domain of the thyroid hormone (TH) receptor (TR)-β is a TH-dependent binding site for nuclear coactivators (NCoA), which modulate TH-dependent gene transcription. In contrast, the putative AF-1 domain is a TH-independent region interacting with NCoA. We determined the specificity of the AF-2 domain and NCoA interaction by evaluating thyroid function in mice with combined disruption of the AF-2 domain in TRβ, due to a point mutation (E457A), and deletion of one of the NCoAs, steroid receptor coactivator (SRC)-1. The E457A mutation was chosen because it abolishes NCoA recruitment in vitro while preserving normal TH binding and corepressor interactions resulting in resistance to TH. At baseline, disruption of SRC-1 in the homozygous knock-in (TRβE457A/E457A) mice worsened the degree of resistance to TH, resulting in increased serum T4 and TSH. During TH deprivation, disruption of AF-2 and SRC-1 resulted in a TSH rise 50% of what was seen when AF-2 alone was removed, suggesting that SRC-1 was interacting outside of the AF-2 domain. Therefore, 1) during TH deprivation, SRC-1 is necessary for activating the hypothalamic-pituitary-thyroid axis; 2) ligand-dependent repression of TSH requires an intact AF-2; and 3) SRC-1 may interact with the another region of the TRβ or the TRα to regulate TH action in the pituitary. This report demonstrates the dual interaction of NCoA in vivo: the TH-independent up-regulation possibly through another domain and TH-dependent down-regulation through the AF-2 domain.

scholarly journals Disruption of the Melanin-Concentrating Hormone Receptor 1 (MCH1R) Affects Thyroid Function

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6145-6154 ◽  
Author(s):  
Shinjae Chung ◽  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Jacqueline Van Sande ◽  
Zhiwei Wang ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Hormone Secretion ◽  
Zona Incerta ◽  
Wild Type ◽  
Free T4 ◽  
Thyroid Follicular Cells ◽  
Pituitary Thyroid Axis ◽  
Melanin Concentrating Hormone ◽  
Thyroid Axis ◽  
Follicle Size

Abstract Melanin-concentrating hormone (MCH) is a peptide produced in the hypothalamus and the zona incerta that acts on one receptor, MCH receptor 1 (MCH1R), in rodents. The MCH system has been implicated in the regulation of several centrally directed physiological responses, including the hypothalamus-pituitary-thyroid axis. Yet a possible direct effect of the MCH system on thyroid function has not been explored in detail. We now show that MCH1R mRNA is expressed in thyroid follicular cells and that mice lacking MCH1R [MCH1R-knockout (KO)] exhibit reduced circulating iodothyronine (T4, free T4, T3, and rT3) levels and high TRH and TSH when compared with wild-type (WT) mice. Because the TSH of MCH1R-KO mice displays a normal bioactivity, we hypothesize that their hypothyroidism may be caused by defective thyroid function. Yet expression levels of the genes important for thyroid hormones synthesis or secretion are not different between the MCH1R-KO and WT mice. However, the average thyroid follicle size of the MCH1R-KO mice is larger than that of WT mice and contained more free and total T4 and T3 than the WT glands, suggesting that they are sequestered in the glands. Indeed, when challenged with TSH, the thyroids of MCH1R-KO mice secrete lower amounts of T4. Similarly, secretion of iodothyronines in the plasma upon 125I administration is significantly reduced in MCH1R-KO mice. Therefore, the absence of MCH1R affects thyroid function by disrupting thyroid hormone secretion. To our knowledge, this study is the first to link the activity of the MCH system to the thyroid function.

scholarly journals Reversal of Physiological Deficits Caused by Diminished Levels of Peptidylglycine α-Amidating Monooxygenase by Dietary Copper

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1739-1747 ◽  
Author(s):  
D. Bousquet-Moore ◽  
X. M. Ma ◽  
E. A. Nillni ◽  
T. A. Czyzyk ◽  
J. E. Pintar ◽  
...  
Keyword(s):  
Body Temperature ◽  
Mrna Levels ◽  
Wild Type ◽  
Dietary Copper ◽  
Physiological Functions ◽  
Pituitary Thyroid Axis ◽  
Serum T4 ◽  
Thyroid Axis ◽  
Genetic Deletion ◽  
Maintain Body Temperature

Amidated peptides are critically involved in many physiological functions. Genetic deletion of peptidylglycine α-amidating monooxygenase (PAM), the only enzyme that can synthesize these peptides, is embryonically lethal. The goal of the present study was the identification of physiological functions impaired by haploinsufficiency of PAM. Regulation of the hypothalamic-pituitary-thyroid axis and body temperature, functions requiring contributions from multiple amidated peptides, were selected for evaluation. Based on serum T4 and pituitary TSH-β mRNA levels, mice heterozygous for PAM (PAM+/−) were euthyroid at baseline. Feedback within the hypothalamic-pituitary-thyroid axis was impaired in PAM+/− mice made hypothyroid using a low iodine/propylthiouracil diet. Despite their normal endocrine response to cold, PAM+/− mice were unable to maintain body temperature as well as wild-type littermates when kept in a 4 C environment. When provided with additional dietary copper, PAM+/− mice maintained body temperature as well as wild-type mice. Pharmacological activation of vasoconstriction or shivering also allowed PAM+/− mice to maintain body temperature. Cold-induced vasoconstriction was deficient in PAM+/− mice. This deficit was eliminated in PAM+/− mice receiving a diet with supplemental copper. These results suggest that dietary deficiency of copper, coupled with genetic deficits in PAM, could result in physiological deficits in humans.

scholarly journals Assessment of Thyroid Functions in Late Preterm Infants of Mothers on Antenatal Steroids

2021 ◽  
Vol 2 (4) ◽  
pp. 18-29
Author(s):  
Rasha T Hamza ◽  
Amira I Hamed ◽  
Basma B B Hassan ◽  
Wafaa O Ahmed
Keyword(s):  
Preterm Infants ◽  
Late Preterm ◽  
Antenatal Corticosteroids ◽  
Free T4 ◽  
Cross Sectional ◽  
Late Preterm Infants ◽  
The Third ◽  
Antenatal Steroids ◽  
Serum T4 ◽  
Group 1

Purpose: The study examined the effect of antenatal steroids on thyroid functions in late preterm infants on the third to the seventh day of life. Patients and Methods: A comparative Cross-Sectional study was conducted on 75 neonates admitted to NICU in the first week of life. They were divided according to exposure to antenatal steroids into three groups. First group: exposed to complete course of ANS. Second group: exposed to partial course of ANS. The third group: not exposed to ANS. Serum samples were obtained from selected cases free T3, Free T4, and TSH levels in the third day of life, compared to the cut of levels currently available (the TSH reference range is (1.7 to 9.1 mU per L), T4 should be greater than( 10 mcg per dL). Using Eleusis and Cubase analyzers kits (Roche Diagnostics, Indianapolis, IN, USA) by ELISA (enzyme-linked immune sorbent assay) technique. Results: The study showed that there were significantly higher serum T4 levels in group 1 that was exposed to a complete course compared to group 2 (partial course) and 3 (Third group). There were no significant differences in serum TSH, T3 levels between groups. The current study found a decreased incidence of the ROP, NEC and BPD among group 1 as compared to the other two groups although was non statistically significant. In addition, the complete course of ANS had delayed the date of delivery (P=0.04) as compared to the partial course in the current study. Conclusion: Antenatal corticosteroids can influence thyroid function in late preterm infants as serum T4 was significantly higher in infants exposed to complete course compared to those who were exposed to partial course or did not receive antenatal corticosteroids.

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