scholarly journals Prenatal Phthalates Exposure and Cord Thyroid Hormones: A Birth Cohort Study in Southern Taiwan

2021 ◽  
Vol 18 (8) ◽  
pp. 4323
Author(s):  
Po-Chin Huang ◽  
Pao-Lin Kuo ◽  
Wei-Hsiang Chang ◽  
Shu-Fang Shih ◽  
Wan-Ting Chang ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Cord Blood ◽  
Pregnant Women ◽  
Phthalate Metabolites ◽  
Cord Serum ◽  
Serum T4 ◽  
Southern Taiwan ◽  
Hormone Homeostasis ◽  
Serum Tsh

Background: The regulation of thyroid hormones in the early stages of gestation plays a crucial role in the outcome of a pregnancy. Furthermore, thyroid hormones are fundamental for the fetal development of all organs, including endocrine hormone changes in uterus. Endocrine disrupting chemicals have been shown to have an effect on thyroid hormone homeostasis in newborns, which affects their later development. Few studies have proposed how phthalates could alter thyroid function through several mechanisms and the possible effects on thyroid hormone homeostasis of phthalates on pregnant women. However, the effects of cord blood phthalates and prenatal phthalate exposure on thyroid hormones in newborns remain unclear. Objectives: We aim to follow up on our previous established subjects and determine the correlation between phthalate exposure and thyroid hormones in pregnant women and newborns. Materials and methods: We recruited 61 pregnant women from the Obstetrics and Gynecology Department of a medical hospital in southern Taiwan and followed up. High performance liquid chromatography electrospray ionization tandem mass spectrometry (HPLC-ESI-MS/MS) was used to analyze urine samples for five phthalate metabolites. Serum levels of thyroid hormones were analyzed using electrochemoluminescence immunoassay (ECLIA) method. We used Spearman and Pearson correlation coefficients to evaluate the correlation between each phthalate metabolites in serum and the thyroid hormone levels in fetus and parturient. Finally, multiple logistic regression was used to explore the relationship between hormones and their corresponding phthalate metabolites in cord blood. Results: High MBP in cord blood was correlated with negative cord serum TSH in newborns (r = −0.25, p < 0.06). By using multiple linear regression after adjusting for potential confounders (gestational and maternal age), cord serum MBP levels showed a negative association with cord serum TSH (β = 0.217, p < 0.05), cord serum T4 (β = 1.71, p < 0.05) and cord serum T4 × TSH (β = 42.8, p < 0.05), respectively. Conclusion: We found that levels of cord serum TSH and T4 in newborns was significantly negatively associated with cord serum MBP levels after adjusting for significant covariate. The fall in TSH in newborns may potentially be delaying their development.

Treatment of maternal hyperthyroidism with antithyroid agents and changes in thyrotrophin and thyroxine in the newborn

1981 ◽  
Vol 97 (2) ◽  
pp. 186-195 ◽  
Author(s):  
B.-A. Lamberg ◽  
E. Ikonen ◽  
K. Teramo ◽  
G. Wägar ◽  
K. Österlund ◽  
...  
Keyword(s):  
Laboratory Test ◽  
Cord Blood ◽  
Pregnant Women ◽  
Newborn Infants ◽  
Antithyroid Drug ◽  
Clinical Indication ◽  
Antithyroid Drugs ◽  
Serum Thyroxine ◽  
Antithyroid Agents ◽  
Serum Tsh

Abstract. Eleven pregnant women with concomitant hyperthyroidism were treated with antithyroid drugs. At monthly intervals serum thyroxine (T4) and triiodothyronine (T3) were measured with radioimmunoassay, the Sephadex uptake of radioactive triiodothyronine (T3U) determined and the free T4 and T3 indices calculated (FT4I, FT3I). TSH-binding inhibiting immunoglobulins (TBII) were determined by the radiomembrane assay. Serum TSH and T4 were measured at delivery from cord blood and/or from the newborn infants some days after birth. Serum TSH was significantly elevated in one infant. There was an inadequate post-partal rise in serum T4 concentration in this child and in another who showed only a marginal elevation of TSH. The mothers of these infants were given carbimazole in doses of 30 and 25 mg/day, respectively, at the time of delivery. No significant changes were seen in other infants, the daily doses being 20 mg of carbimazole or less. There was no clinical indication of hypo- or hyperthyroidism in any of the newborn. The TBII were positive in most patients and there was a trend of normalization during treatment. No relationship between the dose of antithyroid drug and the level of TBII could be seen. During treatment the dose was adjusted according to the FT3I values. This seems to be an adequate laboratory test for this purpose.

Establishment of Early Pregnancy Related Thyroid Hormone Models and Reference Intervals for Pregnant Women in China Based on Real World Data

2021 ◽  
Vol 53 (04) ◽  
pp. 272-279
Author(s):  
Chaochao Ma ◽  
Xiaoqi Li ◽  
Lixin Liu ◽  
Xinqi Cheng ◽  
Fang Xue ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Pregnant Women ◽  
Early Pregnancy ◽  
Gestational Age ◽  
Dynamic Change ◽  
Reference Intervals ◽  
Thyroid Stimulating Hormone ◽  
Free Thyroxine ◽  
Stimulating Hormone

AbstractThyroid hormone reference intervals are crucial for diagnosing and monitoring thyroid dysfunction during early pregnancy, and the dynamic change trend of thyroid hormones during pregnancy can assist clinicians to assess the thyroid function of pregnant women. This study aims to establish early pregnancy related thyroid hormones models and reference intervals for pregnant women. We established two derived databases: derived database* and derived database#. Reference individuals in database* were used to establish gestational age-specific reference intervals for thyroid hormones and early pregnancy related thyroid hormones models for pregnant women. Individuals in database# were apparently healthy non-pregnant women. The thyroid hormones levels of individuals in database# were compared with that of individuals in database* using nonparametric methods and the comparative confidence interval method. The differences in thyroid stimulating hormone and free thyroxine between early pregnant and non-pregnant women were statistically significant (p<0.0001). The reference intervals of thyroid stimulating hormone, free thyroxine and free triiodothyronine for early pregnant women were 0.052–3.393 μIU/ml, 1.01–1.54 ng/dl, and 2.51–3.66 pg/ml, respectively. Results concerning thyroid stimulating hormone and free thyroxine reference intervals of early pregnancy are comparable with those from other studies using the same detection platform. Early pregnancy related thyroid hormones models showed various change patterns with gestational age for thyroid hormones. Early pregnancy related thyroid hormones models and reference intervals for pregnant women were established, so as to provide accurate and reliable reference basis for the diagnosing and monitoring of maternal thyroid disfunction in early pregnancy.

Iodide Metabolism and Effects

2020 ◽  
pp. 25-33
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Dietary Supplement ◽  
Thyroid Function ◽  
Thyroid Stimulating Hormone ◽  
Hormone Synthesis ◽  
Serum Tsh ◽  
Tsh Stimulation ◽  
Sensitive Marker

Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.

scholarly journals A study of vascular endothelial growth factor in the cord blood of pre-eclamptics and healthy pregnant women

2017 ◽  
Vol 8 (1) ◽  
pp. 21-25
Author(s):  
Anita Rawat ◽  
Anil Kumar Gangwar ◽  
Archana Ghildiyal ◽  
Neena Srivastava ◽  
Sunita Tiwari ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Cord Blood ◽  
Pregnant Women ◽  
Assay Method ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Vascular Endothelial ◽  
Cord Serum ◽  
Endothelial Growth Factor

Background: Pre-eclampsia(PE) is  the  most  frequently encountered  medical  complication  during  pregnancy. In developing countries PE   is a principal cause of maternal mortality. A disturbance  in  the  angiogenic/antiangiogenic  factors  and  in  the  hypoxia/placental re-oxygenation  process,  seems  to  activate a maternal  endothelial  dysfunction.Aims and Objective: To estimate Vascular Endothelial Growth Factor ( VEGF )  level  in the cord blood of healthy and Preeclamptic ( PEc ) pregnant women and to associate this with Preeclamptic pregnancy.Material and Methods: A case-control study ofUmbilical cord serum VEGF levels from women with uncomplicated pregnancies (control group, n=60) and pregnancies complicated by Pre-eclampsia (n=40). VEGF in the cord serum was estimated by SANDWICH Enzyme Linked Immunosorbent Assay method by using ELISA Kit and then compared between the two groups.Results: The mean VEGF concentrations in the women who had pre-eclampsia  (578.62±468.3)  were lower than in the control group( 625.75±533.1) , but the difference was not statistically significant ( p= 0.8548).  Conclusion VEGF plays a key role in the instability between endothelial dysfunction and angiogenesis that occurs during Preeclampsia.  VEGF levels might be a useful tool for the early diagnosis of Pre-eclampsia.Asian Journal of Medical Sciences Vol.8(1) 2017 21-25

The association of thyroid hormones and blood pressure in euthyroid preadolescents

2016 ◽  
Vol 29 (4) ◽  
Author(s):  
Bo Hyun Park ◽  
Sun Jung Baik ◽  
Hye Ah Lee ◽  
Young Sun Hong ◽  
Hae Soon Kim ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Diastolic Blood Pressure ◽  
Pressure Control ◽  
Thyroid Stimulating Hormone ◽  
University Hospital ◽  
Hypertension Status ◽  
Childhood Hypertension ◽  
Serum Tsh

AbstractHypertension is the leading cause of cardiovascular disease worldwide, and both high and low blood pressures are associated with various chronic diseases. Thyroid hormones have profound effects on cardiovascular function, including on blood pressure. Recent studies have shown that childhood hypertension can lead to adult hypertension. Therefore, adequate blood pressure control is important from early life. Employing a life-course approach, we aimed to investigate the association between thyroid hormones and blood pressure in children.A total of 290 children from the Ewha Woman’s University Hospital birth cohort participated in a preadolescent check-up program. We assessed the levels of serum thyroid-stimulating hormone (TSH) and free thyroxine (FT4) and the blood pressure status in these children. Thyroid hormone concentrations were measured using an electro-chemiluminescence immunoassay (ECLIA), and hypertension was defined according to the guideline of the Korea Centers for Disease Control and Prevention.The sex-, age-, and height-adjusted prevalence of hypertension was 27.0% in the present study. On regression analysis, serum FT4 showed significantly negative association with diastolic blood pressure (DBP; β=–8.24, 95% CI: –14.19–2.28, p=0.007). However, these relationships were not significant after adjustment for sex, age, and current body mass index. The levels of serum TSH showed no relationship with mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) after adjustment. No significant differences in serum TSH and FT4 levels according to hypertension status were found.These findings suggest that thyroid hormone is not independently associated with increased blood pressure in euthyroid preadolescents.

scholarly journals A rare mutation of thyroid hormone receptor beta gene in thyroid hormone resistance syndrome

2021 ◽  
Vol 2021 ◽  
Author(s):  
Michela Del Prete ◽  
Fabrizio Muratori ◽  
Irene Campi ◽  
Gianleone Di Sacco ◽  
Federico Vignati ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Genetic Test ◽  
List Type ◽  
Thyroid Function Tests ◽  
Resistance To Thyroid Hormone ◽  
Hereditary Syndrome ◽  
Serum Tsh ◽  
Receptor Beta ◽  
Tsh Levels

Summary Resistance to thyroid hormone (RTH) is a rare hereditary syndrome with impaired sensitivity to thyroid hormones (TH) and reduced intracellular action of triiodothyronine (T3) caused by genetic variants of TH receptor beta (TRB) or alpha (TRA). RTH type beta (RTHβ) due to dominant negative variants in the TRB gene usually occurs with persistent elevation of circulating free TH, non-suppressed serum TSH levels responding to a thyrotropin-releasing hormone (TRH) test, an absence of typical symptoms of hyperthyroidism and goiter. Here, we present a rare variant in the TRB gene reported for the first time in an Italian patient with generalized RTHβ syndrome. The patient showed elevated TH, with non-suppressed TSH levels and underwent thyroid surgery two different times for multinodular goiter. The genetic test showed a heterozygous mutation in exon 9 of the TRB gene resulting in the replacement of threonine (ACG) with methionine (ATG) at codon 310 (p.M310T). RTHβ syndrome should be considered in patients with elevated TH, non-suppressed TSH levels and goiter. Learning points Resistance to thyroid hormone (RTH) is a rare autosomal dominant hereditary syndrome with impaired tissue responsiveness to thyroid hormones (TH). Diagnosis of RTH is usually based on the clinical finding of discrepant thyroid function tests and confirmed by a genetic test. RTH is a rare condition that must be considered for the management of patients with goiter, elevation of TH and non-suppressed serum TSH levels in order to avoid unnecessary treatments.

scholarly journals Combined effects of cadmium and decabrominated diphenyl ether on thyroid hormones in rats

2012 ◽  
Vol 63 (3) ◽  
pp. 255-262 ◽  
Author(s):  
Marijana Ćurčić ◽  
Saša Janković ◽  
Vesna Jaćević ◽  
Sanja Stanković ◽  
Slavica Vučinić ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Thyroid Function ◽  
Wistar Rats ◽  
Diphenyl Ether ◽  
Thyroid Stimulating Hormone ◽  
Combined Effects ◽  
Single Substance ◽  
Hormone Homeostasis ◽  
Stimulating Hormone

The aim of this study was to see how a mixture of cadmium (Cd) and decabrominated diphenyl ether (BDE209) affect thyroid function, namely thyroid-stimulating hormone (TSH), thyroxin (T4), free thyroxin (FT4), triiodothyronin (T3), and free triiodothyronin (FT3) in Wistar rats (eight per group) receiving either a single substance or their combination by gavage for 28 days. Three groups were receiving Cd alone in the doses of 2.5 mg kg-1, 7.5 mg kg-1, or 15 mg kg-1 b. w. a day, three groups were receiving BDE209 in the doses of 1000 mg kg-1, 2000 mg kg-1, or 4000 mg kg-1 b. w. a day, while nine groups were receiving different mixtures of Cd and BDE209 in these doses (3x3 design). The results have indicated that the Cd+BDE209 mixtures more potently disrupt thyroid hormone homeostasis than would be expected from these chemicals alone.

scholarly journals Modern concepts of primary thyroid gland failure

1996 ◽  
Vol 42 (1) ◽  
pp. 179-182 ◽  
Author(s):  
E C Ridgway
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Thyroid Hormones ◽  
Hormone Deficiency ◽  
Clinical Effects ◽  
Normal Range ◽  
Medical Disorder ◽  
Clinical Detection ◽  
Key Genes ◽  
Serum Tsh

Abstract Primary thyroid gland failure is a common medical disorder occurring in mild or severe forms in 10% to 15% of our population. Symptoms may be classical and easy to recognize or very subtle, escaping clinical detection. This disorder is more common in females and increases with advancing age. The most important diagnostic test is measurement of the serum thyrotropin (TSH) concentration, which will increase above the normal range in both mild and severe cases. Most clinical effects of thyroid hormone deficiency can be explained by the "nuclear thyroid hormone hypothesis," which states that thyroid hormones act predominantly by effecting the transcription of key genes in affected tissues. Therapy of hypothyroidism is easy, inexpensive, and precise, involving pure L-thyroxine and measuring dose requirements and efficacy by monitoring serum TSH concentrations.

scholarly journals Consequences of Monocarboxylate Transporter 8 Deficiency for Renal Transport and Metabolism of Thyroid Hormones in Mice

Endocrinology ◽  
2010 ◽  
Vol 151 (2) ◽  
pp. 802-809 ◽  
Author(s):  
Marija Trajkovic-Arsic ◽  
Theo J. Visser ◽  
Veerle M. Darras ◽  
Edith C. H. Friesema ◽  
Bernhard Schlott ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Psychomotor Retardation ◽  
High Serum ◽  
Monocarboxylate Transporter ◽  
Iodothyronine Deiodinase ◽  
Serum T4 ◽  
Mct8 Deficiency ◽  
Low Serum

Patients carrying inactivating mutations in the gene encoding the thyroid hormone transporting monocarboxylate transporter (MCT)-8 suffer from a severe form of psychomotor retardation and exhibit abnormal serum thyroid hormone levels. The thyroidal phenotype characterized by high-serum T3 and low-serum T4 levels is also found in mice mutants deficient in MCT8 although the cause of these abnormalities is still unknown. Here we describe the consequences of MCT8 deficiency for renal thyroid hormone transport, metabolism, and function by studying MCT8 null mice and wild-type littermates. Whereas serum and urinary parameters do not indicate a strongly altered renal function, a pronounced induction of iodothyronine deiodinase type 1 expression together with increased renal T3 and T4 content point to a general hyperthyroid state of the kidneys in the absence of MCT8. Surprisingly, accumulation of peripherally injected T4 and T3 into the kidneys was found to be enhanced in the absence of MCT8, indicating that MCT8 deficiency either directly interferes with the renal efflux of thyroid hormones or activates indirectly other renal thyroid hormone transporters that preferentially mediate the renal uptake of thyroid hormones. Our findings indicate that the enhanced uptake and accumulation of T4 in the kidneys of MCT8 null mice together with the increased renal conversion of T4 into T3 by increased renal deiodinase type 1 activities contributes to the generation of the low-serum T4 and the increase in circulating T3 levels, a hallmark of MCT8 deficiency.

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