Maternal thyroid hormone programs cardiovascular functions in the offspring

Thyroid ◽  
2021 ◽  
Author(s):  
Mehdi Pedaran ◽  
Rebecca Oelkrug ◽  
Qian Sun ◽  
Julia Resch ◽  
Lutz Schomburg ◽  
...  
2011 ◽  
Vol 4 (3) ◽  
pp. 357-358
Author(s):  
Dr. Aditi Choubey ◽  
◽  
Dr. T.M. Panchanadikar Dr. T.M. Panchanadikar ◽  
Dr. Alpesh Patel ◽  
Dr. Deven Jogal

PEDIATRICS ◽  
1993 ◽  
Vol 91 (6) ◽  
pp. 1203-1209
Author(s):  

Congenital hypothyroidism (CH) represents one of the most common preventable causes of mental retardation. The fetal hypothalamic-pituitary-thyroid axis begins to function by midgestation and is mature in the term infant at delivery. If fetal hypothyroidism develops, untoward effects may be demonstrated in certain organ systems, including the central nervous system and skeleton. However, most infants with CH appear normal at birth. Recent data suggest that the hypothyroid fetus is protected to a certain extent by placental transfer of maternal thyroid hormone; serum thyroxine (T4) levels in the cord blood of athyroid fetuses approximate one third of maternal levels.1 In addition, studies in animal models of hypothyroidism demonstrate increased levels of brain iodothyronine deiodinase, the enzyme which converts T4 to triiodothyronine (T3). In the hypothyroid fetus, this increased enzyme acting on T4 of maternal origin is sufficient to produce near normal fetal brain T3 concentrations.2 Thus, it appears that early detection and treatment of congenital hypothyroidism should have the potential to completely reverse the effects of fetal hypothyroidism in all but the most severe cases, for example, athyreotic infants born to mothers with thyroid problems resulting in inadequate placental transfer of maternal thyroid hormone. Since the development of pilot screening programs for CH in Quebec and Pittsburgh in 1974,3 newborn screening for CH has become routine in essentially all developed countries of the world and is under development in Eastern Europe, South America, Asia, and Africa. In North America it is estimated that more than 5 million newborns are screened, with approximately 1400 infants with congenital hypothyroidism detected annually.


1993 ◽  
pp. 171-180 ◽  
Author(s):  
Gabriella Morreale de Escobar ◽  
María Jesús Obregón ◽  
Rosa Calvo ◽  
Francisco Escobar del Rey

2012 ◽  
Vol 237 (2) ◽  
pp. 477-488 ◽  
Author(s):  
Vishwa Mohan ◽  
Rohit A. Sinha ◽  
Amrita Pathak ◽  
Leena Rastogi ◽  
Praveen Kumar ◽  
...  

2017 ◽  
Vol 21 (1) ◽  
pp. 17-21
Author(s):  
Nandita Hazra ◽  
Binay Mitra ◽  
Reetika Pal

ABSTRACT Aim Maternal thyroid hormone levels during pregnancy are vital for the health of the mother as well as the developing child. Fetal growth is affected by maternal thyroid levels. Various physiological changes like alterations of thyroxine-binding globulins, human chorionic gonadotropin level, and changes in iodide metabolism affect maternal thyroid hormone levels. Therefore, reference intervals (RIs) for thyroid hormones in pregnant population require to be established separately from the general population. Materials and methods The RIs of serum triiodothyronine (T3), thyroxine (T4), and thyroid-stimulating hormone (TSH) were determined in healthy pregnant women by enzyme-linked immunosorbent assay (ELISA) technique after segregating them into three trimesters. This study was conducted in a 492-bedded zonal-level hospital. The reference population was chosen from a study population of pregnant women by strict inclusion and exclusion criteria. The assays were done by the most-commonly used, economical ELISA method employing standard kits. Tests were done using accurate and precise methods with proper quality control measures. Results The RIs were calculated from the central 95% of distribution of total T3, total T4, and TSH values located between 2.5 and 97.5 percentile values. The 0.90 confidence intervals for the upper and lower reference limits were calculated. The values thus obtained were different from those provided by the manufacturer kit literature. Conclusion It is recommended to determine one's own laboratory-specific, method-specific, trimester-wise RIs for maternal thyroid hormone status and use them for screening of pregnant women. How to cite this article Chakrabarty BK, Mitra B, Pal R, Hazra N. Specific Reference Intervals of Serum Triiodothyronine, Thyroxine, and Thyroid-stimulating Hormone in Normal Pregnant Indian Women as per Trimester. Indian J Med Biochem 2017;21(1):17-21.


2018 ◽  
Vol 88 (4) ◽  
pp. 575-584 ◽  
Author(s):  
William Thompson ◽  
Ginny Russell ◽  
Genevieve Baragwanath ◽  
Justin Matthews ◽  
Bijay Vaidya ◽  
...  

2019 ◽  
Vol 51 (06) ◽  
pp. 381-388 ◽  
Author(s):  
Jorge Tapia-Martínez ◽  
Alejandra Paola Torres-Manzo ◽  
Margarita Franco-Colín ◽  
Marisol Pineda-Reynoso ◽  
Edgar Cano-Europa

AbstractEnvironmental stimuli during critical developmental stages establish long-term physiological and structural patterns that “program” health during adult life. Little is known about how alterations in hormonal supply might have consequences in metabolic and thyroid programming. This work aims to prove that alterations in the supply of thyroid hormones during gestation and lactation have long-term consequences in the metabolic and thyroid programming of the offspring. Female Wistar rats were divided into euthyroid, hypothyroid, and hypothyroid with 20 μg/day of s.c. thyroxine (T4), replacement wet nurses. Rats were mating, and after birth, pups were grouped according to their wet nurses group. Milk quality of wet nurses was assessed on days 7, 14, and 21. Body mass gain and energy intake of the offspring were monitored for 28 weeks after weaning. At sacrifice, we extracted and weighed their thyroid gland and adipose reserves, and collected blood to measure its metabolic and thyroid profiles. Hypothyroid wet nurses presented a persistent low quality of milk, while both male and female hypothyroid offspring presented lower body mass gain, higher blood glucose, dyslipidemia, hyperinsulinemia, and hyperleptinemia, as well as lower total adipose reserves, but higher visceral reserve, diminished T3 and T4 concentrations, and lower weight of thyroid gland. Thyroxine replacement prevented all changes in both wet nurses and pups. We conclude that maternal thyroid hormone deficiency during congenital and lactation stages alters the metabolic and thyroid programming of the offspring, while the reestablishment of maternal thyroid status during critical periods of development can prevent these alterations.


2019 ◽  
Vol 194 (4) ◽  
pp. E96-E108 ◽  
Author(s):  
Bin-Yan Hsu ◽  
Irene Verhagen ◽  
Phillip Gienapp ◽  
Veerle M. Darras ◽  
Marcel E. Visser ◽  
...  

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