| Reference | [1]. Levothyroxine.<br />
Drugs and Lactation Database (LactMed) [Internet]. Bethesda (MD): National Library of Medicine (US); 2006–. 2021 Jun 21.<br />
Levothyroxine (T4) is a normal component of human milk. Limited data on exogenous replacement doses of levothyroxine during breastfeeding indicate no adverse effects in infants. The American Thyroid Association recommends that subclinical and overt hypothyroidism should be treated with levothyroxine in lactating women seeking to breastfeed.[1] Levothyroxine dosage requirement may be increased in the postpartum period compared to prepregnancy requirements patients with Hashimoto's thyroiditis.[2]<br />
PMID: 30000062<br />
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[2]. Front Endocrinol (Lausanne). 2019 Jun 4;10:350. doi: 10.3389/fendo.2019.00350. eCollection 2019.<br />
Thyroid Hormone Action on Innate Immunity.<br />
Montesinos MDM(1), Pellizas CG(1).<br />
Author information: (1)Facultad de Ciencias Químicas, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI-CONICET) and Departamento de Bioquímica Clínica, Universidad Nacional de Córdoba, Córdoba, Argentina.<br />
Erratum in Front Endocrinol (Lausanne). 2019 Jul 19;10:486.<br />
The interplay between thyroid hormone action and the immune system has been established in physiological and pathological settings. However, their connection is complex and still not completely understood. The thyroid hormones (THs), 3,3',5,5' tetraiodo-L-thyroxine (T4) and 3,3',5-triiodo-L-thyronine (T3) play essential roles in both the innate and adaptive immune responses. Despite much research having been carried out on this topic, the available data are sometimes difficult to interpret or even contradictory. Innate immune cells act as the first line of defense, mainly involving granulocytes and natural killer cells. In turn, antigen presenting cells, macrophages and dendritic cells capture, process and present antigens (self and foreign) to naïve T lymphocytes in secondary lymphoid tissues for the development of adaptive immunity. Here, we review the cellular and molecular mechanisms involved in T4 and T3 effects on innate immune cells. An overview of the state-of-the-art of TH transport across the target cell membrane, TH metabolism inside these cells, and the genomic and non-genomic mechanisms involved in the action of THs in the different innate immune cell subsets is included. The present knowledge of TH effects as well as the thyroid status on innate immunity helps to understand the complex adaptive responses achieved with profound implications in immunopathology, which include inflammation, cancer and autoimmunity, at the crossroads of the immune and endocrine systems.<br />
DOI: 10.3389/fendo.2019.00350 PMCID: PMC6558108 PMID: 31214123<br />
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[3]. J Pharm Biomed Anal. 2010 Nov 2;53(3):688-92. doi: 10.1016/j.jpba.2010.03.018. Epub 2010 Mar 27.<br />
Ion-trap mass spectrometry for determination of 3,5,3'-triiodo-L-thyronine and 3,5,3',5'-tetraiodo-L-thyronine in neonatal rat cardiomyocytes.<br />
Vacek J(1), Kosina P, Gabrielová E, Modrianský M, Ulrichová J.<br />
Author information: (1)Department of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacký University, Hnevotínská 3, 775 15 Olomouc, Czech Republic. [email protected]<br />
Our short report describes a method employing electrospray ion-trap mass spectrometry (MS) connected to a reversed phase (C(8)) HPLC system for monitoring of 3,5,3'-triiodo-L-thyronine (T3) and its precursor 3,5,3',5'-tetraiodo-L-thyronine (T4) in neonatal rat cardiomyocytes. The experimental protocol allows simultaneous analysis of the free thyroid hormones in nanomolar concentration range and enables observation of their distribution in cultivation medium over time. The method is a useful tool for MS(2) identification of T3/T4 and analysis of their uptake into mammalian cells.<br />
DOI: 10.1016/j.jpba.2010.03.018 PMID: 20403674 [Indexed for MEDLINE]<br />
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[4]. Gene Expr. 2017 Nov 27;17(4):265-275. doi: 10.3727/105221617X14968563796227. Epub 2017 Jun 13.<br />
GC-1: A Thyromimetic With Multiple Therapeutic Applications in Liver Disease.<br />
Columbano A(1), Chiellini G(2), Kowalik MA(1).<br />
Author information: (1)Department of Biomedical Sciences, Unit of Oncology and Molecular Pathology, University of Cagliari, Cagliari, Italy. (2)Department of Surgical, Medical and Molecular Pathology, University of Pisa, Pisa, Italy.<br />
Thyroid hormones (THs), namely, 3,5,3'-triiodo-l-thyronine (T3) and 3,5,3',5'-tetraiodo-l-thyronine (thyroxine or T4), influence a variety of physiological processes that have important implications in fetal development, metabolism, cell growth, and proliferation. While THs elicit several beneficial effects on lipid metabolism and improve myocardial contractility, these therapeutically desirable effects are associated to a thyrotoxic state that severely limits the possible use of THs as therapeutic agents. Therefore, several efforts have been made to develop T3 analogs that could retain the beneficial actions (triglyceride, cholesterol, obesity, and body mass lowering) without the adverse TH-dependent side effects. This goal was achieved by the synthesis of TRβ-selective agonists. In this review, we summarize the current knowledge on the effects of one of the best characterized TH analogs, the TRβ1-selective thyromimetic, GC-1. In particular, we review some of the effects of GC-1 on different liver disorders, with reference to its possible clinical application. A brief comment on the possible therapeutic use of GC-1 in extrahepatic disorders is also included.<br />
DOI: 10.3727/105221617X14968563796227 PMCID: PMC5885148 PMID: 28635586 [Indexed for MEDLINE]<br />
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[5]. Front Endocrinol (Lausanne). 2014 Mar 31;5:40. doi: 10.3389/fendo.2014.00040. eCollection 2014.<br />
Thyroid hormones, t3 and t4, in the brain.<br />
Schroeder AC(1), Privalsky ML(1).<br />
Author information: (1)Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California Davis , Davis, CA , USA.<br />
Thyroid hormones (THs) are essential for fetal and post-natal nervous system development and also play an important role in the maintenance of adult brain function. Of the two major THs, T4 (3,5,3',5'-tetraiodo-l-thyronine) is classically viewed as an pro-hormone that must be converted to T3 (3,5,3'-tri-iodo-l-thyronine) via tissue-level deiodinases for biological activity. THs primarily mediate their effects by binding to thyroid hormone receptor (TR) isoforms, predominantly TRα1 and TRβ1, which are expressed in different tissues and exhibit distinctive roles in endocrinology. Notably, the ability to respond to T4 and to T3 differs for the two TR isoforms, with TRα1 generally more responsive to T4 than TRβ1. TRα1 is also the most abundantly expressed TR isoform in the brain, encompassing 70-80% of all TR expression in this tissue. Conversion of T4 into T3 via deiodinase 2 in astrocytes has been classically viewed as critical for generating local T3 for neurons. However, deiodinase-deficient mice do not exhibit obvious defectives in brain development or function. Considering that TRα1 is well-established as the predominant isoform in brain, and that TRα1 responds to both T3 and T4, we suggest T4 may play a more active role in brain physiology than has been previously accepted.<br />
DOI: 10.3389/fendo.2014.00040 PMCID: PMC3978256 PMID: 24744751
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