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Clinical Applications of Immunoassays
Published in Richard O’Kennedy, Caroline Murphy, Immunoassays, 2017
Thyroid hormone abnormalities are usually due to thyroid gland dysfunction. Thyroid-stimulating hormone (TSH) stimulates the release of thyroxine (T4) and triiodothyronine (T3) from the thyroid gland, which exerts a negative feedback on TSH production. In hyperthyroidism, serum concentrations of TSH are low, while T4 and T3 are elevated. Conversely in hypothyroidism, serum concentrations of TSH are high, while T4 and T3 are low. Thyroid function is assessed by measuring the serum concentrations of TSH, total T4, total T3 and free T4 or T3. The normal range for TSH is 0.4 to 5 mU L−1. Current methods used to measure TSH include chemiluminometric assays, which have very low detection limits (0.01 U L−1) and can diagnose the mildest forms of hyperthyroidism [46]. Serum total T4 and T3 are usually measured by radioimmunoassay (RIA) or chemiluminometric assay, measuring both the bound and unbound T4 to the carrier protein thyroxine binding globulin (TBG). The unbound or free T4 or T3 is more useful in the interpretation of thyroid disease as TBG levels are altered in various conditions including pregnancy, drug use, hepatitis and malnutrition [47]. Autoimmunity also plays a major role in hypo- and hyperthyroidism and can be detected using immunoassays [48]. Anti-thyroglobulin autoantibodies are present in 60% of cases in a hypothyroid condition known as Hashimoto’s thyroiditis, while anti-microsomal antibodies are present in 90%. In Graves’ disease, thyroid stimulating hormone receptor antibodies (TSHR-Abs) stimulate the release of T4 and T3 leading to a hyperthyroid condition known as Graves’ thyrotoxicosis. Almost all patients with Graves’ disease have detectable TSHR-Abs, which can be measured using immunoassays; however, lower concentrations of both anti-thyroglobulin and anti-microsomal antibodies can also found in Graves’ disease.
Urinary levels of phthalate esters and heavy metals in adolescents with thyroid colloid cysts
Published in International Journal of Environmental Health Research, 2022
S. Songül Yalçin, İzzet Erdal, Semra Çetinkaya, Berna Oğuz
Phthalates are added to food packages, drugs, toys, cosmetics, detergents and pesticides for technological and industrial purposes (Wang et al. 2019). Heavy metals are found in nature and can be consumed through different routes with dietary supplements or cigarettes, and contaminated air, water and food in daily life (Tchounwou et al. 2012). WHO has announced four heavy metals including As, Cd, Pb and Hg in ‘ten chemicals of major public health concern’ (WHO, 2010). Their uncontrolled usage poses serious threat to the environment and increases the possibility of adverse effects on human health. In addition, children are more sensitive to the toxicity of contaminants than adults and exposures in children are reported to be higher than adults (Wang et al. 2019; Zhou and Ma 2019). Phthalates and heavy metals are shown to interfere with hormonal processes, including endocrine disruptions in both children and adults (Boas et al. 2006; Meeker and Ferguson 2011; de Cock et al. 2014). Some endocrine disrupting chemicals (EDCs) may change thyrotropin-releasing hormone (TRH)-stimulated thyroid-stimulating hormone (TSH) secretion or inhibit iodide uptake and thyroid peroxidase (TPO). Moreover, the proposed indirect effects include changing thyroxine-binding globulin (TBG) and albumin levels, the T4:T3 ratio, the levels of deiodinase enzyme, and the clearance of thyroid hormones with glucuronyltransferase (UDP-GT) (Price et al. 1988; Sutcliffe and Harvey 2015). The suggested direct and indirect effects of EDCs on thyroid hormone homeostasis require additional studies on the thyroid gland.
Association between polychlorinated biphenyl exposure and thyroid hormones: a systematic review and meta-analysis
Published in Journal of Environmental Science and Health, Part C, 2022
Christine C. Little, Joshua Barlow, Mathilda Alsen, Maaike van Gerwen
In addition to effects mediated by structural homology, PCBs are known to disrupt metabolism of thyroid hormones through alterations in the enzymatic processes of deiodination and glucuronidation. PCBs have been shown to upregulate T4 glucuronidation via induction of hepatic UDP-glucuronosyltransferase in rat models, thereby reducing levels of circulating T4.7,44 Additionally, PCBs may impact thyroid homeostasis by disrupting extrathyroidal conversion of T4 to T3. Conversion of T4 to its biologically active form T3 is tightly controlled by three types of deiodinases in human metabolism. Type-I and type-II deiodinases catalyze the removal of iodine residues from the outer ring of T4 to form T3, whereas type-III deiodinase catalyzes the removal of iodine from the inner ring of T4 or T3 to form the biologically inactive hormone reverse T3 (rT3).45 PCBs have been demonstrated to decrease activity of type-I and type-II deiodinases,7,45,46 while increasing activity of type-III deiodinase,47 though it is important to note that many of these effects appear to be tissue-dependent and vary between studies. Thus, PCB exposure may decrease circulating levels of T3 by impairing conversion of T4 into T3 and by promoting inactivation of T3 into rT3. In addition, PCBs have been shown to alter male and female reproductive hormones due to their estrogen-like structure.48–50 Reproductive hormones are known to directly influence thyroid hormone levels through regulation of the transport protein thyroxine binding globulin, providing an indirect pathway through which PCBs may disrupt thyroid hormone homeostasis.51–53
Nexus between perfluoroalkyl compounds (PFCs) and human thyroid dysfunction: A systematic review evidenced from laboratory investigations and epidemiological studies
Published in Critical Reviews in Environmental Science and Technology, 2021
Weiping Xie, Wei Zhong, Brice M. R. Appenzeller, Jianqing Zhang, Muhammad Junaid, Nan Xu
T3 and T4 are the only halogenated (-iodine) functional biological molecules inside the human body. Similarly, PFCs are also halogenated (-fluorine) compounds, exhibiting active sites that structurally resemble T3 and T4 (Berg et al., 2015). Therefore, binding of PFCs to serum proteins can affect the transport and metabolism of these hormones. Competitive binding of PFCs with transport proteins could displace THs and disturb their normal circulating levels in serum. For instance, in rats, the reduction of the responsiveness of the HPT axis and displacement of circulating THs from blood protein (albumin) binding sites were suggested as the earliest evidence of potential mechanisms of PFDA-mediated thyroid toxicity (Gutshall et al., 1988; Langley & Pilcher, 1985). Weiss et al. (2009) also showed that PFOS could compete with T4 for binding sites on transthyretin (TTR), which could reduce blood THs levels. Among many in vivo studies, an interesting common observation is that the PFC exposure frequently decreased TH levels without a compensatory increase in TSH levels, which supports the hypothesis that PFCs displaces THs to bind with transport proteins (Chang et al., 2009; Shi et al., 2009; Thibodeaux et al., 2003; Yu et al., 2009). A competitive binding assay evaluated by combining protein mutagenesis and computational modeling revealed that the binding affinities of TTR were much stronger than those of thyroxine-binding globulin (TBG) for the same congener of PFCs (Ren et al., 2016). This potential competitive mechanism, if indeed present, could also explain why an epidemiological study reported negative associations of perfluorotridecanoic acid (PFTrDA) with circulating T4 levels, but a positive association with TSH among people with elevated PFC exposure (Ji et al., 2012).