China
Africa
Explore chapters and articles related to this topic
Thyroid
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
The thyroid follicular cell can give rise to a wide variety of neoplasms, ranging from incidental papillary microcarcinoma, which has no effect on life expectancy despite minimal treatment, to lethal anaplastic cancer, which is invariably fatal despite aggressive treatment. The majority of cases occur in young adults, but thyroid cancer can affect any age group. The age-standardized incidence in the United Kingdom has increased by around two-and-a-half times over the last 30 years from only 900 cases per year being diagnosed between 1990 and 1994 (1.7 per 100,000) to 3500 between 2014 and 2016 (5.7 per 100,000).1 This figure is predicted to rise by 74% in the UK between 2014 and 2035, to 11 cases per 100,000 people by 2035.
Thyroid Hormones and Calcium Metabolism
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Thyroglobulin, a large glycoprotein that contains 70 tyrosine residues, is synthesized in the endoplasmic reticulum and Golgi apparatus of the follicular cell and secreted into the follicular cavity. The iodination of thyroglobulin residues occurs at the apical membrane of the thyroid follicular cell. Iodine leaves the follicular cell via the chloride-iodide transporting protein or channel. In follicular lumen, the iodine rapidly binds to the 3 position of tyrosine in thyroglobulin within seconds, in the presence of thyroid peroxidase enzyme. The iodination of tyrosine in thyroglobulin forms mono-iodotyrosine (MIT) and di-iodotyrosine (DIT). Following iodination in thyroglobulin, oxidative condensation of two di-iodotyrosine residues forms T4 and a serine residue. The condensation of mono-iodotyrosine and di-iodotyrosine leads to the formation of T3 and a serine residue. These condensation reactions are catalysed by the peroxidase enzyme.
Graves’ Ophthalmopathy: the Role of Cytokines in Pathogenesis
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
The target cell involved in Graves’ hyperthyroidism is the thyroid follicular cell. The TSH receptor is the specific autoantigen against which the autoimmune response is directed.9 Stimulation of TSH receptors on thyroid follicular cells by circulating autoantibodies in Graves’ disease results in unregulated and excessive production of thyroid hormones. Although still a matter of some controversy, the fibroblast in the orbit and pretibial skin is thought to be the target cell involved in GO and pretibial dermopathy.10,11 Because of the close clinical association between Graves’ hyperthyroidism, GO, and pretibial dermopathy, it is reasonable to suspect that a single pathogenic mechanism involving a common antigen may be responsible for all three conditions. The demonstration of RNA encoding the TSH receptor in human fibroblasts12 and orbital tissue specimens13 allows for the possibility that the TSH receptor is that common autoantigen. It has been suggested that an autoimmune reaction against TSH receptors on fibroblasts throughout the body occurs in Graves’ disease.11 That the clinically apparent connective tissue manifestations are generally limited to the orbit and pretibial skin may be explained by the known phenotypic differences between fibroblasts from various anatomic sites with regard to their biosynthetic capabilities and sensitivity to stimuli.14–17
Oxidative damage to membrane lipids in the thyroid – no differences between sexes
Published in Drug and Chemical Toxicology, 2021
Jan Stepniak, Andrzej Lewinski, Malgorzata Karbownik-Lewinska
H2O2, a form of reactive oxygen species (ROS), is synthesized in the thyroid gland by certain enzymes belonging to the NADPH oxidase (NOX) family, namely, dual oxidases (DUOX1/2) and NOX4. Both DUOX1 and DUOX2 are expressed at the apical membrane and their activation depends on the rise of intracellular calcium levels. Additionally both enzymes are active only in the presence of DUOX maturation factors (Carvalho and Dupuy 2017). H2O2 produced by DUOX2 is an indispensable factor in thyroid hormone biosynthesis. Stimulated thyroid follicular cell generates a lot of H2O2, i.e., as much as an activated leukocyte (Song et al.2007). These large quantities of produced H2O2 and membrane permeable nature of this molecule can lead to its diffusion from the luminal side of the apical membrane back to the cell, potentially creating conditions for enhanced oxidative stress.
Simultaneous measurement of twenty-nine circulating cytokines and growth factors in female patients with overt autoimmune thyroid diseases
Published in Autoimmunity, 2020
Chao-Wen Cheng, Chung-Ze Wu, Kam-Tsun Tang, Wen-Fang Fang, Jiunn-Diann Lin
Despite serum IL-4 and TNF-α being comparable between the GD, HT, and AITD, and control groups, our results showed that serum IL-4 levels were correlated with FT4 levels in GD patients, while TNF-α levels were associated with FT4 levels in HT patients, which indicated that IL-4 or TNF-α could be a regulator of thyroid activity in GD and HT, respectively. It is well-documented that IL-4, a central component of type 2 T helper cell (Th2) cytokines, can facilitate B-cell proliferation, human leukocyte antigen (HLA) class II expression, and immunoglobulin production [30]. Because GD is driven by B-cell mediated immune responses, it would not be surprising if IL-4 can promote antibody-mediated autoimmunity and regulate thyroid function in GD after disease onset [2]. TNF-α, secreted by macrophages, contributes to the inflammatory process, anti-viral function, and immunoregulatory effects [30,31]. Sato et al. showed that TNF-α can suppress TSH-stimulated radioiodine uptake and restrain thyroid follicular cell proliferation in cell experiments, and from clinical data, Yamamoto et al. observed that serum TNF-α levels were correlated with thyroid function, which implied that it could be implicated in regulating thyroid function in GD [32–34]. Inconsistent with the results of earlier reports, we were unable to document an association of serum TNF-α with FT4 levels in GD. Moreover, the mechanism of TNF-α in controlling thyroid function in HT remains unclear. A further large sample size recruiting more patients is required to elucidate the role of TNF-α in the occurrence of HT.
Comparison of the hepatic and thyroid gland effects of sodium phenobarbital and pregnenolone-16α-carbonitrile in wild-type and constitutive androstane receptor (CAR)/pregnane X receptor (PXR) knockout rats
Published in Xenobiotica, 2019
Corinne Haines, Lynsey R. Chatham, Audrey Vardy, Clifford R. Elcombe, John R. Foster, Brian G. Lake
A number of non-genotoxic chemicals, including some CAR activators, have also been shown to produce thyroid gland tumours in rodents by a MOA in which circulating thyroid hormone levels are decreased as a result of increased hepatic metabolism and clearance (Capen, 2001; Dellarco et al., 2006; Hill et al., 1998; McClain et al., 1989; Meek et al., 2003). In this MOA, thyroxine (T4) conjugation is enhanced due to the stimulation of hepatic microsomal UDP-glucuronosyltransferase (UGT) enzymes towards T4 as substrate resulting in increased biliary excretion of T4, a decrease in serum triiodothyronine (T3) and/or T4 levels and a compensatory increase in serum thyroid stimulating hormone (TSH) levels. In the rodent thyroid gland, the increase in TSH levels results in thyroid follicular cell hypertrophy and hyperplasia, with chronic stimulation subsequently producing thyroid follicular cell tumours (Capen, 2001; Curran and DeGroot, 1991; Hill et al., 1998).