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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 Isoflavones Levels in Relation to Serum Thyroid Hormone Concentrations in Female and Male Adults in the U.S. General Population
Published in International Journal of Environmental Health Research, 2021
Patricia A. Janulewicz, Jeffrey M. Carlson, Amelia K. Wesselink, Lauren A. Wise, Elizabeth E. Hatch, Lariah M. Edwards, Junenette L. Peters
Thyroid hormones (TH) are controlled through the hypothalamic-pituitary-thyroid (HPT) axis and are crucial for the regulation of many biological systems. The HPT axis is complex and sensitive to perturbations. The hypothalamus, located in the central nervous system, produces thyrotropin-releasing hormone (TRH), and sends it to the pituitary gland, which releases thyroid stimulating hormone (TSH). TSH binds to receptors on the thyroid gland and stimulates the synthesis and release of thyroid hormones, thyroxine (T4) and triiodothyronine (T3), into peripheral circulation. Proper production of these hormones is largely dependent on iodine levels (Rousset et al. 2000). Circulating TH levels are maintained by a feedback mechanism between the hypothalamus, pituitary gland, and thyroid gland (Rousset et al. 2000; Pearce and Braverman 2009; Gilbert et al. 2012). Optimal circulating TH levels are essential for normal fetal and child growth (Meeker 2012; DiVall 2013) and brain development (Meeker 2012), reproductive function, and metabolism (Meeker and Ferguson 2014).