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Evaluation and Investigation of Thyroid Disease
Published in R James A England, Eamon Shamil, Rajeev Mathew, Manohar Bance, Pavol Surda, Jemy Jose, Omar Hilmi, Adam J Donne, Scott-Brown's Essential Otorhinolaryngology, 2022
TSH is measured using antibody immunoassays. Generally, normal TSH rules out thyroid dysfunction, but an elevated or suppressed TSH level should be considered in association with the serum free thyroxine (FT4) and free serum triiodothyronine (FT3) levels. Primary hypothyroidism causes elevated TSH, whereas primary thyrotoxicosis causes TSH suppression (Table 80.1). The normal reference range for TSH is 0.4–4.5 mU/L, but it can be affected by pregnancy, age, genetic factors, obesity, and nonthyroidal conditions.
Thyroid
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
TSH is the main regulator of thyroid function, differentiation, and proliferation. Binding of TSH to its receptor on thyroid cells primarily activates a cyclic adenosine monophosphate cascade, leading to thyroid hormone synthesis and release as well as to the expression of thyroid-specific genes, including those encoding Tg and thyroperoxidase. DTC retains some degree of thyroid-specific gene expression and function similar to normal thyroid cells; therefore, it is responsive to stimulation by TSH. In thyroid cancer cell lines, TSH has been shown to stimulate vascular endothelial growth factor (VEGF) secretion and angiogenesis. Thus, TSH may promote growth in some thyroid cancers.57
Endocrinology, growth and puberty
Published in Rachel U Sidwell, Mike A Thomson, Concise Paediatrics, 2020
Rachel U Sidwell, Mike A Thomson
Grossly elevated levels of TSH are most likely due to severe congenital hypothyroidism. Mildly elevated TSH levels (5–20 mU/L) in the presence of normal free T4 levels require close monitoring as they may represent transient hyper-thyrotropinaemia.
Low awareness and under-diagnosis of hypothyroidism
Published in Current Medical Research and Opinion, 2022
Ulrike Gottwald-Hostalek, Barbara Schulte
Current guidance for the management of subclinical hypothyroidism supports a trial of levothyroxine for patients aged <65 y with symptoms36. Conversely, some older subjects or those without symptoms of hypothyroidism (presumably diagnosed opportunistically or via population screening for thyroid disease) are not considered to require thyroid hormone replacement36,37. It could be argued that a diagnosis of subclinical hypothyroidism in the latter group would be moot, as it would not affect their management, while burdening them with an additional medical diagnosis. In addition, it will be important in future to identify and manage appropriately those subjects with modestly elevated TSH that is due to causes other than thyroid dysfunction, such as obesity and/or psychological stress, as described below38,39.
Pituitary hyperplasia mimicking thyrotropin-producing pituitary adenoma in the patient with resistance to thyroid hormone: a case report
Published in International Journal of Neuroscience, 2021
Onnicha Suntornlohanakul, Chutintorn Sriphrapradang
In normal physiological conditions, elevated serum thyroid hormone levels feedback negatively on the hypothalamus and pituitary leading to TSH suppression. Syndrome of inappropriate thyroid-stimulating hormone (TSH) secretion is characterized by high serum free thyroxine (T4) and triiodothyronine (T3) levels with measurable serum TSH concentrations. This syndrome is rare, but the interpretation of discordant thyroid function tests (TFTs) is challenging. The differential diagnoses of this syndrome include the assay interference, resistance to thyroid hormone-beta (RTH-β), and TSH-secreting pituitary adenoma (TSHoma). Although a rare disease, the correct differential diagnosis is mandatory to prevent improper management because therapeutic approaches are extremely different. Patients with TSHoma require pituitary surgery, while most patients with RTH-β do not require treatment.
Prevalence and aetiology of thyrotoxicosis in patients with hyperemesis gravidarum presenting to a tertiary hospital in Cape Town, South Africa
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2021
T van der Made, M van de Vyver, M Conradie-Smit, Magda Conradie
Serum TSH, free T4 (fT4) and free T3 (fT3) in this study were measured on the Roche Cobas e 601 analyser (Roche Diagnostics, Mannheim, Germany). A competition principle immunoassay is used for the determination of free thyroxine fT4 and fT3 and results determined via a calibration curve. The measuring ranges for fT4 and fT3 are 0.3–100 pmol/l and 0.3–10 nmol/l and the normal reference intervals are 12–22 pmol/l and 3.1–6.8 nmol/l respectively. A non-competitive sandwich immunoassay is applied for TSH with the same principle as for fT3 and fT4. The TSH measuring range is 0.005–100 μIU/ml with a normal reference interval of 0.27–4.2 mIU/l. The local NHLS does not report trimester-specific normal ranges. The inter-assay coefficient of variance at various clinically significant cut-off points for serum TSH, fT4 and fT3 was less than 3%.