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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.
Effect of chemoradiation on the size of the thyroid gland
Published in Baylor University Medical Center Proceedings, 2020
Ana Marcella Rivas, Eneko Larumbe-Zabala, Olaia Diaz-Trastoy, Ryan Nicholas Schurr, Catherine Jones, Ramzi Abdulrahman, Nabeel Dar, Joaquin Lado-Abeal
The effects of severe illness or the systemic response to the cancer process itself on thyroid hormone axis homeostasis is among the factors that could explain the decrease in thyroid gland size in our study. The high mortality rate at 3 months of patients in our study is an indirect indicator of the illness severity of our sample. A study in which thyroid function tests were measured before and after a cycle of chemotherapy for breast cancer in 180 patients revealed that the prevalence of nonthyroidal illness increased during chemotherapy, from 16.5% prior to the cycle to 87.1% after the initial cycle.14 During severe illness, serum TSH usually remains inappropriately low-normal despite low levels of thyroid hormone.18 TSH is a trophic factor for the thyroid gland, and a decrease in serum TSH levels even within the low-normal range could impact the size of the gland. Nevertheless, our data did not show a correlation between 3-month mortality and the degree of reduction of the gland, which could as well be explained by a lack of statistical power due to the small size of our sample.