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On the Importance of Monitoring Blood Sugar and Other “Vital Signs”
Published in Robert Fried, Richard M. Carlton, Type 2 Diabetes, 2018
Robert Fried, Richard M. Carlton
Parenthetically, a study published in the Canadian Medical Association Journal also reported that metformin is associated with an increased incidence of low TSH levels in Type 2 diabetes patients with treated hypothyroidism, but not in euthyroid patients (Fournier, Yin, Yu et al. 2014). “Euthyroid sick syndrome” is a condition characterized by low serum levels of thyroid hormones in patients with nonthyroid systemic illness.
Electrolyte disturbances and endocrinal care
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Raffaele Di Fenza, Giuseppe Citerio
After TBI, 8% to 15% of patients will develop central hypothyroidism, characterized by inappropriately low TSH in the presence of low serum free tetraiodothyronine (T4).58,68 Acute patients often show the so-called “euthyroid sick syndrome” which may be difficult to distinguish from central hypothyroidism because TSH may be low as well. Current evidence suggests postponing an evaluation of the hypothalamic-pituitary-thyroid axis for at least 4 weeks after the onset of TBI in patients without suspected or documented preexisting hypothyroidism. Treatment in the acute setting is not usually indicated, and is also given the average half-life of T4 (7 days). A full replacement dose of 1.6 µg/kg qd (lower doses may be warranted in older patients and in those with cardiovascular comorbidities) should be administered carefully in patients with documented central hypothyroidism and after evidence of intact adrenal function or ongoing adequate glucocorticoid therapy, in order to avoid adrenal crisis.58
Thyroid disorders, dementia and Down syndrome
Published in Vee P. Prasher, Down Syndrome and Alzheimer’s Disease, 2018
This term refers to abnormalities in thyroid function that are not caused by primary thyroid or pituitary dysfunction.87 Causes are thought to include hypothalamic and pituitary suppression, decreased conversion of T4 to T3, alterations in serum binding of thyroid hormones, and decreased TSH production and/or its effect on the thyroid. Cytokines such as tumour necrosis factor alpha, interleukin-1, interleukin-6, free fatty acids, Cortisol and glucagon all have effects on thyroid function. Abnormalities of thyroid function also result from conditions such as surgical stress and serious infection. It is not clear whether these changes reflect a protective response in the face of a serious illness, or a maladaptive process that needs to be corrected. Some patterns of abnormalities that fall into the category of euthyroid ‘sick syndrome’ include the following. Low T3 with an increase in rT3. This is thought to be due to a decrease in the conversion of T4 to T3 by the hepatic deiodinase system.Low T3 and low T4 with normal to low TSH. This may be due to low TBG levels or the presence of a thyroid-hormone-binding inhibitor.Low TSH, low T3 and low T4. This suggests an alteration in pituitary or hypothalamic responsiveness.Elevated T4 with normal or elevated TSH and normal or elevated T3. This may be seen in primary biliary cirrhosis and acute or chronic hepatitis in which TBG synthesis and release are increased, in acute psychiatric illnesses, and as a result of use of certain drugs.83,106
Association between Thyroid Function and Prognosis of COVID-19: A Retrospective Observational Study
Published in Endocrine Research, 2021
Shan Lang, Ye Liu, Xue Qu, Ran Lu, Wei Fu, Wenhui Zhang, Haining Wang, Tianpei Hong
COVID-19’s impact on the thyroid gland remains largely unknown. Increasing evidence has demonstrated that angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2), which are the key entry sites for SARS-CoV-2, are highly expressed in the thyroid gland and are more abundant than in the lungs.4–7 The onset of subacute thyroiditis has been reported in patients with COVID-19, indicative of viral infections as an etiology.8–11 Data from the previous coronavirus pandemic caused by the SARS-associated coronavirus (SARS-CoV), a member of the Coronaviridae family, demonstrated that SARS-CoV could damage thyroid follicular and parafollicular cells and decrease the number of thyroid stimulating hormone (TSH)-positive cells in the pituitary.12,13 Thus, thyroid dysfunction may be a comorbidity in patients with COVID-19. Moreover, a low triiodothyronine (T3) state is considered an indicator of nonthyroidal illness syndrome (NTIs), also known as euthyroid sick syndrome,14–16 and is observed in critically ill patients. Therefore, changes in thyroid function during coronavirus infection have attracted attention.
Current and future immunotherapies for thyroid cancer
Published in Expert Review of Anticancer Therapy, 2018
Alessandro Antonelli, Silvia Martina Ferrari, Poupak Fallahi
Primary hypothyroidism is diagnosed if thyroid stimulating hormone (TSH) levels are increased in presence of a low free thyroxine (T4) level, whereas hypophysitis is characterized by a low TSH and low free T4. In case of primary hypothyroidism, immune checkpoint inhibitor therapy can be continued with appropriate levothyroxine replacement [42]. Hypophysitis can present as fatigue, headaches, and visual field defects. Diagnosis is established according to levels of pituitary hormones (ACTH, TSH, FSH, LH, GH, IGF-1, and prolactin) and nuclear magnetic resonance imaging showing an enlarged pituitary, with/without necrosis. For grade ≥2 toxicity, it is advised to withhold immune checkpoint inhibitor therapy and start high-dose corticosteroids (methylprednisolone 125 mg daily intravenously for 3 days with a switch to oral prednisone 1–2 mg/kg daily upon improvement of symptoms). The corticosteroid therapy (which is quite frequent in neoplastic subjects) may have a direct effect on the pituitary by reducing TSH levels. Furthermore, corticosteroid therapy can be associated with an ‘euthyroid sick syndrome’ (also known as non-thyroidal illness syndrome) characterized by low serum triiodothyronine (T3) and elevated reverse T3 (rT3). This might affect differential diagnosis when evaluating thyroid function tests [42].
Thyroid dysfunction and survival in cancer patients treated with immune checkpoint inhibitors: analyses from a large single tertiary cancer center database
Published in Acta Oncologica, 2021
Ruth Percik, Yair Liel, Damien Urban, Jair Bar, Eytan Ben-Ami, Muhammad Abu Tailakh
Despite rare reports on severe thyrotoxicosis and even ‘thyroid storm’ in CPIs-treated patients [32], the typical presentation of CPI-induced TD is exceptionally clinically indolent. The mild clinical presentation of the thyrotoxic phase can be explained by concurrent alterations in thyroid hormone metabolism and peripheral response to thyroid hormones during the CPI-induced intense immune reaction, characteristic of the ‘euthyroid-sick syndrome’, which often accompanies inflammatory and no-inflammatory conditions [33]. Alterations in thyroid hormones and activity due to ‘euthyroid-sick syndrome’ include decreased expression of the thyroid hormone cell transporters MCT8 and MCT10, responsible for T4 uptake by peripheral tissues. Alterations in deiodinase expression result in reduced production of T3, simultaneous increased production of the biologically inactive metabolite, reverse-T3, and possibly a decrease in thyroid hormone receptors expression and their nuclear binding to DNA resulting in ‘tissue hypothyroidism’ [33]. Due to its mild clinical presentation, unless there are clinical awareness and specific laboratory surveillance, the early phase of thyroiditis can be easily missed. Levothyroxine should be initiated for patients with hypothyroidism and immunotherapy should not be interrupted. Finally, whereas most other drug-induced thyroid abnormalities result in the recovery of normal thyroid function, with only 5–20% of cases resulting in permanent hypothyroidism [19], most patients with CPI-induced TD progress to overt hypothyroidism requiring permanent treatment with a full replacement dose of thyroxine [17].