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Acquired hypothyroidism
Published in Pallavi Iyer, Herbert Chen, Thyroid and Parathyroid Disorders in Children, 2020
With the increased ease of thyroid function screening, thyroid lab abnormalities still require explanation in the absence of symptoms. In non-thyroidal illness syndrome, the severity of underlying disease and starvation can result in low T3 and low T4 levels. TSH is low or normal and pituitary and hypothalamic pathology are not likely. Treatment is not usually indicated, and the severity and duration of the underlying illness is reflected in the suppression of the serum thyroxine level (20).
Endocrinology
Published in Fazal-I-Akbar Danish, Essential Lists of Differential Diagnoses for MRCP with diagnostic hints, 2017
Sick euthyroid syndrome (non-thyroidal illness syndrome) – ↓ T4 and T3; normal or ↓ TSH:1 Starvation.2 Any severe illness (ITU; severe infection; renal/hepatic/cardiac failure; end-stage malignancy).
Complications of Hypovolemic and Septic Shock
Published in Stephen M. Cohn, Matthew O. Dolich, Complications in Surgery and Trauma, 2014
Meghann L. Kaiser, Matthew O. Dolich
Hypothyroidism is another very common complication of hemorrhagic or septic shock, but, again, treatment in the acute setting of critical illness remains controversial. The terms “sick euthyroid syndrome” and “nonthyroidal illness syndrome (NTIS)” have arisen to describe a state of suppressed triiodothyronine (T3), with normal or decreased thyroxine (T4) and thyroid-stimulating hormone (TSH). It would seem logical that low thyroid hormone levels would exert deleterious metabolic and cardiovascular effects, and in some specific scenarios, such as severe traumatic brain injury, T4 supplementation may prove key to maintaining hemodynamic stability. In 10% of patients with shock, hypothyroidism may coincide with hypoadrenalism, and the concern for synergistic effects frequently prompts thyroid hormone supplementation. However, despite many studies on the subject, no clear evidence exists that correcting the apparent thyroid hormone deficiency will alter outcome, and the clinical significance of the syndrome itself remains in question.25
Free thyroxine measurement in clinical practice: how to optimize indications, analytical procedures, and interpretation criteria while waiting for global standardization
Published in Critical Reviews in Clinical Laboratory Sciences, 2023
Federica D’Aurizio, Jürgen Kratzsch, Damien Gruson, Petra Petranović Ovčariček, Luca Giovanella
The interpretation of TFT can be difficult in hospitalized patients and those recently discharged from the hospital [34]. Non-thyroidal illness syndrome is recognized as a nonspecific adaptive mechanism for illness and an indirect marker of disease severity in various conditions, including hospitalization in the critical care setting [35]. The underlying mechanisms include multiple and complex alterations (i.e. inhibition of iodide uptake and organification, suppression of thyroglobulin synthesis and reduction of thyroid hormone secretion, inhibition of the hypothalamus-pituitary-thyroid axis) mediated by cytokines such as interleukin-6 and tumor necrosis factor-alpha that have specific effects on the thyroid gland [36]. The hallmark of non-thyroidal illness syndrome is low FT3, with or without low FT4, in combination with normal or low TSH in clinically euthyroid patients. Furthermore, in the prolonged phase of critical illness, non-thyroidal illness syndrome is associated with adverse outcomes. In general, TFT are discouraged in these conditions whenever possible.
Stable thyroid function despite regular use of povidone-iodine throat spray for SARS-CoV-2 prophylaxis
Published in Annals of Medicine, 2022
Amy May Lin Quek, Mei Yen Ng, Ooiean Teng, Nicole-Ann Lim, Geelyn Jeng Lin Ng, Samantha Peiling Yang, Mikael Hartman, Paul Anantharajah Tambyah, Alex R. Cook, Raymond Chee Seong Seet
The SARS-CoV-2 virus enters cells using the angiotensin-converting enzyme type 2 (ACE2) receptor. This receptor is also highly expressed in thyroid glands, at levels greater than those present in lung tissues [23,24]. Among infected patients, serum ACE2 levels have been shown to correlate closely with circulatory T3 and T4 levels [25]. Despite these preliminary data linking SARS-CoV-2 and its biological propensity to infect thyroid tissues, we did not observe significant differences in thyroid function between infected and non-infected controls, and the following seroconversion. These findings are consistent with a previous report that observed no change in thyroid function during convalescence [26] but differ from studies that observed significant differences in thyroid parameters during acute infection [27], although it remains unclear whether these changes occur as a result of a nonthyroidal illness syndrome or direct infection of thyroid tissues. Compared to autopsy findings in patients with SARS-CoV infection [28], existing observations suggest either mild or no damage to thyroid follicles among those with SARS-CoV-2 infection [29–32]. These findings suggest that SARS-CoV-2 could have a less pronounced effect on thyroid tissues, contrary to its biological predisposition to infection given the abundance of ACE2 receptors.
Possible Contributions of Nongenomic Actions of Thyroid Hormones to the Vasculopathic Complex of COVID-19 Infection
Published in Endocrine Research, 2022
Paul J. Davis, Hung-Yun Lin, Aleck Hercbergs, Kelly A. Keating, Shaker A. Mousa
Integrin αvβ3 has been implicated in the cellular internalization of certain viruses, including porcine coronavirus,10 and we have shown that T4 promotes the uptake and recycling of this integrin.11 These observations caused us to propose that this T4-activated integrin may interact with angiotensin-converting enzyme-2 (ACE-2), designated a receptor for SARS-CoV-2, the virus responsible for COVID-19 infection.10,12 ACE2 supports virus uptake.10 Serious COVID-19 infection occurs more commonly in patients with preexisting medical illnesses and such patients are more likely to have a panel of changes in circulating levels of thyroid hormones that define the nonthyroidal illness syndrome (NTIS).13 A small subgroup of NTIS patients have elevated free T4 (FT4) levels,14,15 whereas elevation of rT3 is common in the syndrome.16–19 We propose that changes in each of these hormones may be relevant to the vasculopathic complications of COVID-19 infection. In addition to its occurrence in NTIS, FT4 elevation may also occur in the subacute thyroiditis that complicates COVID-19 infection.20 Reduced circulating T3 is a hallmark of NTIS, but this change is not seen by us to relate to vasculopathy.