The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Mechanisms behind the non-thyroidal illness syndrome: an update
Open accessAbstract
The mechanisms behind the changes in serum triiodothyronine (T 3), thyroxine (T 4) and TSH that occur in the non-thyroidal illness syndrome (NTIS) are becoming clearer. Induction of a central hypothyroidism occurs due to a diminution in hypothalamic thyrotropin-releasing hormone. This can be signalled by a decrease in leptin caused by malnutrition and possibly a localised increase in hypothalamic T 3 catalyzed by altered expression of hypothalamic iodothyronine deiodinases D2 and D3. Data from D1 and D2 knockout mice suggest that these enzymes may have little contribution to the low serum T 3 found in acute illness. The decline in serum T 3 and T 4 in models of acute illness precedes the fall in hepatic D1, suggesting that much of the initial fall in these hormones may be attributable to an acute phase response giving rise to a reduction in the thyroid hormone binding capacity of plasma. When measured by reliable methods, changes in serum free T 4 and free T 3 are modest in comparison to the fall seen in total thyroid hormone. Thyroid hormone transporter expression is up-regulated in many models of the NTIS, thus if diminished tissue uptake of hormone occurs in vivo, it is likely to be the result of impaired transporter function caused by diminished intracellular ATP or plasma inhibitors of transporter action. In man, chronic illness leads to an upregulation of thyroid hormone receptor (THR) expression at least in liver and renal failure. In contrast, human and animal models of sepsis and trauma indicate that expression of THRs and their coactivators are decreased in acute illness.
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Cellular and Molecular Basis of Deiodinase-Regulated Thyroid Hormone Signaling1
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Deiodinases: implications of the local control of thyroid hormone action
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Type 2 iodothyronine deiodinase is the major source of plasma T3 in euthyroid humans
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Abnormal thyroid hormone metabolism in mice lacking the monocarboxylate transporter 8
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Association between serum interleukin-6 and serum 3,5,3'-triiodothyronine in nonthyroidal illness.
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Cited by
Central Hypothyroidism: Pathogenic, Diagnostic, and Therapeutic Challenges
Persani, L. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2012-1616 · Cited by 295
Pitfalls in the measurement and interpretation of thyroid function tests
Koulouri, O., Moran, C., Halsall, D., Chatterjee, K., & Gurnell, M. (2013) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2013.10.003 · Cited by 282
Ruiz-Núñez, B., Pruimboom, L., Dijck-Brouwer, D. A. J., & Muskiet, F. A. J. (2013) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2013.02.009 · Cited by 246
Raiten, D. J., Ashour, F. A. S., Ross, A. C., Meydani, S. N., Dawson, H. D., Stephensen, C. B., Brabin, B. J., Suchdev, P. S., & van Ommen, B. (2015) · The Journal of Nutrition · doi:10.3945/jn.114.194571 · Cited by 234
TSH and thyrotropic agonists: key actors in thyroid homeostasis
Dietrich, J. W., Landgrafe, G., & Fotiadou, E. H. (2012) · Journal of Thyroid Research · doi:10.1155/2012/351864 · Cited by 146
Metadata
- Authors
- Warner, M. H., & Beckett, G. J.
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2009-12-16
- Volume
- 205
- Issue
- 1
- Pages
- 1-13
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2168760648
- Cited by
- 432
- References
- 27
- FWCI
- 14.14
- Type
- journal article
- Language
- en
- Open access
- bronze
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