Research Progress of Non-Thyroidal Illness Syndrome in Sepsis

Yaqian QU, Huiling ZANG, Zhenghao ZHOU, Hui GUO, Jianguo LI

Acta Academiae Medicinae Sinicae ›› 2025, Vol. 47 ›› Issue (6) : 1015-1027.

PDF(935 KB)
Home Journals Acta Academiae Medicinae Sinicae
Acta Academiae Medicinae Sinicae

Abbreviation (ISO4): Acta Academiae Medicinae Sinicae      Editor in chief: Xuetao CAO

About  /  Aim & scope  /  Editorial board  /  Indexed  /  Contact  / 
PDF(935 KB)
Acta Academiae Medicinae Sinicae ›› 2025, Vol. 47 ›› Issue (6) : 1015-1027. DOI: 10.3881/j.issn.1000-503X.16534
Review Articles

Research Progress of Non-Thyroidal Illness Syndrome in Sepsis

Author information +
History +

Abstract

Non-thyroidal illness syndrome(NTIS)is commonly observed in critically ill patients.Sepsis is one of the leading causes of mortality among patients in intensive care units,where the incidence of NTIS is higher than that in general wards.Recently,increasing attention has been paid to thyroid metabolic abnormalities in sepsis patients.This article reviews the pathogenesis and clinical significance of NTIS in sepsis,aiming to offer evidence-based medical insights for future research directions for clinicians.

Key words

non-thyroidal illness syndrome / sepsis / thyroid function / inflammation

Cite this article

Download Citations
Yaqian QU , Huiling ZANG , Zhenghao ZHOU , et al . Research Progress of Non-Thyroidal Illness Syndrome in Sepsis[J]. Acta Academiae Medicinae Sinicae. 2025, 47(6): 1015-1027 https://doi.org/10.3881/j.issn.1000-503X.16534

References

[1]
Lee S, Farwell AP. Euthyroid sick syndrome[J]. Compr Physiol, 2016, 6(2):1071-1080.DOI:10.1002/cphy.c150017.
[2]
中华医学会内分泌学分会. 成人甲状腺功能减退症诊治指南[J]. 中华内分泌代谢杂志, 2017(2):167-180.DOI:10.3760/cma.j.issn.1000-6699.2017.02.018.
[3]
Fliers E, Boelen A. An update on non-thyroidal illness syndrome[J]. J Endocrinol Invest, 2021, 44(8):1597-1607.DOI:10.1007/s40618-020-01482-4.
[4]
Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock(sepsis-3)[J]. JAMA, 2016, 315(8):801-810.DOI:10.1001/jama.2016.0287.
[5]
Xie J, Wang H, Kang Y, et al. The epidemiology of sepsis in Chinese ICUs:a national cross-sectional survey[J]. Crit Care Med, 2020, 48(3):e209-e218.DOI:10.1097/ccm.0000000000004155.
[6]
Ray DC, Macduff A, Drummond GB, et al. Endocrine measurements in survivors and non-survivors from critical illness[J]. Intensive Care Med, 2002, 28(9):1301-1308.DOI:10.1007/s00134-002-1427-y.
[7]
曾媛媛, 谢云, 陈道南, 等. 脓毒症患者发生正常甲状腺性病态综合征的相关因素[J]. 北京大学学报(医学版), 2024, 56(3):526-532.DOI:10.19723/j.issn.1671-167X.2024.03.021.
[8]
王庭槐. 生理学[M]. 9版. 北京: 人民卫生出版社, 2018.
[9]
Bianco AC, Kim BW. Deiodinases:implications of the local control of thyroid hormone action[J]. J Clin Invest, 2006, 116(10):2571-2579.DOI:10.1172/jci29812.
[10]
Warner MH, Beckett GJ. Mechanisms behind the non-thyroidal illness syndrome:an update[J]. J Endocrinol, 2010, 205(1):1-13.DOI:10.1677/joe-09-0412.
[11]
Visser TJ. Thyroid hormone transporters[J]. Horm Res, 2007, 68(Suppl 5):28-30.DOI:10.1159/000110469.
[12]
Visser WE, Friesema EC, Jansen J, et al. Thyroid hormone transport in and out of cells[J]. Trends Endocrinol Metab, 2008, 19(2):50-56.DOI:10.1016/j.tem.2007.11.003.
[13]
Dayan CM, Panicker V. Novel insights into thyroid hormones from the study of common genetic variation[J]. Nat Rev Endocrinol, 2009, 5(4):211-218.DOI:10.1038/nrendo.2009.19.
[14]
Davis PJ, Davis FB, Lin HY. Promotion by thyroid hormone of cytoplasm-to-nucleus shuttling of thyroid hormone receptors[J]. Steroids, 2008, 73(9-10):1013-1017.DOI:10.1016/j.steroids.2007.12.030.
[15]
Oetting A, Yen PM. New insights into thyroid hormone action[J]. Best Pract Res Clin Endocrinol Metab, 2007, 21(2):193-208.DOI:10.1016/j.beem.2007.04.004.
[16]
Inan M, Koyuncu A, Aydin C, et al. Thyroid hormone supplementation in sepsis:an experimental study[J]. Surg Today, 2003, 33(1):24-29.DOI:10.1007/s005950300004.
[17]
Hesch RD, Hüsch M, Ködding R, et al. Treatment of dopamine-dependent shock with triiodothyronine[J]. Endocr Res Commun, 1981, 8(4):229-237.DOI:10.3109/07435808109045741.
[18]
徐梅先, 刘刚, 曹利静, 等. 脓毒症危重患儿非甲状腺疾病综合征的发生及其与IL-6和IL-10的相关性[J]. 中国当代儿科杂志, 2020, 22(11):1215-1220.DOI:10.7499/j.issn.1008-8830.2004137.
[19]
Yildizdaş D, Onenli-Mungan N, Yapicioqlu H,et al. Thyroid hormone levels and their relationship to survival in children with bacterial sepsis and septic shock[J]. J Pediatr Endocrinol Metab,2004,17(10):1435-1442.DOI:10.1515/jpem.2004.17.10.1435.
[20]
Purwanto D, Astrawinata D. Mekanisme kompleks sepsis dan syok septik[J]. J Biomedika dan Biosains, 2018, 10(3):143.DOI:10.35790/jbm.10.3.2018.21979.
[21]
周易, 陈影, 陈尔真. 甲状腺激素对脓毒症脏器功能维护作用的研究进展[J]. 内科理论与实践, 2022, 17(5):408-412.DOI:10.16138/j.1673-6087.2022.05.013.
[22]
王凤, 严宗逊. 正常甲状腺病态综合征研究进展[J]. 中国医药导刊, 2020, 22(8):544-548.DOI:10.3969/j.issn.1009-0959.2020.08.011.
[23]
Wasyluk W, Wasyluk M, Zwolak A. Sepsis as a pan-endocrine illness-endocrine disorders in septic patients[J]. J Clin Med, 2021, 10(10):2075-2075.DOI:10.3390/jcm10102075.
[24]
Schett G, Neurath MF. Resolution of chronic inflammatory disease:universal and tissue-specific concepts[J]. Nat Commun, 2018, 9(1):3261.DOI:10.1038/s41467-018-05800-6.
[25]
Medzhitov R. Origin and physiological roles of inflammation[J]. Nature, 2008, 454(7203):428-435.DOI:10.1038/nature07201.
[26]
Lasa M, Contreras-Jurado C. Thyroid hormones act as modulators of inflammation through their nuclear receptors[J]. Front Endocrinol(Lausanne), 2022, 13:937099.DOI:10.3389/fendo.2022.937099.
[27]
Hotchkiss RS, Moldawer LL, Opal SM, et al. Sepsis and septic shock[J]. Nat Rev Dis Primers, 2016, 2:16045.DOI:10.1038/nrdp.2016.45.
[28]
Bartalena L, Bogazzi F, Brogioni S, et al. Role of cytokines in the pathogenesis of the euthyroid sick syndrome[J]. Eur J Endocrinol, 1998, 138(6):603-614.DOI:10.1530/eje.0.1380603.
[29]
Siampa VN, Abadi S, Aman AM, et al. Association between severity of sepsis and thyroid function profile[J]. Acta Biomed, 2023, 94(6):e2023239.DOI:10.23750/abm.v94i6.15076.
[30]
Vidart J, Axelrud L, Braun AC, et al. Relationship among low T3 levels,type 3 deiodinase,oxidative stress,and mortality in sepsis and septic shock:defining patient outcomes[J]. Int J Mol Sci, 2023, 24(4):3935.DOI:10.3390/ijms24043935.
[31]
Boelen A, Platvoet-Ter Schiphorst MC, Wiersinga WM. Association between serum interleukin-6 and serum 3,5,3’-triiodothyronine in nonthyroidal illness[J]. J Clin Endocrinol Metab, 1993, 77(6):1695-1699.DOI:10.1210/jcem.77.6.8263160.
[32]
Mönig H, Arendt T, Meyer M, et al. Activation of the hypothalamo-pituitary-adrenal axis in response to septic or non-septic diseases-implications for the euthyroid sick syndrome[J]. Intensive Care Med, 1999, 25(12):1402-1406.DOI:10.1007/s001340051088.
[33]
Boelen A, Platvoet-Ter Schiphorst MC, Bakker O, et al. The role of cytokines in the lipopolysaccharide-induced sick euthyroid syndrome in mice[J]. J Endocrinol, 1995, 146(3):475-483.DOI:10.1677/joe.0.1460475.
[34]
Van Haasteren GA, Van Der Meer MJ, Hermus AR, et al. Different effects of continuous infusion of interleukin-1 and interleukin-6 on the hypothalamic-hypophysial-thyroid axis[J]. Endocrinology, 1994, 135(4):1336-1345.DOI:10.1210/endo.135.4.7925094.
[35]
Stouthard JM, Van Der Poll T, Endert E, et al. Effects of acute and chronic interleukin-6 administration on thyroid hormone metabolism in humans[J]. J Clin Endocrinol Metab, 1994, 79(5):1342-1346.DOI:10.1210/jcem.79.5.7962327.
[36]
Hermus AR, Sweep CG, Demacker PN, et al. Continuous infusion of interleukin-1 beta in rats induces a profound fall in plasma levels of cholesterol and triglycerides[J]. Arterioscler Thromb, 1992, 12(9):1036-1043.DOI:10.1161/01.atv.12.9.1036.
[37]
Van Der Poll T, Van Zee KJ, Endert E, et al. Interleukin-1 receptor blockade does not affect endotoxin-induced changes in plasma thyroid hormone and thyrotropin concentrations in man[J]. J Clin Endocrinol Metab, 1995, 80(4):1341-1346.DOI:10.1210/jcem.80.4.7714108.
[38]
Van Der Poll T, Endert E, Coyle SM, et al. Neutralization of TNF does not influence endotoxininduced changes in thyroid hormone metabolism in humans[J]. Am J Physiol, 1999, 276(2):R357-R362.DOI:10.1152/ajpregu.1999.276.2.R357.
[39]
Rubingh J, Van Der Spek A, Fliers E, et al. The role of thyroid hormone in the innate and adaptive immune response during infection[J]. Compr Physiol, 2020, 10(4):1277-1287.DOI:10.1002/cphy.c200003.
[40]
De Castro AL, Fernandes RO, Ortiz VD, et al. Thyroid hormones decrease the proinflammatory TLR4/NF-κβ pathway and improve functional parameters of the left ventricle of infarcted rats[J]. Mol Cell Endocrinol, 2018, 461:132-142.DOI:10.1016/j.mce.2017.09.003.
[41]
Furuya F, Ishii T, Tamura S, et al. The ligand-bound thyroid hormone receptor in macrophages ameliorates kidney injury via inhibition of nuclear factor-κB activities[J]. Sci Rep, 2017, 7:43960.DOI:10.1038/srep43960.
[42]
Contreras-Jurado C, Alonso-Merino E, Saiz-Ladera C, et al. The thyroid hormone receptors inhibit hepatic interleukin-6 signaling during endotoxemia[J]. Sci Rep, 2016, 6:30990.DOI:10.1038/srep30990.
[43]
Alamino VA, Montesinos MDM, Soler MF, et al. Dendritic cells exposed to triiodothyronine deliver pro-inflammatory signals and amplify IL-17-driven immune responses[J]. Cell Physiol Biochem, 2019, 52(2):354-367.DOI:10.33594/000000025.
[44]
Perrotta C, Buldorini M, Assi E, et al. The thyroid hormone triiodothyronine controls macrophage maturation and functions:protective role during inflammation[J]. Am J Pathol, 2014, 184(1):230-247.DOI:10.1016/j.ajpath.2013.10.006.
[45]
Takano APC, Munhoz CD, Moriscot AS, et al. S100A8/MYD88/NF-кB:a novel pathway involved in cardiomyocyte hypertrophy driven by thyroid hormone[J]. J Mol Med(Berl), 2017, 95(6):671-682.DOI:10.1007/s00109-017-1511-y.
[46]
Chiloeches A, Sánchez-Pacheco A, Gil-Araujo B, et al. Thyroid hormone-mediated activation of the ERK/dual specificity phosphatase 1 pathway augments the apoptosis of GH4C1 cells by down-regulating nuclear factor-kappaB activity[J]. Mol Endocrinol, 2008, 22(11):2466-2480.DOI:10.1210/me.2008-0107.
[47]
Lasa M, Gil-Araujo B, Palafox M, et al. Thyroid hormone antagonizes tumor necrosis factor-alpha signaling in pituitary cells through the induction of dual specificity phosphatase 1[J]. Mol Endocrinol, 2010, 24(2):412-422.DOI:10.1210/me.2009-0298.
[48]
Mussbacher M, Salzmann M, Brostjan C, et al. Cell type-specific roles of NF-κB linking inflammation and thrombosis[J]. Front Immunol, 2019, 10:85.DOI:10.3389/fimmu.2019.00085.
[49]
Dorrington MG, Fraser IDC. NF-κB signaling in macrophages:dynamics,crosstalk,and signal integration[J]. Front Immunol, 2019, 10:705.DOI:10.3389/fimmu.2019.00705.
[50]
Viatour P, Merville MP, Bours V, et al. Phosphorylation of NF-kappaB and IkappaB proteins:implications in cancer and inflammation[J]. Trends Biochem Sci, 2005, 30(1):43-52.DOI:10.1016/j.tibs.2004.11.009.
[51]
Sabio G, Davis RJ. TNF and MAP kinase signalling pathways[J]. Semin Immunol, 2014, 26(3):237-245.DOI:10.1016/j.smim.2014.02.009.
[52]
Taniguchi K, Karin M. NF-κB,inflammation,immunity and cancer:coming of age[J]. Nat Rev Immunol, 2018, 18(5):309-324.DOI:10.1038/nri.2017.142.
[53]
Canovas B, Nebreda AR. Diversity and versatility of p38 kinase signalling in health and disease[J]. Nat Rev Mol Cell Biol, 2021, 22(5):346-366.DOI:10.1038/s41580-020-00322-w.
[54]
Hui L, Yao Y, Wang S, et al. Inhibition of Janus kinase 2 and signal transduction and activator of transcription 3 protect against cecal ligation and puncture-induced multiple organ damage and mortality[J]. J Trauma, 2009, 66(3):859-865.DOI:10.1097/TA.0b013e318164d05f.
[55]
李莉, 吴彩军. 危重症患者低T3综合征研究进展[J]. 中国急救医学, 2019, 39(2):165-169.DOI:10.3969/j.issn.1002-1949.2019.02.019.
[56]
De Vries EM, Surovtseva O, Vos WG, et al. Downregulation of type 3 deiodinase in the hypothalamus during inflammation[J]. Thyroid, 2019, 29(9):1336-1343.DOI:10.1089/thy.2019.0201.
[57]
Fekete C, Gereben B, Doleschall M, et al. Lipopolysaccharide induces type 2 iodothyronine deiodinase in the mediobasal hypothalamus:implications for the nonthyroidal illness syndrome[J]. Endocrinology, 2004, 145(4):1649-1655.DOI:10.1210/en.2003-1439.
[58]
Fekete C, Singru PS, Sarkar S, et al. Ascending brainstem pathways are not involved in lipopolysaccharide-induced suppression of thyrotropin-releasing hormone gene expression in the hypothalamic paraventricular nucleus[J]. Endocrinology, 2005, 146(3):1357-1363.DOI:10.1210/en.2004-1429.
[59]
Prummel MF, Brokken LJ, Wiersinga WM. Ultra short-loop feedback control of thyrotropin secretion[J]. Thyroid, 2004, 14(10):825-829.DOI:10.1089/thy.2004.14.825.
[60]
Boelen A, Platvoet-Ter Schiphorst MC, Wiersinga WM. Soluble cytokine receptors and the low 3,5,3’-triiodothyronine syndrome in patients with nonthyroidal disease[J]. J Clin Endocrinol Metab, 1995, 80(3):971-976.DOI:10.1210/jcem.80.3.7883859.
[61]
Boelen A, Schiphorst MC, Wiersinga WM. Relationship between serum 3,5,3’-triiodothyronine and serum interleukin-8,interleukin-10 or interferon gamma in patients with nonthyroidal illness[J]. J Endocrinol Invest, 1996, 19(7):480-483.DOI:10.1007/bf03349894.
[62]
Boelen A, Kwakkel J, Platvoet-Ter Schiphorst M, et al. Contribution of interleukin-12 to the pathogenesis of non-thyroidal illness[J]. Horm Metab Res, 2004, 36(2):101-106.DOI:10.1055/s-2004-814219.
[63]
Rimmelé T, Kellum JA. Clinical review:blood purification for sepsis[J]. Crit Care, 2011, 15(1):205.DOI:10.1186/cc9411.
[64]
Peng Z, Singbartl K, Simon P, et al. Blood purification in sepsis:a new paradigm[J]. Contrib Nephrol, 2010, 165:322-328.DOI:10.1159/000313773.
[65]
Kim JG, Shin H, Kim W, et al. The value of decreased thyroid hormone for predicting mortality in adult septic patients:a systematic review and meta-analysis[J]. Sci Rep, 2018, 8(1):14137.DOI:10.1038/s41598-018-32543-7.
[66]
Fliers E, Alkemade A, Wiersinga WM. The hypothalamic-pituitary-thyroid axis in critical illness[J]. Best Pract Res Clin Endocrinol Metab, 2001, 15(4):453-464.DOI:10.1053/beem.2001.0163.
[67]
Fliers E, Alkemade A, Wiersinga WM, et al. Hypothalamic thyroid hormone feedback in health and disease[J]. Prog Brain Res, 2006, 153:189-207.DOI:10.1016/s0079-6123(06)53011-0.
[68]
Fliers E, Boelen A, Van Trotsenburg AS. Central regulation of the hypothalamo-pituitary-thyroid(HPT)axis:focus on clinical aspects[J]. Handb Clin Neurol, 2014, 124:127-138.DOI:10.1016/b978-0-444-59602-4.00009-5.
[69]
Sousa RHCE, Rorato R, Hollenberg AN, et al. Analysis of hypothalamic TRH neurons in regulating thyroid hormone levels[J]. Endocr Soc, 2021, 5(Supple1):A849.DOI:10.1210/jendso/bvab048.1733.
[70]
Chan JL, Heist K, Depaoli AM, et al. The role of falling leptin levels in the neuroendocrine and metabolic adaptation to short-term starvation in healthy men[J]. J Clin Invest, 2003, 111(9):1409-1421.DOI:10.1172/jci17490.
[71]
Bianco AC, Nunes MT, Hell NS, et al. The role of glucocorticoids in the stress-induced reduction of extrathyroidal 3,5,3’-triiodothyronine generation in rats[J]. Endocrinology, 1987, 120(3):1033-1038.DOI:10.1210/endo-120-3-1033.
[72]
Nicoloff JT, Fisher DA, Appleman MD Jr. The role of glucocorticoids in the regulation of thyroid function in man[J]. J Clin Invest, 1970, 49(10):1922-1929.DOI:10.1172/jci106411.
[73]
Alkemade A, Friesema EC, Unmehopa UA, et al. Neuroanatomical pathways for thyroid hormone feedback in the human hypothalamus[J]. J Clin Endocrinol Metab, 2005, 90(7):4322-4334.DOI:10.1210/jc.2004-2567.
[74]
Boelen A, Kwakkel J, Alkemade A, et al. Induction of type 3 deiodinase activity in inflammatory cells of mice with chronic local inflammation[J]. Endocrinology, 2005, 146(12):5128-5134.DOI:10.1210/en.2005-0608.
[75]
Hosoi Y, Murakami M, Mizuma H, et al. Expression and regulation of type Ⅱ iodothyronine deiodinase in cultured human skeletal muscle cells[J]. J Clin Endocrinol Metab, 1999, 84(9):3293-3300.DOI:10.1210/jcem.84.9.5969.
[76]
Jakobs TC, Mentrup B, Schmutzler C, et al. Proinflammatory cytokines inhibit the expression and function of human type Ⅰ5’-deiodinase in HepG2 hepatocarcinoma cells[J]. Eur J Endocrinol, 2002, 146(4):559-566.DOI:10.1530/eje.0.1460559.
[77]
Kwakkel J, Wiersinga WM, Boelen A. Interleukin-1beta modulates endogenous thyroid hormone receptor alpha gene transcription in liver cells[J]. J Endocrinol, 2007, 194(2):257-265.DOI:10.1677/joe-06-0177.
[78]
Casey LC, Balk RA, Bone RC. Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome[J]. Ann Intern Med, 1993, 119(8):771-778.DOI:10.7326/0003-4819-119-8-199310150-00001.
[79]
Wajner SM, Goemann IM, Bueno AL, et al. IL-6 promotes nonthyroidal illness syndrome by blocking thyroxine activation while promoting thyroid hormone inactivation in human cells[J]. J Clin Invest, 2011, 121(5):1834-1845.DOI:10.1172/jci44678.
[80]
Lehnen TE, Marschner R, Dias F, et al. Oxidative remote induction of type 3 deiodinase impacts nonthyroidal illness syndrome[J]. J Endocrinol, 2020, 246(3):237-246.DOI:10.1530/joe-19-0574.
[81]
Boelen A, Kwakkel J, Thijssen-Timmer DC, et al. Simultaneous changes in central and peripheral components of the hypothalamus-pituitary-thyroid axis in lipopolysaccharide-induced acute illness in mice[J]. J Endocrinol, 2004, 182(2):315-323.DOI:10.1677/joe.0.1820315.
[82]
Debaveye Y, Ellger B, Mebis L, et al. Regulation of tissue iodothyronine deiodinase activity in a model of prolonged critical illness[J]. Thyroid, 2008, 18(5):551-560.DOI:10.1089/thy.2007.0287.
[83]
Peeters RP, Wouters PJ, Kaptein E, et al. Reduced activation and increased inactivation of thyroid hormone in tissues of critically ill patients[J]. J Clin Endocrinol Metab, 2003, 88(7):3202-3211.DOI:10.1210/jc.2002-022013.
[84]
Kwakkel J, Surovtseva OV, De Vries EM, et al. A novel role for the thyroid hormone-activating enzyme type 2 deiodinase in the inflammatory response of macrophages[J]. Endocrinology, 2014, 155(7):2725-2734.DOI:10.1210/en.2013-2066.
[85]
Boelen A, Wiersinga WM, Fliers E. Fasting-induced changes in the hypothalamus-pituitary-thyroid axis[J]. Thyroid, 2008, 18(2):123-129.DOI:10.1089/thy.2007.0253.
[86]
Everts ME, De Jong M, Lim CF, et al. Different regulation of thyroid hormone transport in liver and pituitary:its possible role in the maintenance of low T3 production during nonthyroidal illness and fasting in man[J]. Thyroid, 1996, 6(4):359-368.DOI:10.1089/thy.1996.6.359.
[87]
Jirasakuldech B, Schussler GC, Yap MG, et al. A characteristic serpin cleavage product of thyroxine-binding globulin appears in sepsis sera[J]. J Clin Endocrinol Metab, 2000, 85(11):3996-3999.DOI:10.1210/jcem.85.11.6966.
[88]
Reilly CP, Wellby ML. Slow thyroxine binding globulin in the pathogenesis of increased dialysable fraction of thyroxine in nonthyroidal illnesses[J]. J Clin Endocrinol Metab, 1983, 57(1):15-18.DOI:10.1210/jcem-57-1-15.
[89]
Costante G, Sand G, Reding P, et al. Absence of circulating desialylated thyroxine-binding globulin in patients with hepatobiliary disease[J]. Acta Endocrinol(Copenh), 1985, 108(3):392-400.DOI:10.1530/acta.0.1080392.
[90]
Bloise FF, Santos AT, De Brito J, et al. Sepsis impairs thyroid hormone signaling and mitochondrial function in the mouse diaphragm[J]. Thyroid, 2020, 30(7):1079-1090.DOI:10.1089/thy.2019.0124.
[91]
Mebis L, Debaveye Y, Ellger B, et al. Changes in the central component of the hypothalamus-pituitary-thyroid axis in a rabbit model of prolonged critical illness[J]. Crit Care, 2009, 13(5):R147.DOI:10.1186/cc8043.
[92]
Mebis L, Paletta D, Debaveye Y, et al. Expression of thyroid hormone transporters during critical illness[J]. Eur J Endocrinol, 2009, 161(2):243-250.DOI:10.1530/eje-09-0290.
[93]
Phani Kumar AC, Arepalli S, Chintalapudi V, et al. Study of thyroid function in patients admitted in intensive care unit[J]. Int J Res Med Sci, 2022, 10(8):1806-1811.DOI:10.18203/2320-6012.ijrms20223258.
[94]
Kothiwale VA, Patil P, Gaur S. Correlation of thyroid hormone profile with the acute physiology and chronic health evaluation Ⅱ score as a prognostic marker in patients with sepsis in the intensive care unit[J]. J Assoc Physicians India, 2018, 66(7):59-62.
[95]
Li X, Zhu Z, Zhou T, et al. Predictive value of combined serum FGF21 and free T3 for survival in septic patients[J]. Clin Chim Acta, 2019, 494:31-37.DOI:10.1016/j.cca.2019.03.005.
[96]
袁荆, 吴敬医, 鲁卫华, 等. 游离三碘甲状腺原氨酸联合血乳酸评估成人脓毒症患者的预后[J]. 齐齐哈尔医学院学报, 2023, 44(6):511-514.DOI:10.3969/j.issn.1002-1256.2023.06.003.
[97]
徐跃文, 陈福进, 赵晶晶, 等. 基于重症监护医学信息数据库-Ⅳ分析低三碘甲状腺原氨酸综合征与脓毒症患者病死率的相关性[J]. 临床内科杂志, 2024, 41(3):179-183.DOI:10.3969/j.issn.1001-9057.2024.03.009.
[98]
蒋天雨. 脓毒症早期甲状腺功能改变的特点及临床意义[D]. 天津: 天津医科大学, 2021.DOI:10.27366/d.cnki.gtyku.2021.000699.
[99]
Liu YC, Jiang TY, Chen ZS, et al. Thyroid hormone disorders:a predictor of mortality in patients with septic shock defined by sepsis-3[J]. Intern Emerg Med, 2021, 16(4):967-973.DOI:10.1007/s11739-020-02546-2.
[100]
Ning N, Li J, Sun W, et al. Different subtypes of nonthyroidal illness syndrome on the prognosis of septic patients:a two-centered retrospective cohort study[J]. Front Endocrinol(Lausanne), 2023, 14:1227530.DOI:10.3389/fendo.2023.1227530.
[101]
Wang S, Chen M, Sun D, et al. Total triiodothyronine level associated with disease severity for patients with emergent status[J]. Sci Rep, 2024, 14(1):17170.DOI:10.1038/s41598-024-68195-z.
[102]
Lado-Abeal J. Non-thyroidal illness syndrome,the hidden player in the septic shock induced myocardial contractile depression[J]. Med Hypotheses, 2020, 142:109775.DOI:10.1016/j.mehy.2020.109775.
[103]
Kovacevic M, Adam VN, Causevic S. Triiodothyronine hormone supplementation therapy in septic shock patients with euthyroid sick syndrome:two pilot,placebo-controlled,randomized trials[J]. Anaesth Crit Care Pain Med, 2024, 43(2):101336.DOI:10.1016/j.accpm.2023.101336.
[104]
Rocchi R, Kimura H, Tzou SC, et al. Toll-like receptor-MyD88 and Fc receptor pathways of mast cells mediate the thyroid dysfunctions observed during nonthyroidal illness[J]. Proc Natl Acad Sci U S A, 2007, 104(14):6019-6024.DOI:10.1073/pnas.0701319104.
[105]
Van Den Berghe G. Non-thyroidal illness in the ICU:a syndrome with different faces[J]. Thyroid, 2014, 24(10):1456-1465.DOI:10.1089/thy.2014.0201.
[106]
Van Den Berghe G, Wouters P, Weekers F, et al. Reactivation of pituitary hormone release and metabolic improvement by infusion of growth hormone-releasing peptide and thyrotropin-releasing hormone in patients with protracted critical illness[J]. J Clin Endocrinol Metab, 1999, 84(4):1311-1323.DOI:10.1210/jcem.84.4.5636.
[107]
Van Den Berghe G, Baxter RC, Weekers F, et al. The combined administration of GH-releasing peptide-2(GHRP-2),TRH and GnRH to men with prolonged critical illness evokes superior endocrine and metabolic effects compared to treatment with GHRP-2 alone[J]. Clin Endocrinol(Oxf), 2002, 56(5):655-669.DOI:10.1046/j.1365-2265.2002.01255.x.
[108]
Vidart J, Wajner SM, Leite RS, et al. N-acetylcysteine administration prevents nonthyroidal illness syndrome in patients with acute myocardial infarction:a randomized clinical trial[J]. J Clin Endocrinol Metab, 2014, 99(12):4537-4545.DOI:10.1210/jc.2014-2192.
PDF(935 KB)

Accesses

Citation

Detail

Sections
Recommended

/