An update on non-thyroidal illness syndrome
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SHORT REVIEW
An update on non‑thyroidal illness syndrome E. Fliers1 · A. Boelen2 Received: 22 October 2020 / Accepted: 30 November 2020 © The Author(s) 2020
Abstract The non-thyroidal illness syndrome (NTIS) was first reported in the 1970s as a remarkable ensemble of changes in serum TH (TH) concentrations occurring in probably any severe illness. Ever since, NTIS has remained an intriguing phenomenon not only because of the robustness of the decrease in serum triiodothyronine (T3), but also by its clear correlation with morbidity and mortality. In recent years, it has become clear that (parenteral) feeding in patients with critical illness should be taken into account as a major determinant not only of NTIS but also of clinical outcome. Moreover, both experimental animal and clinical studies have shown that tissue TH concentrations during NTIS do not necessarily reflect serum low TH concentrations and may decrease, remain unaltered, or even increase according to the organ and type of illness studied. These differential changes now have a solid basis in molecular studies on organ-specific TH transporters, receptors and deiodinases. Finally, the role of inflammatory pathways in these non-systemic changes has begun to be clarified. A fascinating role for TH metabolism in innate immune cells, including neutrophils and monocytes/macrophages, was reported in recent years, but there is no evidence at this early stage that this may be a determinant of susceptibility to infections. Although endocrinologists have been tempted to correct NTIS by TH supplementation, there is at present insufficient evidence that this is beneficial. Thus, there is a clear need for adequately powered randomized clinical trials (RCT) with clinically relevant endpoints to fill this knowledge gap. Keywords TH · Low T3 syndrome · Sick euthyroid syndrome · T3 · rT3 · T4 · TRH · TSH · Deiodinase
Introduction Soon after the development of radioimmunoassays for thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH) in the 1970s, a drop in serum thyroid hormone (TH) levels was reported both during starvation and illness. In mild illness, only a decrease in serum T3 levels was seen but with increasing severity and duration of the illness there appeared to be a drop in serum T4 as well. This decrease of serum TH levels was reported in a variety of species and pathologies including sepsis, myocardial infarction, * E. Fliers [email protected] 1
Department of Endocrinology and Metabolism, Amsterdam Gastroenterology Endocrinology and Metabolism, Amsterdam UMC, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
Endocrine Laboratory, Department of Clinical Chemistry, Amsterdam Gastroenterology Endocrinology and Metabolism, Amsterdam UMC, University of Amsterdam, 1105 AZ Amsterdam, The Netherlands
2
and many more diseases. In contrast to the situation during primary hypothyroidism, however, decreased serum TH concentrations did not coincide with increased serum TSH. This typical ensemble of cha
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