Volume 17 Supplement 3
Effect of N-acetylcysteine on serum thyroid hormone levels in nonthyroidal illness syndrome
© Vidart et al; licensee BioMed Central Ltd. 2013
Published: 19 June 2013
Nonthyroidal illness syndrome (NTIS) refers to changes in thyroid hormone levels affecting up to 75% of critically ill patients. Cytokines and oxidative stress have been implicated as causative factors, as they derange deiodinase reactions. Interestingly, the addition of N-acetylcysteine (NAC) in a cell model prevented the effect of IL-6 on deiodinases, probably through a mechanism that restores catalytic activity of the enzyme . NTIS is an independent marker of poor prognosis during myocardial infarction (MI) . Here, we investigate whether NAC administration would prevent the decrease in serum thyroid hormone levels observed in patients with MI.
This was a randomized, multicenter clinical trial. Patients with MI within 12 hours of evolution who underwent primary percutaneous coronary intervention were eligible. Patients were randomized to receive NAC (1,200 mg, intravenous, every 12 hours) or placebo for 48 hours. Baseline characteristics, clinical history and serial blood samples for measurements of thyroid hormones were collected. Primary outcome was the variation of serum T3 levels. Statistical tests used included χ2 test analyses for proportions and Student's t test analyses for means.
This is the first clinical trial designed to investigate the effect of NAC on NTIS in humans. We show that patients with myocardium infarction who received NAC treatment on admission had attenuation of the degree of T3 level decrease compared with those who received placebo. As expected, NAC did not interfere with central feedback, as TSH levels presented a similar rise in both groups, probably as a marker of recovery from acute illness. However, whether this effect is able to prevent mortality or to ameliorate patient outcome remains to be elucidated.
Clinical Trials: NCT01501110.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.