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Is Thyroid Hormone Therapy Indicated for Euthyroid Sick Syndrome?« Back to Volume 26, Issue 1, September 2010 - Table of Contents From ENDO 2010 The Endocrine Society Annual Meeting, San Diego, June 19-22, 2010 Greet Van de Berghe (pro side, Catholic University of Leuven, Belgium) and Elaine Kaptein (con side, University of Southern California, Los Angeles, USA) debated the use of thyroid hormone therapy for patients with euthyroid sick syndrome (ESS). The debaters discussed four randomized-controlled trials in ICU patients with prolonged illness treated with thyroid hormone replacement (a total of 190 patients with ESS). Two of the trials used T3 and two trials used T4 for the treatment. The T3 trials showed no change in mortality, while the T4 trials showed no change or an increase in mortality. Additionally, in an extensive literature review there were 35 non-randomized controlled studies of thyroid hormone therapy in ESS. For the most part, the results of all 35 trials were inconclusive. All used T3 and/or T4 as the active therapy agent. However, the sample size was much too small; for example an ICU study with 23 patients would have needed 142 patients to show statistically significant results. Also the doses of thyroid hormone used in the studies were high, and the wrong hormone may have been utilized. In addition, the effects of malnutrition, medications and other therapies may have played an important role in the outcome of ESS. Sick patients often fast and their nutrition is poor, this depresses serum T3 levels; proper nutrition quickly corrects the circulating thyroid hormone balance. It was suggested that a combination of thyrotropin-releasing hormone (TRH) plus growth-hormone-releasing peptide (GHRP) may provide benefits in prolonged, critically ill patients. The combination of TRH plus GHRP treatment to correct thyroid hormone levels seemed the most successful in the patients who were receiving adequate nutrition. There were 14 studies in ESS patients with obesity and calorie restriction, but there were no definitive beneficial effects demonstrated in any of them. Seven other studies of patients with abnormal thyroid findings suggestive of ESS, in various clinical conditions that were treated with thyroid hormone, showed inconsistent results, though one study in patients with coronary artery disease showed decreased systemic vascular resistance. Another study showed an increase in mortality from acute renal failure. Of the 14 studies performed in postoperative ESS patients who received thyroid hormone therapy, 13 were inconclusive and one showed an increase in cardiac index. A small study in burn patients (14 patients in each group) showed no therapeutic effect, however it would have needed 313 patients in each arm to detect significance. The evidence in favor of thyroid hormone treatment for ESS is equivocal at best and may increase mortality. Thus, in order to determine the therapy effectiveness and safety in ESS, randomized-controlled trials with adequate sample size and appropriate endpoints are needed. Van de Berghe G, Kaptein E. Catholic University of Leuven, Belgium; University of Southern California, Los Angeles, USA Editor's CommentEuthyroid sick syndrome, also known as low FT3 syndrome, has a high prevalence in hospitalized patients. In a recent study Iglesias et al described the alterations in thyroid hormone levels in up to 85% of patients.1 In obese patients, alterations in thyroid hormone levels are often detected. These may reflect ESS related to dietary intake or other factors, not the cause of weight gain or obesity. In premature infants and infants in the NICU, these circulating thyroid hormone alterations are also prevalent; although the debate did not address this issue, it is one of great interest to pediatric endocrinologists. The experimental treatment with TRH and GHRP appeared to improve the circulating thyroid hormones in some patients without other measurable benefits. ESS may be a defense against oxidative stress leading to lower energy expenditures and calorie sparing. This results from a number of homeostatic adaptations in sick patients ie, an increase in glutathione peroxidase, selenium, deiodinase activity type 3, and cytokine interleukin (IL)-6. These lead to decreasing the activation of T4 and the lowering of T3 levels. Thus, it may be inappropriate to alter the homeostatic process in sick patients with thyroid hormone treatment. The data suggest that there may be no measurable benefit and there may be increased risks - so, why treat? Fima Lifshitz, MD Reference - (linked to
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Volume 26 Number 1
September 2010
www.GGHjournal.com
ISSN 1932-9032
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