Objective: Thyroxine (T4) is deiodinated to triiodothyronine (T3) by the hepatic type I iodothyronine deiodinase, a selenoprotein that is sensitive to selenium (Se) deficiency. After severe injury, T4 deiodination is decreased, leading to the low T3 syndrome. Injury increases free radical production, which inactivates the iodothyronine deiodinase. The aims were to study the Se status after major trauma and to investigate its relation to the low T3 syndrome.
Design: Preliminary prospective descriptive study.
Setting: Intensive care unit at a university teaching hospital.
Patients and methods: 11 patients aged 41 +/- 4 years (mean +/- SEM), with severe multiple injuries (Injury Severity Score 29 +/- 2 points). A balance study was performed from day 1 to day 7. Serum and urine samples were collected from the time of admission until day 7, then on days 10, 15, 20, 25 and 30. Non-parametric tests and Pearson's correlation coefficients were used for analysis.
Results: Cumulated Se losses were 0.88 +/- 0.1 mumol/24h. Serum Se was decreased from admission to day 7. T3, free T3, and the T3/T4 ratio were low until day 5, being lowest on day 2; T4 and thyroid stimulating hormone were normal. Serum Se was correlated with T3 (r = 0.55, p = 0.0001), and with free T3 (r = 0.35).
Conclusion: Se status is altered after trauma, with decreased Se serum levels upon admission to the ICU but with no major Se losses. Se is probably redistributed to the tissues. The correlation between Se and T3, along with the parallel decrease in T4 deiodination, indicates that reduced deiodination might be related to the transient decrease in serum Se.