Objective:Thyroxine (T-4) is deiodinated to triiodothyronine (T-3) by
the hepatic type I iodothyronine deiodinase, a selenoprotein that is s
ensitive to selenium (Se) deficiency. After severe injury, T-4 deiodin
ation is decreased, leading to the low T-3 syndrome. Injury increases
free radical production, which inactivates the iodothyronine deiodinas
e. The aims were to study the Se status after major trauma and to inve
stigate its relation to the low T-3 syndrome. Design: Preliminary pros
pective descriptive study. Setting: Intensive care unit at a universit
y teaching hospital. Patients and methods: 11 patients aged 41 +/- 4 y
ears (mean +/- SEM), with severe multiple injuries (Injury Severity Sc
ore 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 unt
il day 7, then on days 10, 15, 20, 25 and 30. Nonparametric tests and
Pearson's correlation coefficients were used for analysis. Results: Cu
mulated Se losses were 0.88+/-0.1 mu mol/24 h. Serum Se was decreased
from admission to day 7. T-3, free T-3, and the T-3/T-4 ratio were low
until day 5, being lowest on day 2; T-4 and thyroid stimulating hormo
ne were normal. Serum Se was correlated with T-3 (r = 0.55, p = 0.0001
), and with free T-3 (r = 0.35). Conclusion: Se status is altered afte
r 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 T-3, along with the parallel decrease
in T-4 deiodination, indicates that reduced deiodination might be rela
ted to the transient decrease in serum Se.