Critical Care Medicine:
June 2016 -
Volume 44 - Issue 6 - p 1034–1041
Cohen, J et al
Objectives: To measure tissue glucocorticoid sensitivity in
patients with septic shock and determine its relationship to standard
measurements of adrenal function and of outcome. Design: Prospective observational
trial. Setting: Teaching hospital ICU. Subjects: Forty-one patients and 20
controls were studied. Interventions: Glucocorticoid sensitivity was measured
by in vitro suppression of cytokine production from
lipopolysaccharide-stimulated leukocytes. Measurements and Main Results: There
was no significant difference between the groups in the relative suppression of
cytokine production, although there was a greater range and variance in the
patient data. Patients in the lowest quartile of glucocorticoid sensitivity had
higher Acute Physiology and Chronic Health Evaluation II scores (25 [24–28] vs
20 [14–23]; p = 0.02) and a trend toward higher mortality (30% vs 0%; p = 0.2)
compared to those in the highest. The mRNA expression of the β variant of the glucocorticoid
receptor and the 11-β hydroxysteroid dehydrogenase 2 isozyme were significantly
higher in patients compared to controls (8.6-fold, p = 0.002 and 10.1-fold, p =
0.0002, respectively). Changes in mRNA expression of these genes did not
correlate with measurements of glucocorticoid sensitivity. Conclusions:
Patients with septic shock and controls do not differ in their median
glucocorticoid sensitivity. However, patients exhibited a greater variability
in glucocorticoid responsiveness and had evidence of association between
increased sickness sensitivity and reduced glucocorticoid sensitivity.
Sensitivity to glucocorticoids did not appear to be mediated by changes in the
expression of the β variant of the glucocorticoid receptor or the 11-β hydroxysteroid
dehydrogenase 2 isozyme.
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