Data from: Corticosteroid-binding globulin deficiency independently predicts mortality in septic shock

Context Hydrocortisone administration in septic shock remains
controversial. Corticosteroid-binding globulin (CBG) transports cortisol
to inflammatory sites and is depleted in septic shock. Objective To
determine if severely deficient serum CBG <200 nmol/L (Ref range
269-641 nmol/L) independently predicts septic shock mortality. Methods A
prospective observational study in patients with septic shock. Patients
were categorised into two groups: mean plasma CBG concentrations
<200 nmol/L and ≥200 nmol/L (day 1/2), with additional
categorisation by nadir CBG. Primary outcome was ICU mortality. Secondary
outcomes were 28- and 90-day mortality, norepinephrine requirements,
renal-replacement therapy, and clinician-instituted hydrocortisone.
Results 135 patients were included. Mortality rates in ICU were higher in
the CBG <200 nmol/L vs the CBG ≥200 nmol/L group: 32.4% vs 13.9%;
Odds ratio (OR), 2.97, (95% confidence intervals (CI) 1.19,7.41); P=0.02:
28-days; OR 2.25 (95% CI 0.99,5.11): 90-days; OR 2.21 (95% CI 0.99,4.91).
Multivariate analysis revealed 4 factors independently associated with ICU
mortality: CBG <200 nmol/L (OR 3.23, 95% CI 1.06,9.88), Acute
Physiology and Chronic Health Evaluation II >25 (OR 3.58, 95% CI
1.20,10.68); SOFA liver score (OR 1.98, 95% CI 1.04,3.72); and
renal-replacement therapy (OR 6.59, 95% CI 2.17,20.01). Nadir CBG levels
were associated with higher SOFA cardiovascular scores, norepinephrine
total dose (ug) P<0.01 and duration (days) P<0.01. Plasma
cortisol concentrations and hydrocortisone administration did not relate
to ICU mortality. Conclusion Septic shock patients with CBG <200
nmol/L had higher norepinephrine requirements and 3.2-fold higher ICU
mortality. CBG concentration was the only directly reversible independent
mortality risk factor.