Prognostic Value of Serum Cortisol, DHEA, and SOFA Score in Adult Sepsis Patients: A Retrospective Single-Center...

Background/Objectives: Sepsis and septic shock remain leading causes of morbidity and mortality in intensive care units (ICUs) worldwide. While activation of the hypothalamic-pituitary-adrenal (HPA) axis is a vital adaptive response, the dissociation between cortisol and adrenal androgens like dehydroepiandrosterone (DHEA) is hypothesized to correlate with poor outcomes. This study aimed to evaluate the prognostic value of serum cortisol, DHEA, and the Cortisol/DHEA ratio in patients with sepsis admitted to the ICU. Methods: Clinical and laboratory data from 106 adult sepsis patients in a tertiary care hospital were retrospectively analyzed. Disease severity was assessed using Sequential Organ Failure Assessment (SOFA), Acute Physiology and Chronic Health Evaluation II (APACHE II), and Glasgow Coma Scale (GCS) scores. Baseline cortisol and DHEA levels were measured at the time of diagnosis. Logistic regression and Cox proportional hazards models were employed to identify predictors of in-hospital mortality and time to death, respectively. Results: A total of 106 adult sepsis patients with a mean age of 73.63 ± 13.70 years (55 female, 51.9%) were included in the study population. In the final logistic regression model, higher SOFA score was associated with greater odds of in-hospital mortality Odds ratio (OR) = 1.39 per 1-point increase, 95% Confidence interval (CI): 1.15-1.69, p < 0.001). Higher platelet count (PLT) was associated with lower odds of mortality (OR = 0.958 per 10 × 10⁹/L increase, 95% CI: 0.919-0.998, p = 0.042), whereas higher urea was associated with greater odds of mortality (OR = 1.112 per 10 mg/dL increase, 95% CI: 1.020-1.212, p = 0.016). The model area under the curve (AUC) was 0.7956. In univariable Cox analysis, higher baseline DHEA was associated with a greater hazard of death (Hazard ratio (HR) = 1.03, 95% CI: 1.014-1.046, p = 0.0002). In the final multivariable Cox proportional hazards model, baseline cortisol remained independently associated with the hazard of death (HR = 1.014, 95% CI: 1.007-1.022, p < 0.001), whereas DHEA was not retained. Notably, the Cortisol/DHEA ratio did not demonstrate independent prognostic value in either modeling approach. Conclusions: Higher baseline DHEA levels were associated with an increased hazard of death in univariable Cox proportional hazards analysis but did not retain independent prognostic significance in the final multivariable Cox proportional hazards model. While SOFA score remains the central prognostic tool, integrating continuous markers such as platelets and urea enhances risk stratification. The Cortisol/DHEA ratio offers no incremental prognostic utility over established clinical parameters.