Cortisol Response to Low-dose (1 µg) ACTH Stimulation for the Prediction of Outcome in Patients with Systemic Inflammatory Response Syndrome

Summary Background: Systemic inflammatory response syndrome (SIRS) changes cortisol dynamics and indicates dissociation between the adrenal cortex and the hypothalamo-pituitary unit. The aim of this study was to assess the cortisol response after stimulation with ACTH1-24 in patients with SIRS at admission to the Respiratory Intensive Care Unit (RICU) and seven days later. Methods: Fifty-four subjects were included in the study, and SIRS was defined according to the Consensus Conference criteria from 1992. Severity of the disease was determined using the APACHE II score, and organ dysfunction using the SOFA score. Low-dose (1 μg) ACTH test (LDT) was performed in all patients, and cortisol was determined along with basal ACTH. Data were analyzed using parametric and nonparametric tests and regression analysis. The results are presented as mean ± standard deviation, and P<0.05 was considered statistically significant. Results: There were no differences in cortisol values between the two LDTs. Cortisol increment lower than 250 nmol/L during the LDT was found in 14/54 (25.9%) subjects at the onset of SIRS. Five out of 54 (9.6%) patients died within 7 days from the onset of SIRS. Female sex and maximal cortisol response (Δ max) on LDT predicted the duration of hospitalization in RICU, while APACHE II and SOFA scores best predicted the duration of hospitalization, mortality outcome as well as overall survival outcome. Conclusions: A difference was found in Δ max at the diagnosis of SIRS and seven days later. Δ max, and primarily the clinical scores APACHE II and SOFA predicted the outcomes of hospitalization and overall survival.

• Publication year

  2016

• Venue

  Journal of Medical Biochemistry

• Publication date

  2016-10-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.1515/jomb-2016-0015PMID 28670195PMCID 5471638
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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