title: Adrenocortical hormones in survivors and nonsurvivors of severe sepsis: diverse time course of dehydroepiandrosterone, dehydroepiandrosterone-sulfate, and cortisol.
abstract: OBJECTIVE
  Activation and suppression of immune responses are crucial events during sepsis. Based on substantial new data, a complex picture of differential immune-enhancing and immunosuppressive actions of adrenocortical steroids is emerging. The adrenal androgen dehydroepiandrosterone and its precursor, dehydroepiandrosterone-sulfate, show a considerable decrease with increasing age and serve as functional antagonists to endogenous glucocorticoids. Therefore, we examined time-dependent changes in dehydroepiandrosterone, dehydroepiandrosterone-sulfate, cortisol, adrenocorticotropin, and inflammatory variables in surviving and nonsurviving patients with severe sepsis.
  
  
  METHODS
  Prospective observational study in consecutive patients.
  
  
  METHODS
  Medical and interdisciplinary intensive care units in two university hospitals and one city hospital.
  
  
  METHODS
  Thirty nonsurgical patients (25 men and 5 women) with severe sepsis (American College of Chest Physicians/Society of Critical Care Medicine criteria); 15 survivors (mean age, 54 +/- 14 yrs; Acute Physiology and Chronic Health Evaluation III score, 59 +/- 35) and 15 nonsurvivors (mean age, 63 +/- 15 yrs; Acute Physiology and Chronic Health Evaluation III score, 67 +/- 24) were included. Hormones were compared individually and between survivors/nonsurvivors by sequential blood drawings from early sepsis till time of recovery/death.
  
  
  METHODS
  None.
  
  
  RESULTS
  During early sepsis, cortisol (nmol/L) was not significantly higher in survivors than nonsurvivors (750 +/- 121 vs. 454 +/- 92, p <.08) and decreased in survivors (p <.01) during late sepsis. During early sepsis, dehydroepiandrosterone-sulfate (percentage of age-matched normal levels) was higher in survivors than nonsurvivors (85 +/- 19 vs. 22 +/- 7, p <.01). Dehydroepiandrosterone-sulfate decreased in survivors (p =.0001) but remained low in nonsurvivors during late sepsis. Dehydroepiandrosterone (percentage of age-matched normal levels) was not significantly elevated in survivors compared to nonsurvivors during early sepsis (282 +/- 42 vs. 214 +/- 63, p <.08). Dehydroepiandrosterone decreased in survivors (p <.01) but not in nonsurvivors during late sepsis. Linear regression for dehydroepiandrosterone levels showed a reconstitution of age dependence only in survivors during recovery. Adrenocorticotropin levels did not change. The dehydroepiandrosterone-sulfate/cortisol ratio decreased significantly in both survivors and nonsurvivors, whereas dehydroepiandrosterone/cortisol ratio only decreased in survivors during course of sepsis.
  
  
  CONCLUSIONS
  During sepsis, adrenal androgens and glucocorticoids show a diverse time-dependent course in survivors and nonsurvivors.
authors.affiliation: Department of Internal Medicine I, University Hospital Carl Gustav Carus, Technical University Dresden, Germany. marx@mk1.med.tu-dresden.de
authors.forename: Christian
authors.initials: C
authors.lastname: Marx
authors.forename: Sirak
authors.initials: S
authors.lastname: Petros
authors.forename: Stefan R
authors.initials: SR
authors.lastname: Bornstein
authors.forename: Matthias
authors.initials: M
authors.lastname: Weise
authors.forename: Matthias
authors.initials: M
authors.lastname: Wendt
authors.forename: Mario
authors.initials: M
authors.lastname: Menschikowski
authors.forename: Lothar
authors.initials: L
authors.lastname: Engelmann
authors.forename: Gert
authors.initials: G
authors.lastname: Höffken
mesh_terms: D018806:APACHE; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000276:immunology; D000367:Age Factors; D000368:Aged; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D002116:Calcitonin / Q000097:blood / Q000276:immunology; D003687:Dehydroepiandrosterone / Q000097:blood* / Q000276:immunology; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood* / Q000276:immunology; D005260:Female; D005938:Glucocorticoids / Q000037:antagonists & inhibitors; D006801:Humans; D006854:Hydrocortisone / Q000097:blood* / Q000276:immunology; D007249:Inflammation; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011498:Protein Precursors / Q000097:blood / Q000276:immunology; D012307:Risk Factors; D018805:Sepsis / Q000097:blood* / Q000276:immunology / Q000401:mortality*; D016019:Survival Analysis; D013997:Time Factors
chemical_list: D005938:Glucocorticoids; D011498:Protein Precursors; D003687:Dehydroepiandrosterone; D019314:Dehydroepiandrosterone Sulfate; D000324:Adrenocorticotropic Hormone; D002116:Calcitonin; D002097:C-Reactive Protein; D006854:Hydrocortisone