title: Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease.
abstract: OBJECTIVE
  Dehydroepiandrosterone sulfate (DHEAS) and cortisol are multifunctional adrenal hormones with immunomodulating properties. DHEAS levels were found to be very low in chronic inflammatory diseases. This study aimed to shed more light on the interrelation between DHEAS and cortisol (and humoral markers of inflammation) in chronic inflammatory bowel disease.
  
  
  METHODS
  DHEAS and cortisol serum levels were measured by ELISA in the serum of 66 normal subjects, 115 patients with Crohn's disease (CD) and 64 patients with ulcerative colitis (UC). Humoral markers of inflammation and disease activity scores were assessed by standard techniques.
  
  
  RESULTS
  DHEAS was lower in patients with CD (p < 0.005) and UC (p < 0.005) than in controls, which was, in part, dependent on previous corticosteroid treatment (p < 0.01). In CD patients, z-normalized DHEAS was inversely correlated with blood sedimentation rate (p = 0.017). Z-normalized DHEAS was negatively correlated with interleukin-6 (IL-6) in the form of a trend (p = 0.068), and z-normalized DHEAS was significantly positively correlated with hemoglobin (p = 0.001) but not with the Crohn's disease activity index. Cortisol, however, was positively correlated with blood sedimentation rate (p = 0.034) and C-reactive protein (p = 0.006). In contrast, in UC patients no such correlation of z-normalized DHEAS or cortisol and parameters of humoral inflammatory activity or Rachmilewitz index exist.
  
  
  CONCLUSIONS
  DHEAS as a marker of inflammation was low in CD and UC. In CD patients, low DHEAS and high cortisol serum levels were associated with higher humoral inflammatory activity. With respect to humoral inflammatory activity in CD patients, DHEAS and cortisol seem to be inversely regulated, which may have an impact on several immune functions, such as IL-6 secretion.
authors.affiliation: Department of Internal Medicine I, University Medical Center, Regensburg, Germany.
authors.forename: R H
authors.initials: RH
authors.lastname: Straub
authors.forename: D
authors.initials: D
authors.lastname: Vogl
authors.forename: V
authors.initials: V
authors.lastname: Gross
authors.forename: B
authors.initials: B
authors.lastname: Lang
authors.forename: J
authors.initials: J
authors.lastname: Schölmerich
authors.forename: T
authors.initials: T
authors.lastname: Andus
mesh_terms: D000293:Adolescent; D000328:Adult; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000032:analysis; D015815:Cell Adhesion Molecules / Q000032:analysis; D003093:Colitis, Ulcerative / Q000097:blood; D003424:Crohn Disease / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood*; D018836:Inflammation Mediators / Q000097:blood*; D015212:Inflammatory Bowel Diseases / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors; D015375:Receptors, Interleukin-2 / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015815:Cell Adhesion Molecules; D018836:Inflammation Mediators; D015850:Interleukin-6; D017472:Receptors, Interleukin-1; D015375:Receptors, Interleukin-2; D014409:Tumor Necrosis Factor-alpha; D019314:Dehydroepiandrosterone Sulfate; D002097:C-Reactive Protein; D006854:Hydrocortisone