title: Hypothalamic-pituitary-adrenal axis function in ankylosing spondylitis.
abstract: OBJECTIVE
  To assess basal function and responsiveness of the hypothalamic-pituitary-adrenal (HPA) axis in patients with ankylosing spondylitis during dynamic testing.
  
  
  METHODS
  Insulin induced hypoglycaemia (IIH) (Actrapid HM 0.1 IU/kg, as intravenous bolus) was induced in 17 patients and 11 healthy controls matched for age, sex, and body mass index. Concentrations of glucose, adrenocorticotrophic hormone (ACTH), cortisol, insulin, dehydroepiandrosterone sulphate (DHEAS), 17alpha-hydroxyprogesterone, interleukin 6 (IL-6), and tumour necrosis factor alpha (TNFalpha) were determined in plasma.
  
  
  RESULTS
  Comparable basal cortisol levels were found in the two groups, with a trend to be lower in ankylosing spondylitis. In the ankylosing spondylitis group, there were higher concentrations of IL-6 (mean (SEM): 16.6 (2.8) pg/ml v 1.41 (0.66) pg/ml in controls; p<0.001) and TNFalpha (8.5 (1.74) pg/ml v 4.08 (0.42) pg/ml in controls; p<0.01). Glucose, insulin, ACTH, DHEAS, and 17alpha-hydroxyprogesterone did not differ significantly from control. The IIH test was carried out successfully in 11 of the 17 patients with ankylosing spondylitis, and the ACTH and cortisol responses were comparable with control. General linear modelling showed a different course of glycaemia (p = 0.041) in the ankylosing spondylitis patients who met the criteria for a successful IIH test compared with the controls.
  
  
  CONCLUSIONS
  The results suggest there is no difference in basal HPA axis activity and completely preserved responsiveness of the HPA axis in patients with ankylosing spondylitis. The interpretation of the different course of glycaemia during IIH in ankylosing spondylitis requires further investigation.
authors.affiliation: Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 833 06 Bratislava, Slovakia. richard.imrich@savba.sk
authors.forename: R
authors.initials: R
authors.lastname: Imrich
authors.forename: J
authors.initials: J
authors.lastname: Rovensky
authors.forename: M
authors.initials: M
authors.lastname: Zlnay
authors.forename: Z
authors.initials: Z
authors.lastname: Radikova
authors.forename: L
authors.initials: L
authors.lastname: Macho
authors.forename: M
authors.initials: M
authors.lastname: Vigas
authors.forename: J
authors.initials: J
authors.lastname: Koska
mesh_terms: D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000328:Adult; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D001786:Blood Glucose / Q000032:analysis; D016022:Case-Control Studies; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000502:physiology; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D010913:Pituitary-Adrenal System / Q000502:physiology*; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001786:Blood Glucose; D007328:Insulin; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone